Inputs
Defining mutations, FLT3, cytogenetics, sAML genes, disease context, age and MRD.
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Delphi Poll AML Treatment Explorer
Algorithm and lookup sheet
A complete explanation of how the explorer turns clinical selections into ELN context, workbook flags, consensus-case matching and displayed treatment guidance.
279Workbook rows
30Direct recommendation rows
249Similar-case rows
26Current scenario cards
26Direct scenario rows
End-to-end decision flow
Normalisation
Selections are converted into workbook flags and a separate ELN 2022 context input.
Cytogenetic branch
One primary cytogenetic category is selected; complex and monosomal are stored as modifiers.
Workbook lookup
The resolver searches the static Delphi poll workbook rows for an exact flag combination.
Recommendation source
Direct treatment fields are used when present; otherwise a populated Similar Case row borrows that case’s recommendation.
Result
Preferred treatment, reasonable treatments, transplant text, Ven-Aza/non-intensive text, trial/funding notes, and explanatory trace are displayed.
Branching principles
No cytogenetics
If cytogenetics are unavailable, the calculator shows provisional ELN context but does not force a Coats case.
Defining biology
CBF, NPM1, CEBPA bZIP, DDX41, TP53, KMT2A and MECOM-related flags remain explicit in lookup matching.
Intermediate branch
Normal and other non-adverse cytogenetics route through the intermediate-karyotype flag; DNMT3A refines NPM1 + FLT3-ITD rows.
Adverse branch
MDS-associated, KMT2A adverse, MECOM/other adverse and complex/monosomal modifiers are represented as separate flags.
No exact match
If the selected combination is not represented in the lookup table and no workbook Similar Case applies, no treatment recommendation is extrapolated.
Cytogenetics engine
Cytogenetics model
The calculator treats cytogenetics as a controlled decision model: status first, one primary branch, then separate complex/three-or-more and monosomal modifiers where clinically eligible.
Available cytogenetics opens the branch selector. Unavailable cytogenetics prevents Coats case forcing and shows provisional ELN context only.
Exactly one primary cytogenetic branch can be active. Other primary options are greyed out until the selected branch is cleared.
Complex/three-or-more and monosomal karyotype are captured separately. They are not part of the non-adverse trisomy branch.
CBF and KMT2A remain biologically controlling when a complex modifier is present; the lookup uses workbook similar-case guidance where supplied.
Complex or monosomal karyotype can matter, but it should not accidentally convert CBF AML or KMT2A AML into a generic adverse branch when the workbook keeps the primary biology in control.
APL, BCR::ABL, other non-adverse MDS-associated cytogenetics and other adverse are visible for transparency when not yet polled or not currently selectable for this consensus calculator.
Mutation and context inputs
Inputs are converted into Boolean workbook flags. sAML mutations are counted as present when any of the listed genes are selected; DNMT3A is used only for the NPM1 + FLT3-ITD refinement branch.
NPM1TP53DDX41CEBPA bZIPFLT3-ITDFLT3-TKDDNMT3AASXL1BCOREZH2SF3B1SRSF2STAG2U2AF1ZRSR2RUNX1
Lookup matching
The page converts selected findings into workbook flags, searches for an exact static lookup row, then uses direct recommendation text or a workbook Similar Case reference. No match means no treatment recommendation is extrapolated.
Profile flags+Workbook row=Direct or borrowed recommendation
Cytogenetics decision guardrails
Report status
Choose available or unavailable. Unavailable prevents Coats case forcing.
Primary category
Choose one primary category only: normal, CBF, t(9;11), other KMT2A, MDS-associated, MECOM/other adverse, or other non-adverse.
Incompatibility guard
Once a primary branch is chosen, incompatible primary branches are greyed out until the branch is cleared.
Modifier prompt
For eligible primary branches, the separate prompt asks whether complex/three-or-more or monosomal karyotype is also reported.
Clinical exception
Complex/three-or-more does not make CBF or KMT2A become generic adverse for Coats lookup; the primary biology remains controlling.
Scenario layer
Current consensus scenarios
These are the scenario-labelled rows represented in the current workbook-driven lookup. Older 2+ sAML scenario labels are documented separately below because the updated workbook uses a present/absent sAML flag.
Scenario 01CBF AML (Core Binding Factor)~10%
Preferred: DA+gemtuzumab - strong consensus
Flags: Core binding factor AML
strong consensusmoderate consensus
Scenario 02NPM1 favourable risk~13%
Preferred: DA + gemtuzumab - strong consensus
Flags: Intermediate cytogenetics, NPM1
strong consensusmoderate consensus
Scenario 03NPM1 favourable with FLT3-TKD~2.25%
Preferred: DA+midostaurin - moderate consensus
Flags: Intermediate cytogenetics, NPM1, FLT3-TKD
moderate consensusstrong consensus
Scenario 04NPM1 with secondary AML mutation~1.5%
Preferred: DA+gemtuzumab - strong consensus
Flags: Intermediate cytogenetics, sAML mutation present, NPM1
strong consensusmoderate consensus
Scenario 06NPM1 AML arising from prior MDS<1%
Preferred: No consensus on preferred treatment
Flags: Intermediate cytogenetics, NPM1, Prior MDS
strong consensusstrong consensusstrong consensus
Scenario 07Therapy-related AML with NPM1~0.75%
Preferred: DA + gemtuzumab - moderate consensus
Flags: Intermediate cytogenetics, NPM1, Therapy-related AML
moderate consensusstrong consensusstrong consensusstrong consensus
Scenario 08CEBPA bZIP mutation~7%
Preferred: DA + gemtuzumab - strong consensus
Flags: Intermediate cytogenetics, CEBPA bZIP
strong consensusmoderate consensus
Scenario 09Intermediate cytogenetics AML~1%
Preferred: DA+ gemtuzumab - strong consensus
Flags: Intermediate cytogenetics
strong consensus
Scenario 10Intermediate cytogenetics: NPM1 + FLT3-ITD, wild-type DNMT3A~7%
Preferred: No consensus for preferred treatment
Flags: Intermediate cytogenetics, NPM1, FLT3-ITD
strong consensusstrong consensus
Scenario 11Intermediate cytogenetics: NPM1 + FLT3-ITD + DNMT3A~8%
Preferred: DA + quizartinib - moderate consensus
Flags: Intermediate cytogenetics, NPM1, FLT3-ITD, DNMT3A
moderate consensusstrong consensusstrong consensus
Scenario 12Intermediate cytogenetics with FLT3-ITD only~12%
Preferred: No consensus on preferred treatment
Flags: Intermediate cytogenetics, FLT3-ITD
strong consensusstrong consensus
Scenario 13Intermediate cytogenetics with FLT3-TKD~5%
Preferred: DA + midostaurin - strong consensus
Flags: Intermediate cytogenetics, FLT3-TKD
strong consensusmoderate consensus
Scenario 14Intermediate cytogenetics with FLT3-ITD and TKD~1%
Preferred: DA + midostaurin - strong consensus
Flags: Intermediate cytogenetics, FLT3-ITD, FLT3-TKD
strong consensus
Scenario 15Intermediate cytogenetics with therapy-related AML~5%
Preferred: CPX-351 - moderate consensus
Flags: Intermediate cytogenetics, Therapy-related AML
moderate consensusstrong consensusmoderate consensus
Scenario 16t(9;11) KMT2A rearrangement~1%
Preferred: FLAG-Ida - moderate consensus
Flags: KMT2A::MLLT3 t(9;11)
moderate consensusstrong consensusstrong consensus
Scenario 17Adverse KMT2A rearrangement~1%
Preferred: FLAG-Ida - strong consensus
Flags: Other KMT2A rearranged
strong consensus
Scenario 18Complex or MDS-associated karyotype, wild-type TP53~4%
Preferred: CPX - moderate consensus
Flags: MDS-associated adverse cytogenetics
moderate consensusstrong consensusstrong consensus
Scenario 19Complex or MDS-associated karyotype with TP53 mutation~10%
Preferred: No consensus on preferred treatment
Flags: MDS-associated adverse cytogenetics, TP53, Complex / monosomal modifier
strong consensusstrong consensus
Scenario 20Intermediate cytogenetics with secondary AML mutation~4%
Preferred: No consensus on preferred treatment
Flags: Intermediate cytogenetics, sAML mutation present
strong consensusmoderate consensus
Scenario 22Adverse karyotype with NPM1<1%
Preferred: No consensus on preferred treatment
Flags: MDS-associated adverse cytogenetics, NPM1
strong consensusmoderate consensus
Scenario 23Adverse karyotype with FLT3-ITD<1%
Preferred: DA+ quizartinib - moderate consensus
Flags: MDS-associated adverse cytogenetics, FLT3-ITD
moderate consensusstrong consensusmoderate consensus
Scenario 24Adverse karyotype with FLT3-TKD<1%
Preferred: No consensus on preferred treatment
Flags: MDS-associated adverse cytogenetics, FLT3-TKD
strong consensusstrong consensus
Scenario 25Secondary AML with FLT3-ITD<1%
Preferred: DA + quizartinib - moderate consensus
Flags: Intermediate cytogenetics, sAML mutation present, FLT3-ITD
moderate consensusstrong consensusstrong consensus
Scenario 26Secondary AML with FLT3-TKD<1%
Preferred: DA + midostaurin - moderate consensus
Flags: Intermediate cytogenetics, sAML mutation present, FLT3-TKD
moderate consensusstrong consensusstrong consensus
Scenario 27GATA2::MECOM or other adverse karyotype~2%
Preferred: FLAG-Ida - strong consensus
Flags: Other adverse / MECOM
strong consensus
Scenario 28DDX41 mutation~5%
Preferred: DA+ gemtuzumab - strong consensus
Flags: Intermediate cytogenetics, DDX41
strong consensus
Current workbook handling: NPM1 + any sAML mutation is represented by Scenario 4.
The updated lookup rows do not carry a distinct scenario for 2+ sAML mutations; the static flags contain sAML mutation present/absent rather than a mutation-count category.Current workbook handling: intermediate cytogenetics + any sAML mutation is represented by Scenario 20.
The updated lookup rows do not carry a distinct scenario for 2+ sAML mutations; the static flags contain sAML mutation present/absent rather than a mutation-count category.Worked examples
Example case traces
These examples show the intended behaviour for common and edge-case combinations, including complex/three-or-more modifiers.
CBF AML with complex/three-or-more abnormalities
- Core binding factor selected
- Complex karyotype / 3+ abnormalities modifier selected
- No TP53 or DDX41
Routes through the CBF pathway and borrows the direct recommendation from Scenario 1 when the exact modifier combination has no treatment fields.
Other KMT2A rearranged with complex karyotype
- Other KMT2Ar AML selected
- Complex/monosomal modifier selected
- No DDX41 or TP53
Keeps the adverse KMT2A biology and uses the workbook similar-case guidance rather than a generic adverse fallback.
NPM1 + FLT3-ITD with DNMT3A
- NPM1 detected
- FLT3-ITD detected
- Intermediate cytogenetics
- DNMT3A detected
Resolves to the DNMT3A-refined NPM1 + FLT3-ITD consensus scenario when the workbook flags match.
CEBPA bZIP with normal cytogenetics
- CEBPA bZIP detected
- FLT3 not detected
- Normal cytogenetics
- De novo AML
Matches the CEBPA bZIP consensus case and shows direct preferred treatment, reasonable treatment, transplant and non-intensive guidance.
Incomplete cytogenetics
- Molecular findings entered
- Cytogenetics unavailable
Shows provisional ELN 2022 risk context but does not invent a Delphi poll treatment case.
Recommendation rows
Direct recommendation table
Rows below contain direct treatment or transplant text in the workbook. Other rows may borrow from these via Similar Case.
| Row | Case | Scenario | Flags | Preferred | Reasonable | Trial / funding / age |
|---|---|---|---|---|---|---|
| 2 | 13313 | 1 | Core binding factor AML | DA+gemtuzumab - strong consensus | No other treatments reasonable (moderate consensus) | Trial: No | Non-NHS: No | Age: No |
| 3 | 513 | 2 | Intermediate cytogenetics, NPM1 | DA + gemtuzumab - strong consensus | FLAG-Ida (moderate consensus) | Trial: VICTOR | Non-NHS: FLAG-Ida-GO | Age: No |
| 4 | 641 | 3 | Intermediate cytogenetics, NPM1, FLT3-TKD | DA+midostaurin - moderate consensus | DA+ midostaurin (strong consensus) | Trial: Optimise FLT3 | Non-NHS: No | Age: No |
| 5 | 1537 | 4 | Intermediate cytogenetics, sAML mutation present, NPM1 | DA+gemtuzumab - strong consensus | FLAG-Ida (moderate consensus) | Trial: VICTOR | Non-NHS: Possibly FLAG-Ida-GO | Age: No |
| 6 | 517 | 6 | Intermediate cytogenetics, NPM1, Prior MDS | No consensus on preferred treatment | DA+ gemtuzumab (strong consensus), FLAG-Ida (strong consensus), CPX (strong consensus) | Trial: No | Non-NHS: Possibly FLAG-Ida-GO | Age: Yes (CPX favoured in over 60s, FLAG-Ida in younger patients) |
| 7 | 515 | 7 | Intermediate cytogenetics, NPM1, Therapy-related AML | DA + gemtuzumab - moderate consensus | DA+ gemtuzumab (strong consensus), FLAG-Ida (strong consensus), CPX (strong consensus) | Trial: No | Non-NHS: Possibly FLAG-Ida-GO | Age: Yes (FLAG-Ida less favoured in older patients) |
| 8 | 65 | 8 | Intermediate cytogenetics, CEBPA bZIP | DA + gemtuzumab - strong consensus | No other treatments reasonable (moderate consensus) | Trial: No | Non-NHS: No | Age: No |
| 9 | 1 | 9 | Intermediate cytogenetics | DA+ gemtuzumab - strong consensus | No consensus on use of alternative treatments | Trial: No | Non-NHS: No | Age: No |
| 10 | 769 | 10 | Intermediate cytogenetics, NPM1, FLT3-ITD | No consensus for preferred treatment | DA + midostaurin (strong consensus), DA + quizartinib (strong consensus) | Trial: Optimise FLT3 | Non-NHS: FLAG-Ida-GO | Age: No |
| 11 | 777 | 11 | Intermediate cytogenetics, NPM1, FLT3-ITD, DNMT3A | DA + quizartinib - moderate consensus | DA + quizartinib (strong consensus), DA + midostaurin (strong consensus) | Trial: Optimise FLT3 | Non-NHS: Possibly FLAG-Ida-GO | Age: No |
| 12 | 257 | 12 | Intermediate cytogenetics, FLT3-ITD | No consensus on preferred treatment | DA + quizartinib (strong consensus), DA + midostaurin (strong consensus) | Trial: Optimise FLT3 | Non-NHS: Possibly FLAG-Ida-GO | Age: No |
| 13 | 129 | 13 | Intermediate cytogenetics, FLT3-TKD | DA + midostaurin - strong consensus | No other treatments reasonable (moderate consensus) | Trial: Optimise FLT3 | Non-NHS: No | Age: No |
| 14 | 385 | 14 | Intermediate cytogenetics, FLT3-ITD, FLT3-TKD | DA + midostaurin - strong consensus | No consensus on reasonable other treatments | Trial: Optimise FLT3 | Non-NHS: Possibly FLAG-Ida-GO | Age: No |
| 15 | 3 | 15 | Intermediate cytogenetics, Therapy-related AML | CPX-351 - moderate consensus | CPX-351 (strong consensus), DA + gemtuzumab (moderate consensus) | Trial: No | Non-NHS: No | Age: Yes (CPX favoured in over 60s, FLAG-Ida preferred by some clinicians in younger patients although note that no consensus reached as to whether FLAG-Ida is a reasonable option) |
| 16 | 5121 | 16 | KMT2A::MLLT3 t(9;11) | FLAG-Ida - moderate consensus | FLAG-Ida (strong consensus), DA+GO (strong consensus) | Trial: Menin-inhibitor trials | Non-NHS: Possibly FLAG-Ida-GO | Age: Yes (DA+GO preferred for older patients) |
| 17 | 7169 | 17 | Other KMT2A rearranged | FLAG-Ida - strong consensus | No consensus on reasonable alternative treatments. | Trial: Menin-inhibitor trials | Non-NHS: No | Age: Yes (FLAG-Ida if younger, DA if older) |
| 18 | 2049 | 18 | MDS-associated adverse cytogenetics | CPX - moderate consensus | CPX (strong consensus), FLAG-Ida (strong consensus) | Trial: No | Non-NHS: Yes (Ven-Aza) | Age: Yes (FLAG-Ida if younger) |
| 19 | 2082 | 19 | MDS-associated adverse cytogenetics, TP53, Complex / monosomal modifier | No consensus on preferred treatment | CPX (strong consensus), FLAG-Ida (strong consensus) | Trial: Any | Non-NHS: Yes (ven-aza) | Age: Yes (FLAG-Ida if younger, Ven-Aza if older) |
| 20 | 1025 | 20 | Intermediate cytogenetics, sAML mutation present | No consensus on preferred treatment | FLAG-Ida (strong consensus), CPX (moderate consensus) | Trial: No | Non-NHS: Yes (Ven-Aza) | Age: Yes (DA+GO/CPX in older >60s, FLAG-Ida in younger) |
| 21 | 2817 | 22 | MDS-associated adverse cytogenetics, NPM1 | No consensus on preferred treatment | FLAG-Ida (strong consensus), CPX (moderate consensus) | Trial: No | Non-NHS: Yes (Ven-Aza) | Age: Yes (FLAG-Ida if younger, CPX or Ven-Aza if older) |
| 22 | 2433 | 23 | MDS-associated adverse cytogenetics, FLT3-ITD | DA+ quizartinib - moderate consensus | DA + quizartinib (strong consensus), DA + midostaurin (moderate consensus) | Trial: Optimise FLT3 | Non-NHS: No | Age: No |
| 23 | 2241 | 24 | MDS-associated adverse cytogenetics, FLT3-TKD | No consensus on preferred treatment | DA + midostaurin (strong consensus), CPX (strong consensus) | Trial: Optimise FLT3 | Non-NHS: No | Age: Yes (FLAG-Ida if younger) |
| 24 | 1281 | 25 | Intermediate cytogenetics, sAML mutation present, FLT3-ITD | DA + quizartinib - moderate consensus | DA + quizartinib (strong consensus), DA + midostaurin (strong consensus) | Trial: Optimise FLT3 | Non-NHS: No | Age: No |
| 25 | 1153 | 26 | Intermediate cytogenetics, sAML mutation present, FLT3-TKD | DA + midostaurin - moderate consensus | DA + midostaurin (strong consensus), CPX (strong consensus) | Trial: Optimise FLT3 | Non-NHS: No | Age: No |
| 26 | 9217 | 27 | Other adverse / MECOM | FLAG-Ida - strong consensus | No consensus on reasonable alternative treatments | Trial: No | Non-NHS: Yes (Ven-Aza) | Age: Yes (FLAG-Ida if younger, maybe Ven-Aza if older) |
| 27 | 17 | 28 | Intermediate cytogenetics, DDX41 | DA+ gemtuzumab - strong consensus | No consensus on reasonable other treatments | Trial: No | Non-NHS: Yes (Experts note that patients with DDX41 generally respond well to Venetoclax-Azacitidine) | Age: No |
| 277 | 2049 | Additional | MDS-associated adverse cytogenetics, Complex / monosomal modifier | CPX - moderate consensus | CPX (strong consensus), FLAG-Ida (strong consensus) | Trial: No | Non-NHS: Yes (Ven-Aza) | Age: Yes (FLAG-Ida if younger) |
| 278 | 2817 | Additional | MDS-associated adverse cytogenetics, NPM1, Complex / monosomal modifier | No consensus on preferred treatment | FLAG-Ida (strong consensus), CPX (moderate consensus) | Trial: No | Non-NHS: Yes (Ven-Aza) | Age: Yes (FLAG-Ida if younger, CPX or Ven-Aza if older) |
| 279 | 2433 | Additional | MDS-associated adverse cytogenetics, FLT3-ITD, Complex / monosomal modifier | DA+ quizartinib - moderate consensus | DA + quizartinib (strong consensus), DA + midostaurin (moderate consensus) | Trial: Optimise FLT3 | Non-NHS: No | Age: No |
| 280 | 2241 | Additional | MDS-associated adverse cytogenetics, FLT3-TKD, Complex / monosomal modifier | No consensus on preferred treatment | DA + midostaurin (strong consensus), CPX (strong consensus) | Trial: Optimise FLT3 | Non-NHS: No | Age: Yes (FLAG-Ida if younger) |
Exhaustive lookup
All workbook rows used by the calculator
The static lookup contains every non-empty row converted from the source workbook. This table is intentionally exhaustive so every similar-case and direct row can be inspected.
Show 279 static lookup rows, including 253 rows with Similar Case guidance
| Source row | Case | Scenario | Extra | Active flags | Recommendation source | Preferred / similar case | Expert or workbook comment |
|---|---|---|---|---|---|---|---|
| 2 | 13313 | 1 | - | Core binding factor AML | Direct workbook text | DA+gemtuzumab - strong consensus | The strong consensus is informed by subgroup analyses of phase 3 randomised controlled trials and meta-analyses demonstrating a benefit of combining gemtuzumab ozogamicin with intensive chemotherapy in AML with a CBF translocation, alongside the absence of benefit from allogeneic transplantation in first complete remission. The lack of benefit, and potential excess toxicity, of FLAG-Ida compared with daunorubicin–cytarabine when combined with gemtuzumab ozogamicin in this patient subgroup has been suggested by AML19. Current practice for intensively treated patients incorporates an MRD-informed, risk-adapted strategy in those achieving complete remission . |
| 3 | 513 | 2 | - | Intermediate cytogenetics, NPM1 | Direct workbook text | DA + gemtuzumab - strong consensus | The strong consensus is driven by evidence supporting the addition of gemtuzumab ozogamicin to intensive chemotherapy, reflecting its positive impact on event-free survival and MRD clearance in a German randomised controlled trial. FLAG-Ida has moderate consensus as an effective alternative, possibly informed by AML19 data suggesting superior survival in subgroup analyses. However, it remains unclear whether the apparent benefit observed with FLAG-Ida in AML19 reflects the chemotherapy backbone itself or the addition of gemtuzumab ozogamicin, which likely underlies the residual variation in opinion. There is also strong consensus in favour of an MRD-directed approach to transplantation, based on the absence of a survival benefit from allogeneic transplantation in first complete remission among patients who are peripheral blood MRD-negative after cycle 2, and the perceived benefit of transplantation in those who remain MRD-positive at this corresponding treatment milestone. |
| 4 | 641 | 3 | - | Intermediate cytogenetics, NPM1, FLT3-TKD | Direct workbook text | DA+midostaurin - moderate consensus | The moderate consensus is driven by the results of the RATIFY study, which demonstrated a benefit of a daunorubicin–cytarabine plus midostaurin approach, at least in patients younger than 60 years of age. Subgroup analyses from AML19 suggesting superior survival with FLAG as the chemotherapy backbone compared with daunorubicin–cytarabine when combined with gemtuzumab ozogamicin in NPM1-mutated AML, including patients with FLT3-TKD and within the broader FLT3-mutated subset, have led some participants to express a preference for this option. An MRD-guided, risk-adapted approach to transplantation, using post-cycle 2 peripheral blood assessment as a landmark timepoint and established through clinical trials in younger patients, achieved moderate consensus through extrapolation in older patients. |
| 5 | 1537 | 4 | - | Intermediate cytogenetics, sAML mutation present, NPM1 | Direct workbook text | DA+gemtuzumab - strong consensus | The strong consensus is driven by the benefit of adding gemtuzumab ozogamicin to intensive chemotherapy, reflecting its positive impact on event-free survival and MRD clearance in a German randomised controlled trial. FLAG-Ida has moderate consensus as an effective alternative, based on AML19 subgroup analyses demonstrating superior survival in patients with NPM1-mutated AML. However, it remains unclear whether the benefit observed with FLAG-Ida in AML19 reflects the chemotherapy backbone alone or the addition of gemtuzumab ozogamicin, which likely accounts for the residual variation in opinion. There is also strong consensus in favour of an MRD-directed approach to transplantation, based on the absence of a survival benefit from allogeneic transplantation in first complete remission among patients who are peripheral blood MRD-negative after cycle 2, and the perceived benefit in those who remain MRD-positive at this corresponding treatment stage. Posthoc pooled analysis from AML17&19 suggests that this is also the case in the presence of sAML mutations. |
| 6 | 517 | 6 | - | Intermediate cytogenetics, NPM1, Prior MDS | Direct workbook text | No consensus on preferred treatment | There is no consensus regarding optimal induction therapy, utility of MRD assessments or transplantation, given the absence of evidence to guide practice, resulting from the relative rarity of the combination of clinicopathological/genetic abnormalities. |
| 7 | 515 | 7 | - | Intermediate cytogenetics, NPM1, Therapy-related AML | Direct workbook text | DA + gemtuzumab - moderate consensus | The moderate consensus in favour of a daunorubicin–cytarabine plus gemtuzumab ozogamicin approach reflects the under-representation of this clinicopathological subtype of AML in clinical trials of therapy-related disease, together with the likelihood that such cases may represent de novo AML occurring coincidentally after prior genotoxic therapy, with outcomes not different from those of similarly treated patients without a past history of treatment of a malignancy. Consequently, there is moderate to strong consensus regarding disease monitoring and transplantation strategies aligned with those used in de novo disease. |
| 8 | 65 | 8 | - | Intermediate cytogenetics, CEBPA bZIP | Direct workbook text | DA + gemtuzumab - strong consensus | There is strong consensus regarding treatment in this favourable-risk AML genotype, which is chemotherapy-sensitive, with experts preferring approved and funded standard intensive induction therapy. While there is moderate consensus in favour of allogeneic transplantation in first complete remission for MRD-positive disease, the accompanying comments reflect the absence of a strong evidence base to support this practice. |
| 9 | 1 | 9 | - | Intermediate cytogenetics | Direct workbook text | DA+ gemtuzumab - strong consensus | There is strong consensus regarding induction therapy using agents approved for the treatment of AML, and the use of flow cytometry–based MRD assessment to inform decisions regarding allogeneic transplantation in first complete remission among younger patients. However, there is an absence of consensus regarding an MRD-directed consolidative allograft strategy in older patients, reflecting the high relapse risk observed even among MRD-negative older patients and the lack of additional data in this population to better inform relapse risk. |
| 10 | 769 | 10 | - | Intermediate cytogenetics, NPM1, FLT3-ITD | Direct workbook text | No consensus for preferred treatment | Given the approval of two FLT3 inhibitors with activity against FLT3-ITD, and the absence of a direct comparison between these agents when combined with the same chemotherapy backbone, the lack of consensus is unsurprising. Different experts cite individual reasons for favouring one FLT3 inhibitor over the other, largely based on interpretation of clinical trial data derived from post-hoc subgroup analyses. By contrast, consensus against allogeneic transplantation in first complete remission for patients who are peripheral blood MRD-negative after cycle 2, particularly among younger patients, is informed by the absence of a demonstrated survival benefit with alloSCT in this group. |
| 11 | 777 | 11 | - | Intermediate cytogenetics, NPM1, FLT3-ITD, DNMT3A | Direct workbook text | DA + quizartinib - moderate consensus | There is moderate consensus regarding the use of quizartinib as the FLT3 inhibitor of choice in this triple-mutated patient subset, informed by post hoc subgroup analyses from the QuANTUM-First trial. There is strong consensus in favour of an MRD-directed allogeneic transplantation strategy in first complete remission among younger patients, and moderate consensus regarding the application of this approach in older patients. |
| 12 | 257 | 12 | - | Intermediate cytogenetics, FLT3-ITD | Direct workbook text | No consensus on preferred treatment | Given the approval of two FLT3 inhibitors with activity against FLT3-ITD, and the absence of a direct comparison between these agents when combined with the same chemotherapy backbone, the lack of consensus is unsurprising. Different experts cite individual reasons for favouring one FLT3 inhibitor over the other, largely based on interpretations of clinical trial data derived from post hoc subgroup analyses. Only moderate consensus has been achieved regarding allogeneic transplantation in flow MRD negativity in first complete remission among younger patients, likely reflecting variable confidence in the reliability of MRD monitoring to predict relapse in FLT3-ITD AML. In contrast, the absence of a demonstrated survival benefit with quizartinib in older patients, together with the exclusion of older patients from RATIFY, appears to generate strong consensus in favour of allogeneic transplantation in patients over 60 years of age, irrespective of MRD status. |
| 13 | 129 | 13 | - | Intermediate cytogenetics, FLT3-TKD | Direct workbook text | DA + midostaurin - strong consensus | Strong consensus regarding induction therapy is driven by the approval of a FLT3 inhibitor with activity against FLT3-TKD and supporting evidence from the RATIFY randomised controlled trial. In the absence of definitive evidence, there is no consensus regarding allogeneic transplantation in first complete remission among younger patients acheiving MRD negativity. By contrast, in older patients there appears to be strong consensus in favour of allogeneic transplantation in first complete remission for those with intermediate- or higher-risk disease, as defined by AML60+, irrespective of MRD response. |
| 14 | 385 | 14 | - | Intermediate cytogenetics, FLT3-ITD, FLT3-TKD | Direct workbook text | DA + midostaurin - strong consensus | Strong consensus regarding induction therapy is driven by the approval of a FLT3 inhibitor with activity against both FLT3-TKD and FLT3-ITD, supported by evidence from the RATIFY randomised controlled trial. In older patients, there appears to be strong consensus in favour of allogeneic transplantation in first complete remission for those with intermediate- or higher-risk disease, as defined by AML60+, irrespective of MRD response. |
| 15 | 3 | 15 | - | Intermediate cytogenetics, Therapy-related AML | Direct workbook text | CPX-351 - moderate consensus | Moderate consensus regarding induction therapy is driven by the evidence base supporting, and regulatory approval of, CPX-351 for this indication. There is strong consensus in favour of proceeding to allogeneic transplantation in first complete remission, based on the superior survival outcomes observed in patients undergoing this approach. |
| 16 | 5121 | 16 | - | KMT2A::MLLT3 t(9;11) | Direct workbook text | FLAG-Ida - moderate consensus | There is moderate consensus in favour of induction with FLAG-Ida, informed by superior outcomes observed in retrospective analyses of AML17 and AML19 trial data in this disease subset, both of which recruited younger patients. The absence of strong consensus likely reflects the post hoc nature of these analyses and the lack of KMT2A::r-stratified randomisation within either trial. This uncertainty is mirrored by the absence of consensus regarding allogeneic transplantation in first complete remission among younger patients, particularly in relation to the use of an MRD-directed risk-adapted strategy to inform transplant decisions. In older patients, the consensus appears to be driven by the absence of evidence to guide practice and by expert opinion regarding the perceived benefit of allogeneic transplantation. |
| 17 | 7169 | 17 | - | Other KMT2A rearranged | Direct workbook text | FLAG-Ida - strong consensus | There is strong consensus in favour of induction with FLAG-Ida, informed by superior outcomes observed in retrospective analyses of AML17 and AML19 trial data in this disease subset, both of which recruited younger patients. This strong consensus extends to the role of allogeneic transplantation in first complete remission irrespective of MRD status, with outcomes among MRD-negative patients in this adverse-risk group within these trials not altering transplant decision-making, likely reflecting the small patient numbers involved. |
| 18 | 2049 | 18 | a | MDS-associated adverse cytogenetics | Direct workbook text | CPX - moderate consensus | There is moderate consensus regarding the use of the NICE-approved and funded agent for this indication, with support for alternative approaches driven by individual clinical experience with other combinations and interpretation of trial subgroup analyses. Consensus regarding the role of allogeneic transplantation in first complete remission is strong, acknowledging the limited utility of MRD monitoring in this setting. |
| 19 | 2082 | 19 | - | MDS-associated adverse cytogenetics, TP53, Complex / monosomal modifier | Direct workbook text | No consensus on preferred treatment | The absence of consensus on preferred induction reflects the poor outcomes observed in this patient subgroup, even with the NICE-approved and funded option of CPX-351, together with the perception that an intensified approach using FLAG-Ida may be superior. Somewhat paradoxically, a less intensive approach is favoured in older patients, acknowledging inherent bias in expert-driven treatment allocation. There is strong consensus in favour of allogeneic transplantation in first complete remission among younger patients, while there is an absence of consensus regarding an MRD-directed transplantation strategy in older patients. This reflects the lack of high-quality evidence and variability in expert interpretation of data derived from retrospective analyses. |
| 20 | 1025 | 20 | - | Intermediate cytogenetics, sAML mutation present | Direct workbook text | No consensus on preferred treatment | The absence of consensus regarding the optimal induction approach reflects the lack of high-quality data to guide therapy in this setting. Some experts favour CPX-351 based on post hoc subgroup analyses from the AML19 trial in younger patients, while others prefer either intensified or standard induction strategies, influenced in part by the availability of trial data at the time of treatment initiation. Nevertheless, there is clear recognition of the adverse prognostic impact of this mutation, with strong consensus in favour of allogeneic transplantation in first complete remission irrespective of MRD status. |
| 21 | 2817 | 22 | a | MDS-associated adverse cytogenetics, NPM1 | Direct workbook text | No consensus on preferred treatment | The absence of consensus reflects the relative rarity of this genotype, which precludes an evidence-based approach. Consequently, some experts favour a more intensive induction strategy, perceived to be beneficial in genetically adverse-risk AML among younger patients, while others prefer induction with CPX-351, which has age-agnostic approval for this indication. In older patients, a less intensive approach, presumably to mitigate toxicity, is also considered appropriate. There is, however, strong consensus in favour of proceeding to allogeneic transplantation in first complete remission for all eligible patients. |
| 22 | 2433 | 23 | a | MDS-associated adverse cytogenetics, FLT3-ITD | Direct workbook text | DA+ quizartinib - moderate consensus | There is moderate consensus regarding the use of daunorubicin–cytarabine plus quizartinib as induction therapy, likely reflecting the perceived advantage of incorporating quizartinib as post-transplant maintenance. Strong consensus exists in favour of proceeding to allogeneic transplantation, irrespective of MRD status. |
| 23 | 2241 | 24 | a | MDS-associated adverse cytogenetics, FLT3-TKD | Direct workbook text | No consensus on preferred treatment | The absence of consensus reflects a dichotomy of views between targeting the adverse-risk genetic background with CPX-351, an approved and funded option in this setting, and focusing on the FLT3-TKD mutation through the use of midostaurin. Modest benefits for both strategies have been suggested only in underpowered post hoc subgroup analyses of the respective licensing studies, in the absence of any direct comparative data. By contrast, strong consensus in favour of allogeneic transplantation in first complete remission, irrespective of MRD status, is driven by the predominance of the adverse-risk abnormality, regarded by experts as the principal disease driver. |
| 24 | 1281 | 25 | - | Intermediate cytogenetics, sAML mutation present, FLT3-ITD | Direct workbook text | DA + quizartinib - moderate consensus | There is moderate consensus regarding the optimal induction therapy, primarily driven by the option of incorporating post-allogeneic transplantation maintenance, which is perceived by experts to be of benefit. Given the adverse prognostic impact associated with sAML mutations, there is strong consensus in favour of proceeding to allogeneic transplantation in first complete remission, irrespective of MRD status. |
| 25 | 1153 | 26 | - | Intermediate cytogenetics, sAML mutation present, FLT3-TKD | Direct workbook text | DA + midostaurin - moderate consensus | There is moderate consensus regarding the optimal induction therapy, reflecting the absence of high-quality evidence and a lack of stratified prospective randomised data demonstrating a clear benefit for either approach in pivotal licensing trials. Given the adverse prognostic impact associated with sAML mutations, there is strong consensus in favour of proceeding to allogeneic transplantation in first complete remission, irrespective of MRD status. |
| 26 | 9217 | 27 | - | Other adverse / MECOM | Direct workbook text | FLAG-Ida - strong consensus | The strong consensus for FLAG_Ida is based on the perception that this intensified approach is likely to be more effective as a remission inducing strategy than DA, in the absence of good quality data to inform the decision. There is consensus in mandating alloSCT in all patients achieving CR, independent of the MRD status. |
| 27 | 17 | 28 | - | Intermediate cytogenetics, DDX41 | Direct workbook text | DA+ gemtuzumab - strong consensus | Although not explicitly specified within NICE indications, this AML subtype falls within the approved use of daunorubicin–cytarabine plus gemtuzumab ozogamicin for induction therapy, supporting strong consensus for this approach. The relatively favourable outcomes achieved with standard intensive chemotherapy backbones such as daunorubicin–cytarabine, together with the absence of data supporting intensified regimens, result in a lack of consensus regarding alternative induction strategies. The scarcity of evidence to inform a risk-directed approach to allogeneic transplantation is reflected in the absence of consensus regarding transplantation in younger patients, while moderate consensus exists for allogeneic transplantation in older patients, potentially informed by single-centre data suggesting benefit with careful donor selection. |
| 28 | 19 | - | - | Intermediate cytogenetics, DDX41, Therapy-related AML | Borrow from scenario 28 | 28 | t-AML May be expected to co-occur with DDX41 due to accelerating a pre-disposition syndrome. |
| 29 | 21 | - | - | Intermediate cytogenetics, DDX41, Prior MDS | Borrow from scenario 28 | 28 | Int cytogenetics. Prior MDS. DDX41. Probably doesn’t change recommendation |
| 30 | 33 | - | - | Intermediate cytogenetics, TP53 | No direct text recorded | No case | Adverse risk by ELN. But rare event |
| 31 | 35 | - | - | Intermediate cytogenetics, TP53, Therapy-related AML | No direct text recorded | No case | Therapy AML with TP53 but normal karyotype rare. Likely to be adverse |
| 32 | 37 | - | - | Intermediate cytogenetics, TP53, Prior MDS | No direct text recorded | No case | TP53 with prior MDS. Rare to be non-adverse karyotype and without sAML mutaton. Likely to be poor prognosis. |
| 33 | 49 | - | - | Intermediate cytogenetics, TP53, DDX41 | No direct text recorded | No case | DDX41 and multi-hit TP53 – unclear. 11 patients in Makishima paper 2023. Rare |
| 34 | 67 | - | - | Intermediate cytogenetics, CEBPA bZIP, Therapy-related AML | Borrow from scenario 8 | 8 | Prior clinical history not likely to influence management or prognosis. |
| 35 | 69 | - | - | Intermediate cytogenetics, CEBPA bZIP, Prior MDS | Borrow from scenario 8 | 8 | Prior clinical history not likely to influence management or prognosis. |
| 36 | 81 | - | - | Intermediate cytogenetics, CEBPA bZIP, DDX41 | Borrow from scenario 8 | 8 | CEBPA rarely co-occurs with DDX41. Might suggest that DDX41 is not the predominant driver of the disease. |
| 37 | 97 | - | - | Intermediate cytogenetics, CEBPA bZIP, TP53 | No direct text recorded | No case | Intermediate risk/Normal karyotype with TP53 and CEBPA bzip mutation. Very rare. ELN risk doesn’t state what risk this would be. |
| 38 | 131 | - | - | Intermediate cytogenetics, FLT3-TKD, Therapy-related AML | Borrow from scenario 13 | 13 | Prior clinical history not likely to influence management or prognosis. |
| 39 | 133 | - | - | Intermediate cytogenetics, FLT3-TKD, Prior MDS | Borrow from scenario 13 | 13 | Prior clinical history not likely to influence management or prognosis. |
| 40 | 145 | - | - | Intermediate cytogenetics, FLT3-TKD, DDX41 | Borrow from scenario 13 | 13 | FLT3 rarely co-occurs with DDX41. Might suggest that DDX41 is not the predominant driver of the disease. |
| 41 | 161 | - | - | Intermediate cytogenetics, FLT3-TKD, TP53 | Borrow from scenario 13 | 13 | Rare for FLT3-TKD and TP53 to be co-mutated with VAF>10% and intermediate risk karyotype. Adverse risk by ELN. Suggest MDT discussion |
| 42 | 193 | - | - | Intermediate cytogenetics, FLT3-TKD, CEBPA bZIP | Borrow from scenario 13 | 13 | Favourable risk by ELN. Unclear whether midostaurin or gemtuzumab would be favoured. Suggest MDT discussion |
| 43 | 259 | - | - | Intermediate cytogenetics, FLT3-ITD, Therapy-related AML | Borrow from scenario 12 | 12 | Prior clinical history not likely to influence management or prognosis. |
| 44 | 261 | - | - | Intermediate cytogenetics, FLT3-ITD, Prior MDS | Borrow from scenario 12 | 12 | Prior clinical history not likely to influence management or prognosis. |
| 45 | 273 | - | - | Intermediate cytogenetics, FLT3-ITD, DDX41 | Borrow from scenario 12 | 12 | FLT3 rarely co-occurs with DDX41. Might suggest that DDX41 is not the predominant driver of the disease. |
| 46 | 289 | - | - | Intermediate cytogenetics, FLT3-ITD, TP53 | Borrow from scenario 12 | 12 | Rare for FLT3-ITD and TP53 to be co-mutated with VAF>10% and intermediate risk karyotype. Adverse risk by ELN. Suggest MDT discussion. |
| 47 | 321 | - | - | Intermediate cytogenetics, FLT3-ITD, CEBPA bZIP | Borrow from scenario 12 | 12 | Rare for FLT3-ITD and TP53 to be co-mutated with VAF>10% and intermediate risk karyotype. Adverse risk by ELN. Suggest MDT discussion. |
| 48 | 387 | - | - | Intermediate cytogenetics, FLT3-ITD, FLT3-TKD, Therapy-related AML | Borrow from scenario 14 | 14 | Prior clinical history not likely to influence management or prognosis. |
| 49 | 389 | - | - | Intermediate cytogenetics, FLT3-ITD, FLT3-TKD, Prior MDS | Borrow from scenario 14 | 14 | Prior clinical history not likely to influence management or prognosis. |
| 50 | 401 | - | - | Intermediate cytogenetics, FLT3-ITD, FLT3-TKD, DDX41 | Borrow from scenario 14 | 14 | FLT3 rarely co-occurs with DDX41. Might suggest that DDX41 is not the predominant driver of the disease. |
| 51 | 417 | - | - | Intermediate cytogenetics, FLT3-ITD, FLT3-TKD, TP53 | Borrow from scenario 14 | 14 | Rare for FLT3-ITD and TP53 to be co-mutated with VAF>10% and intermediate risk karyotype. Adverse risk by ELN. Suggest MDT discussion. |
| 52 | 449 | - | - | Intermediate cytogenetics, FLT3-ITD, FLT3-TKD, CEBPA bZIP | Borrow from scenario 14 | 14 | Favourable risk by ELN. Unclear on optimal strategy with regards to transplant. Induction treatment likely to favour FLT3-inhibitor over DA+GO |
| 53 | 529 | - | - | Intermediate cytogenetics, NPM1, DDX41 | Borrow from scenario 2 | 2 | Rare for NPM1 and DDX41 to be co-mutated. Suggests DDX41 may not be the driver variant. |
| 54 | 545 | - | - | Intermediate cytogenetics, NPM1, TP53 | Borrow from scenario 2 | 2 | Rare for NPM1 and TP53 at VAF>10% to co-exist with intermediate risk karyotype. Suggest MDT discussion |
| 55 | 577 | - | - | Intermediate cytogenetics, NPM1, CEBPA bZIP | Borrow from scenario 2 | 2 | Rare to have CEBPA bZIP and NPM1 co-mutated. Not likely to change management |
| 56 | 643 | - | - | Intermediate cytogenetics, NPM1, FLT3-TKD, Therapy-related AML | Borrow from scenario 3 | 3 | Therapy-AML not likely to effect management |
| 57 | 657 | - | - | Intermediate cytogenetics, NPM1, FLT3-TKD, DDX41 | Borrow from scenario 3 | 3 | Rare for NPM1 and DDX41 to be co-mutated. Suggests that DDX41 may not be the driver variant |
| 58 | 673 | - | - | Intermediate cytogenetics, NPM1, FLT3-TKD, TP53 | Borrow from scenario 3 | 3 | Rare for NPM1 and TP53 to co-exist in intermediate risk karyotype. Suggest MDT discussion |
| 59 | 705 | - | - | Intermediate cytogenetics, NPM1, FLT3-TKD, CEBPA bZIP | Borrow from scenario 3 | 3 | Rare for NPM1 and CEBPA bZIP to be co-mutated. Presence of mutated CEBPA bZIP Not likely to change management |
| 60 | 771 | - | - | Intermediate cytogenetics, NPM1, FLT3-ITD, Therapy-related AML | Borrow from scenario 10 | 10 | Prior clinical history not likely to influence management or prognosis. |
| 61 | 773 | - | - | Intermediate cytogenetics, NPM1, FLT3-ITD, Prior MDS | Borrow from scenario 10 | 10 | Prior clinical history not likely to influence management or prognosis. |
| 62 | 779 | - | - | Intermediate cytogenetics, NPM1, FLT3-ITD, DNMT3A, Therapy-related AML | Borrow from scenario 11 | 11 | If clear history then may increase preference for allogeneic stem cell transplant even in MRD negativity. Suggest MDT discussion. |
| 63 | 781 | - | - | Intermediate cytogenetics, NPM1, FLT3-ITD, DNMT3A, Prior MDS | Borrow from scenario 11 | 11 | If clear history then may increase preference for allogeneic stem cell transplant even in MRD negativity. Suggest MDT discussion. |
| 64 | 785 | - | - | Intermediate cytogenetics, NPM1, FLT3-ITD, DDX41 | Borrow from scenario 10 | 10 | Rare for NPM1 and DDX41 to be co-mutated. Suggests that DDX41 may not be the driver variant |
| 65 | 793 | - | - | Intermediate cytogenetics, NPM1, FLT3-ITD, DDX41, DNMT3A | Borrow from scenario 11 | 11 | Rare for NPM1 and DDX41 to be co-mutated. Suggests that DDX41 may not be the driver variant |
| 66 | 801 | - | - | Intermediate cytogenetics, NPM1, FLT3-ITD, TP53 | Borrow from scenario 10 | 10 | Rare for NPM1 and TP53 to co-exist in intermediate risk karyotype. Suggest MDT discussion |
| 67 | 809 | - | - | Intermediate cytogenetics, NPM1, FLT3-ITD, TP53, DNMT3A | Borrow from scenario 11 | 11 | Rare for NPM1 and TP53 to co-exist in intermediate risk karyotype. Suggest MDT discussion |
| 68 | 833 | - | - | Intermediate cytogenetics, NPM1, FLT3-ITD, CEBPA bZIP | Borrow from scenario 10 | 10 | Rare for NPM1 and CEBPA bZIP to be co-mutated. Presence of mutated CEBPA bZIP Not likely to change management |
| 69 | 841 | - | - | Intermediate cytogenetics, NPM1, FLT3-ITD, CEBPA bZIP, DNMT3A | Borrow from scenario 11 | 11 | Rare for NPM1 and CEBPA bZIP to be co-mutated. Presence of mutated CEBPA bZIP Not likely to change management |
| 70 | 1027 | - | - | Intermediate cytogenetics, sAML mutation present, Therapy-related AML | Borrow from scenario 20 | 20 | Normal intermediate karyotype and sAML mutation (with/without MDS karyotype/prior MDS/prior therapy) would likely be managed as per SCENARIO |
| 71 | 1029 | - | - | Intermediate cytogenetics, sAML mutation present, Prior MDS | Borrow from scenario 20 | 20 | Normal intermediate karyotype and sAML mutation (with/without MDS karyotype/prior MDS/prior therapy) would likely be managed as per SCENARIO |
| 72 | 1041 | - | - | Intermediate cytogenetics, sAML mutation present, DDX41 | Borrow from scenario 28 | 28 | ASXL1 is a common co-mutation. Clinical MDS/t-MDS also common so not likely to change management |
| 73 | 1043 | - | - | Intermediate cytogenetics, sAML mutation present, DDX41, Therapy-related AML | Borrow from scenario 28 | 28 | Clinical MDS/t-MDS also common so not likely to change management |
| 74 | 1045 | - | - | Intermediate cytogenetics, sAML mutation present, DDX41, Prior MDS | Borrow from scenario 28 | 28 | Clinical MDS/t-MDS also common so not likely to change management |
| 75 | 1057 | - | - | Intermediate cytogenetics, sAML mutation present, TP53 | Borrow from scenario 19 | 19 | Intermediate risk/Normal karyotype with TP53 and sAML mutation. Adverse risk.Very poor outcomes. Irrespective of t-AML or sMDS. May be appropriate to treat like an AML with TP53 and MDS karyotype. |
| 76 | 1059 | - | - | Intermediate cytogenetics, sAML mutation present, TP53, Therapy-related AML | Borrow from scenario 19 | 19 | Intermediate risk/Normal karyotype with TP53 and sAML mutation. Adverse risk.Very poor outcomes. Irrespective of t-AML or sMDS. May be appropriate to treat like an AML with TP53 and MDS karyotype. |
| 77 | 1061 | - | - | Intermediate cytogenetics, sAML mutation present, TP53, Prior MDS | Borrow from scenario 19 | 19 | Intermediate risk/Normal karyotype with TP53 and sAML mutation. Adverse risk.Very poor outcomes. Irrespective of t-AML or sMDS. May be appropriate to treat like an AML with TP53 and MDS karyotype. |
| 78 | 1073 | - | - | Intermediate cytogenetics, sAML mutation present, TP53, DDX41 | No direct text recorded | No case | Rare to be TP53 and intermediate risk karyotype |
| 79 | 1075 | - | - | Intermediate cytogenetics, sAML mutation present, TP53, DDX41, Therapy-related AML | No direct text recorded | No case | Rare to be TP53 and intermediate risk karyotype |
| 80 | 1077 | - | - | Intermediate cytogenetics, sAML mutation present, TP53, DDX41, Prior MDS | No direct text recorded | No case | Rare to be TP53 and intermediate risk karyotype |
| 81 | 1089 | - | - | Intermediate cytogenetics, sAML mutation present, CEBPA bZIP | Borrow from scenario 8 | 8 | According to ELN would still be favourable risk disease. Rare combination. Caution regarding CHIP |
| 82 | 1091 | - | - | Intermediate cytogenetics, sAML mutation present, CEBPA bZIP, Therapy-related AML | Borrow from scenario 8 | 8 | According to ELN would still be favourable risk disease. Rare combination. Caution regarding CHIP |
| 83 | 1093 | - | - | Intermediate cytogenetics, sAML mutation present, CEBPA bZIP, Prior MDS | Borrow from scenario 8 | 8 | According to ELN would still be favourable risk disease. Rare combination. Caution regarding CHIP |
| 84 | 1105 | - | - | Intermediate cytogenetics, sAML mutation present, CEBPA bZIP, DDX41 | No direct text recorded | No case | RARE |
| 85 | 1107 | - | - | Intermediate cytogenetics, sAML mutation present, CEBPA bZIP, DDX41, Therapy-related AML | No direct text recorded | No case | RARE |
| 86 | 1109 | - | - | Intermediate cytogenetics, sAML mutation present, CEBPA bZIP, DDX41, Prior MDS | No direct text recorded | No case | RARE |
| 87 | 1155 | - | - | Intermediate cytogenetics, sAML mutation present, FLT3-TKD, Therapy-related AML | Borrow from scenario 26 | 26 | Similar to case 26 |
| 88 | 1157 | - | - | Intermediate cytogenetics, sAML mutation present, FLT3-TKD, Prior MDS | Borrow from scenario 26 | 26 | Similar to case 26 |
| 89 | 1185 | - | - | Intermediate cytogenetics, sAML mutation present, FLT3-TKD, TP53 | No direct text recorded | No case | Rare to be TP53 and intermediate risk karyotype |
| 90 | 1283 | - | - | Intermediate cytogenetics, sAML mutation present, FLT3-ITD, Therapy-related AML | Borrow from scenario 25 | 25 | Similar to case 25 |
| 91 | 1285 | - | - | Intermediate cytogenetics, sAML mutation present, FLT3-ITD, Prior MDS | Borrow from scenario 25 | 25 | Similar to case 25 |
| 92 | 1539 | - | - | Intermediate cytogenetics, sAML mutation present, NPM1, Therapy-related AML | Borrow from scenario 4 | 4 | Similar to case 4 |
| 93 | 1541 | - | - | Intermediate cytogenetics, sAML mutation present, NPM1, Prior MDS | Borrow from scenario 4 | 4 | Similar to case 4 |
| 94 | 1553 | - | - | Intermediate cytogenetics, sAML mutation present, NPM1, DDX41 | Borrow from scenario 4 | 4 | Rare for NPM1 and DDX41 to be co-mutated. Suggests that DDX41 may not be the driver variant |
| 95 | 1555 | - | - | Intermediate cytogenetics, sAML mutation present, NPM1, DDX41, Therapy-related AML | Borrow from scenario 4 | 4 | Rare for NPM1 and DDX41 to be co-mutated. Suggests that DDX41 may not be the driver variant |
| 96 | 1557 | - | - | Intermediate cytogenetics, sAML mutation present, NPM1, DDX41, Prior MDS | Borrow from scenario 4 | 4 | Rare for NPM1 and DDX41 to be co-mutated. Suggests that DDX41 may not be the driver variant |
| 97 | 1601 | - | - | Intermediate cytogenetics, sAML mutation present, NPM1, CEBPA bZIP | Borrow from scenario 4 | 4 | Rare for NPM1 and CEBPA bZIP to be co-mutated. Presence of mutated CEBPA bZIP Not likely to change management |
| 98 | 1603 | - | - | Intermediate cytogenetics, sAML mutation present, NPM1, CEBPA bZIP, Therapy-related AML | Borrow from scenario 4 | 4 | Rare for NPM1 and CEBPA bZIP to be co-mutated. Presence of mutated CEBPA bZIP Not likely to change management |
| 99 | 1605 | - | - | Intermediate cytogenetics, sAML mutation present, NPM1, CEBPA bZIP, Prior MDS | Borrow from scenario 4 | 4 | Rare for NPM1 and CEBPA bZIP to be co-mutated. Presence of mutated CEBPA bZIP Not likely to change management |
| 100 | 2051 | - | a | MDS-associated adverse cytogenetics, Therapy-related AML | Borrow from scenario 18 | 18 | Clinical history of t-AML not likely to change prognosis or management |
| 101 | 2051 | - | b | MDS-associated adverse cytogenetics, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 18 | 18 | Clinical history of t-AML not likely to change prognosis or management |
| 102 | 2053 | - | a | MDS-associated adverse cytogenetics, Prior MDS | Borrow from scenario 18 | 18 | Clinical history of MDS not likely to change prognosis or management |
| 103 | 2053 | - | b | MDS-associated adverse cytogenetics, Prior MDS, Complex / monosomal modifier | Borrow from scenario 18 | 18 | Clinical history of MDS not likely to change prognosis or management |
| 104 | 2065 | - | a | MDS-associated adverse cytogenetics, DDX41 | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 105 | 2065 | - | b | MDS-associated adverse cytogenetics, DDX41, Complex / monosomal modifier | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 106 | 2067 | - | a | MDS-associated adverse cytogenetics, DDX41, Therapy-related AML | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 107 | 2067 | - | b | MDS-associated adverse cytogenetics, DDX41, Therapy-related AML, Complex / monosomal modifier | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 108 | 2069 | - | a | MDS-associated adverse cytogenetics, DDX41, Prior MDS | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 109 | 2069 | - | b | MDS-associated adverse cytogenetics, DDX41, Prior MDS, Complex / monosomal modifier | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 110 | 2085 | - | - | MDS-associated adverse cytogenetics, TP53, Therapy-related AML | Borrow from scenario 19 | 19 | Prior clinical history not going to change management |
| 111 | 2086 | - | - | MDS-associated adverse cytogenetics, TP53, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 19 | 19 | Prior clinical history not going to change management |
| 112 | 2089 | - | - | MDS-associated adverse cytogenetics, TP53, Prior MDS | Borrow from scenario 19 | 19 | Prior clinical history not going to change management |
| 113 | 2090 | - | - | MDS-associated adverse cytogenetics, TP53, Prior MDS, Complex / monosomal modifier | Borrow from scenario 19 | 19 | Prior clinical history not going to change management |
| 114 | 2113 | - | - | MDS-associated adverse cytogenetics, TP53, DDX41 | Borrow from scenario 19 | 19 | Unclear whether DDX41 abbrogates some of the poor prognosis. Suggest MDT discussion |
| 115 | 2114 | - | - | MDS-associated adverse cytogenetics, TP53, DDX41, Complex / monosomal modifier | Borrow from scenario 19 | 19 | Unclear whether DDX41 abbrogates some of the poor prognosis. Suggest MDT discussion |
| 116 | 2145 | - | a | MDS-associated adverse cytogenetics, CEBPA bZIP | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 117 | 2145 | - | b | MDS-associated adverse cytogenetics, CEBPA bZIP, Complex / monosomal modifier | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 118 | 2147 | - | a | MDS-associated adverse cytogenetics, CEBPA bZIP, Therapy-related AML | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 119 | 2147 | - | b | MDS-associated adverse cytogenetics, CEBPA bZIP, Therapy-related AML, Complex / monosomal modifier | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 120 | 2149 | - | a | MDS-associated adverse cytogenetics, CEBPA bZIP, Prior MDS | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 121 | 2149 | - | b | MDS-associated adverse cytogenetics, CEBPA bZIP, Prior MDS, Complex / monosomal modifier | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 122 | 2161 | - | a | MDS-associated adverse cytogenetics, CEBPA bZIP, DDX41 | No direct text recorded | No case | Rare. Raises likelihood that DDX41 not the primary driver of disease. Unclear on significance of CEBPA in concert with adverse karyotype |
| 123 | 2161 | - | b | MDS-associated adverse cytogenetics, CEBPA bZIP, DDX41, Complex / monosomal modifier | No direct text recorded | No case | Rare. Raises likelihood that DDX41 not the primary driver of disease. Unclear on significance of CEBPA in concert with adverse karyotype |
| 124 | 2177 | - | - | MDS-associated adverse cytogenetics, CEBPA bZIP, TP53 | Borrow from scenario 19 | 19 | Suggest MDT discussion. Still likely to confer poor prognosis. |
| 125 | 2178 | - | - | MDS-associated adverse cytogenetics, CEBPA bZIP, TP53, Complex / monosomal modifier | Borrow from scenario 19 | 19 | Suggest MDT discussion. Still likely to confer poor prognosis. |
| 126 | 2243 | - | a | MDS-associated adverse cytogenetics, FLT3-TKD, Therapy-related AML | Borrow from scenario 24 | 24 | Clinical history not likely to change management |
| 127 | 2243 | - | b | MDS-associated adverse cytogenetics, FLT3-TKD, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 24 | 24 | Clinical history not likely to change management |
| 128 | 2245 | - | a | MDS-associated adverse cytogenetics, FLT3-TKD, Prior MDS | Borrow from scenario 24 | 24 | Clinical history not likely to change management |
| 129 | 2245 | - | b | MDS-associated adverse cytogenetics, FLT3-TKD, Prior MDS, Complex / monosomal modifier | Borrow from scenario 24 | 24 | Clinical history not likely to change management |
| 130 | 2257 | - | a | MDS-associated adverse cytogenetics, FLT3-TKD, DDX41 | Borrow from scenario 24 | 24 | Rare. Raises likelihood that DDX41 not the primary driver of disease |
| 131 | 2257 | - | b | MDS-associated adverse cytogenetics, FLT3-TKD, DDX41, Complex / monosomal modifier | Borrow from scenario 24 | 24 | Rare. Raises likelihood that DDX41 not the primary driver of disease |
| 132 | 2273 | - | - | MDS-associated adverse cytogenetics, FLT3-TKD, TP53 | Borrow from scenario 19 | 19 | May open up different therapeutic target but not likely to abbrogate poor prognosis |
| 133 | 2274 | - | - | MDS-associated adverse cytogenetics, FLT3-TKD, TP53, Complex / monosomal modifier | Borrow from scenario 19 | 19 | May open up different therapeutic target but not likely to abbrogate poor prognosis |
| 134 | 2337 | - | a | MDS-associated adverse cytogenetics, FLT3-TKD, CEBPA bZIP | Borrow from scenario 24 | 24 | Rare. But presence of CEBPA not likely to change management |
| 135 | 2337 | - | b | MDS-associated adverse cytogenetics, FLT3-TKD, CEBPA bZIP, Complex / monosomal modifier | Borrow from scenario 24 | 24 | Rare. But presence of CEBPA not likely to change management |
| 136 | 2435 | - | a | MDS-associated adverse cytogenetics, FLT3-ITD, Therapy-related AML | Borrow from scenario 23 | 23 | Clinical history not likley to change management |
| 137 | 2435 | - | b | MDS-associated adverse cytogenetics, FLT3-ITD, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 23 | 23 | Clinical history not likley to change management |
| 138 | 2437 | - | a | MDS-associated adverse cytogenetics, FLT3-ITD, Prior MDS | Borrow from scenario 23 | 23 | Clinical history not likley to change management |
| 139 | 2437 | - | b | MDS-associated adverse cytogenetics, FLT3-ITD, Prior MDS, Complex / monosomal modifier | Borrow from scenario 23 | 23 | Clinical history not likley to change management |
| 140 | 2449 | - | a | MDS-associated adverse cytogenetics, FLT3-ITD, DDX41 | Borrow from scenario 23 | 23 | Rare. Raises likelihood that DDX41 is not the primary driver of disease |
| 141 | 2449 | - | b | MDS-associated adverse cytogenetics, FLT3-ITD, DDX41, Complex / monosomal modifier | Borrow from scenario 23 | 23 | Rare. Raises likelihood that DDX41 is not the primary driver of disease |
| 142 | 2451 | - | a | MDS-associated adverse cytogenetics, FLT3-ITD, DDX41, Therapy-related AML | Borrow from scenario 23 | 23 | Rare. Raises likelihood that DDX41 is not the primary driver of disease |
| 143 | 2451 | - | b | MDS-associated adverse cytogenetics, FLT3-ITD, DDX41, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 23 | 23 | Rare. Raises likelihood that DDX41 is not the primary driver of disease |
| 144 | 2453 | - | a | MDS-associated adverse cytogenetics, FLT3-ITD, DDX41, Prior MDS | Borrow from scenario 23 | 23 | Rare. Raises likelihood that DDX41 is not the primary driver of disease |
| 145 | 2453 | - | b | MDS-associated adverse cytogenetics, FLT3-ITD, DDX41, Prior MDS, Complex / monosomal modifier | Borrow from scenario 23 | 23 | Rare. Raises likelihood that DDX41 is not the primary driver of disease |
| 146 | 2465 | - | - | MDS-associated adverse cytogenetics, FLT3-ITD, TP53 | No direct text recorded | No case | FLT3 not likely to abbrogate poor prognsosis of TP53 mutation with complex karyotype. Such MDT discussion. |
| 147 | 2529 | - | a | MDS-associated adverse cytogenetics, FLT3-ITD, CEBPA bZIP | Borrow from scenario 23 | 23 | Rare. Presence of CEBPA not likely to change management |
| 148 | 2529 | - | b | MDS-associated adverse cytogenetics, FLT3-ITD, CEBPA bZIP, Complex / monosomal modifier | Borrow from scenario 23 | 23 | Rare. Presence of CEBPA not likely to change management |
| 149 | 2625 | - | a | MDS-associated adverse cytogenetics, FLT3-ITD, FLT3-TKD | No direct text recorded | No case | Rare. Suggest MDT discussion |
| 150 | 2625 | - | b | MDS-associated adverse cytogenetics, FLT3-ITD, FLT3-TKD, Complex / monosomal modifier | No direct text recorded | No case | Rare. Suggest MDT discussion |
| 151 | 2657 | - | - | MDS-associated adverse cytogenetics, FLT3-ITD, FLT3-TKD, TP53 | Borrow from scenario 19 | 19 | May open up different therapeutic target but not likely to abbrogate poor prognosis |
| 152 | 2658 | - | - | MDS-associated adverse cytogenetics, FLT3-ITD, FLT3-TKD, TP53, Complex / monosomal modifier | Borrow from scenario 19 | 19 | May open up different therapeutic target but not likely to abbrogate poor prognosis |
| 153 | 2658 | - | d | MDS-associated adverse cytogenetics, FLT3-ITD, TP53, Complex / monosomal modifier | Borrow from scenario 19 | 19 | May open up different therapeutic target but not likely to abbrogate poor prognosis |
| 154 | 2819 | - | a | MDS-associated adverse cytogenetics, NPM1, Therapy-related AML | Borrow from scenario 22 | 22 | Prior clinical history not likely to influence management or prognosis. |
| 155 | 2819 | - | b | MDS-associated adverse cytogenetics, NPM1, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 22 | 22 | Prior clinical history not likely to influence management or prognosis. |
| 156 | 2821 | - | a | MDS-associated adverse cytogenetics, NPM1, Prior MDS | Borrow from scenario 22 | 22 | Prior clinical history not likely to influence management or prognosis. |
| 157 | 2821 | - | b | MDS-associated adverse cytogenetics, NPM1, Prior MDS, Complex / monosomal modifier | Borrow from scenario 22 | 22 | Prior clinical history not likely to influence management or prognosis. |
| 158 | 2833 | - | a | MDS-associated adverse cytogenetics, NPM1, DDX41 | Borrow from scenario 22 | 22 | Rare for NPM1 and DDX41 to be co-mutated. Suggests that DDX41 may not be the driver variant |
| 159 | 2833 | - | b | MDS-associated adverse cytogenetics, NPM1, DDX41, Complex / monosomal modifier | Borrow from scenario 22 | 22 | Rare for NPM1 and DDX41 to be co-mutated. Suggests that DDX41 may not be the driver variant |
| 160 | 2849 | - | - | MDS-associated adverse cytogenetics, NPM1, TP53 | Borrow from scenario 19 | 19 | NPM1 not likely to abbrogate poor prognosis. May facilitate trial options. Suggest MDT discussion |
| 161 | 2850 | - | - | MDS-associated adverse cytogenetics, NPM1, TP53, Complex / monosomal modifier | Borrow from scenario 19 | 19 | NPM1 not likely to abbrogate poor prognosis. May facilitate trial options. Suggest MDT discussion |
| 162 | 2913 | - | a | MDS-associated adverse cytogenetics, NPM1, CEBPA bZIP | Borrow from scenario 22 | 22 | Rare for NPM1 and CEBPA bZIP to be co-mutated. Presence of mutated CEBPA bZIP Not likely to change management |
| 163 | 2913 | - | b | MDS-associated adverse cytogenetics, NPM1, CEBPA bZIP, Complex / monosomal modifier | Borrow from scenario 22 | 22 | Rare for NPM1 and CEBPA bZIP to be co-mutated. Presence of mutated CEBPA bZIP Not likely to change management |
| 164 | 3009 | - | a | MDS-associated adverse cytogenetics, NPM1, FLT3-TKD | Borrow from scenario 24 | 24 | Rare combination |
| 165 | 3009 | - | b | MDS-associated adverse cytogenetics, NPM1, FLT3-TKD, Complex / monosomal modifier | Borrow from scenario 24 | 24 | Rare combination |
| 166 | 3201 | - | a | MDS-associated adverse cytogenetics, NPM1, FLT3-ITD | Borrow from scenario 23 | 23 | Rare combination. |
| 167 | 3201 | - | b | MDS-associated adverse cytogenetics, NPM1, FLT3-ITD, Complex / monosomal modifier | Borrow from scenario 23 | 23 | Rare combination. |
| 168 | 3233 | - | - | MDS-associated adverse cytogenetics, NPM1, FLT3-ITD, TP53 | Borrow from scenario 19 | 19 | Suggest MDT discussion |
| 169 | 3234 | - | - | MDS-associated adverse cytogenetics, NPM1, FLT3-ITD, TP53, Complex / monosomal modifier | Borrow from scenario 19 | 19 | Suggest MDT discussion |
| 170 | 3585 | - | a | MDS-associated adverse cytogenetics, sAML mutation present | Borrow from scenario 18 | 18 | Presence of sAML mutation not likely to change prognosis or management |
| 171 | 3585 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, Complex / monosomal modifier | Borrow from scenario 18 | 18 | Presence of sAML mutation not likely to change prognosis or management |
| 172 | 3587 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, Therapy-related AML | Borrow from scenario 18 | 18 | Presence of sAML mutation not likely to change prognosis or management |
| 173 | 3587 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 18 | 18 | Presence of sAML mutation not likely to change prognosis or management |
| 174 | 3589 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, Prior MDS | Borrow from scenario 18 | 18 | Presence of sAML mutation not likely to change prognosis or management |
| 175 | 3589 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, Prior MDS, Complex / monosomal modifier | Borrow from scenario 18 | 18 | Presence of sAML mutation not likely to change prognosis or management |
| 176 | 3601 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, DDX41 | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 177 | 3601 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, DDX41, Complex / monosomal modifier | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 178 | 3603 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, DDX41, Therapy-related AML | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 179 | 3603 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, DDX41, Therapy-related AML, Complex / monosomal modifier | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 180 | 3605 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, DDX41, Prior MDS | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 181 | 3605 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, DDX41, Prior MDS, Complex / monosomal modifier | No direct text recorded | No case | DDX41 usually intermediate risk cytogenetics. Unclear where adverse risk confered by abnormal karyotype. Suggest MDT discussion |
| 182 | 3617 | - | - | MDS-associated adverse cytogenetics, sAML mutation present, TP53 | Borrow from scenario 19 | 19 | Still poor prognosis |
| 183 | 3618 | - | - | MDS-associated adverse cytogenetics, sAML mutation present, TP53, Complex / monosomal modifier | Borrow from scenario 19 | 19 | Still poor prognosis |
| 184 | 3621 | - | - | MDS-associated adverse cytogenetics, sAML mutation present, TP53, Therapy-related AML | Borrow from scenario 19 | 19 | Still poor prognosis |
| 185 | 3622 | - | - | MDS-associated adverse cytogenetics, sAML mutation present, TP53, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 19 | 19 | Still poor prognosis |
| 186 | 3625 | - | - | MDS-associated adverse cytogenetics, sAML mutation present, TP53, Prior MDS | Borrow from scenario 19 | 19 | Still poor prognosis |
| 187 | 3626 | - | - | MDS-associated adverse cytogenetics, sAML mutation present, TP53, Prior MDS, Complex / monosomal modifier | Borrow from scenario 19 | 19 | Still poor prognosis |
| 188 | 3681 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, CEBPA bZIP | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 189 | 3681 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, CEBPA bZIP, Complex / monosomal modifier | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 190 | 3683 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, CEBPA bZIP, Therapy-related AML | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 191 | 3683 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, CEBPA bZIP, Therapy-related AML, Complex / monosomal modifier | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 192 | 3685 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, CEBPA bZIP, Prior MDS | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 193 | 3685 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, CEBPA bZIP, Prior MDS, Complex / monosomal modifier | No direct text recorded | No case | Unclear how best to proceed. Adverse risk cytogenetics and CEBPA – may retain much of it’s favourable risk. Suggest MDT discussion. |
| 194 | 3777 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-TKD | Borrow from scenario 24 | 24 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 195 | 3777 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-TKD, Complex / monosomal modifier | Borrow from scenario 24 | 24 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 196 | 3779 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-TKD, Therapy-related AML | Borrow from scenario 24 | 24 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 197 | 3779 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-TKD, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 24 | 24 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 198 | 3781 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-TKD, Prior MDS | Borrow from scenario 24 | 24 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 199 | 3781 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-TKD, Prior MDS, Complex / monosomal modifier | Borrow from scenario 24 | 24 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 200 | 3969 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-ITD | Borrow from scenario 23 | 23 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 201 | 3969 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-ITD, Complex / monosomal modifier | Borrow from scenario 23 | 23 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 202 | 3971 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-ITD, Therapy-related AML | Borrow from scenario 23 | 23 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 203 | 3971 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-ITD, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 23 | 23 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 204 | 3973 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-ITD, Prior MDS | Borrow from scenario 23 | 23 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 205 | 3973 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, FLT3-ITD, Prior MDS, Complex / monosomal modifier | Borrow from scenario 23 | 23 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 206 | 4353 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, NPM1 | Borrow from scenario 22 | 22 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 207 | 4353 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, NPM1, Complex / monosomal modifier | Borrow from scenario 22 | 22 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 208 | 4355 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, NPM1, Therapy-related AML | Borrow from scenario 22 | 22 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 209 | 4355 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, NPM1, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 22 | 22 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 210 | 4357 | - | a | MDS-associated adverse cytogenetics, sAML mutation present, NPM1, Prior MDS | Borrow from scenario 22 | 22 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 211 | 4357 | - | b | MDS-associated adverse cytogenetics, sAML mutation present, NPM1, Prior MDS, Complex / monosomal modifier | Borrow from scenario 22 | 22 | Additional presence of a sAML mutation is not likely to change management or prognosis |
| 212 | 4385 | - | - | MDS-associated adverse cytogenetics, sAML mutation present, NPM1, TP53 | Borrow from scenario 19 | 19 | Still poor prognosis |
| 213 | 5123 | - | - | KMT2A::MLLT3 t(9;11), Therapy-related AML | Borrow from scenario 16 | 16 | Unlikely to change recommendations |
| 214 | 5125 | - | - | KMT2A::MLLT3 t(9;11), Prior MDS | Borrow from scenario 16 | 16 | sAML can confer worse prognosis |
| 215 | 5137 | - | - | KMT2A::MLLT3 t(9;11), DDX41 | Borrow from scenario 16 | 16 | Rare co-existence of DDX41 and this fusion. Might suggest that DDX41 is not the pathological driver variant. |
| 216 | 5153 | - | - | KMT2A::MLLT3 t(9;11), TP53 | Borrow from scenario 16 | 16 | We don't know if this makes prognosis worse |
| 217 | 5153 | - | b | KMT2A::MLLT3 t(9;11), TP53, Complex / monosomal modifier | Borrow from scenario 16 | 16 | We don't know if this makes prognosis worse |
| 218 | 5155 | - | - | KMT2A::MLLT3 t(9;11), TP53, Therapy-related AML | Borrow from scenario 16 | 16 | We don't know if this makes prognosis worse |
| 219 | 5155 | - | b | KMT2A::MLLT3 t(9;11), TP53, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 16 | 16 | We don't know if this makes prognosis worse |
| 220 | 5185 | - | - | KMT2A::MLLT3 t(9;11), CEBPA bZIP | No direct text recorded | No case | Rare co-existence |
| 221 | 5249 | - | - | KMT2A::MLLT3 t(9;11), FLT3-TKD | Borrow from scenario 16 | 16 | Unclear if targeted therapy should be used ie FLT3-i. Presence of FLT3 not an independent prognostic factor |
| 222 | 5377 | - | - | KMT2A::MLLT3 t(9;11), FLT3-ITD | Borrow from scenario 16 | 16 | Unclear if targeted therapy should be used ie FLT3-i. Presence of FLT3 not an independent prognostic factor |
| 223 | 5505 | - | - | KMT2A::MLLT3 t(9;11), FLT3-ITD, FLT3-TKD | Borrow from scenario 16 | 16 | Unclear if targeted therapy should be used ie FLT3-i. Presence of FLT3 not an independent prognostic factor |
| 224 | 5633 | - | - | KMT2A::MLLT3 t(9;11), NPM1 | No direct text recorded | No case | Super rare combination |
| 225 | 6145 | - | - | KMT2A::MLLT3 t(9;11), sAML mutation present | Borrow from scenario 16 | 16 | Presence of sAML mutation not likely to modfiy management or prognosis |
| 226 | 6147 | - | - | KMT2A::MLLT3 t(9;11), sAML mutation present, Therapy-related AML | Borrow from scenario 16 | 16 | Probably doesn’t change management |
| 227 | 6149 | - | - | KMT2A::MLLT3 t(9;11), sAML mutation present, Prior MDS | Borrow from scenario 16 | 16 | Probably doesn’t change managemetn |
| 228 | 7171 | - | - | Other KMT2A rearranged, Therapy-related AML | Borrow from scenario 17 | 17 | Unchanged |
| 229 | 7173 | - | - | Other KMT2A rearranged, Prior MDS | Borrow from scenario 17 | 17 | sAML may mark a worse prognosis. Suggest MDT discussion |
| 230 | 7185 | - | - | Other KMT2A rearranged, DDX41 | Borrow from scenario 17 | 17 | Rare co-existence of DDX41 and this fusion. Might suggest that DDX41 is not the pathological driver variant. |
| 231 | 7201 | - | - | Other KMT2A rearranged, TP53 | Borrow from scenario 17 | 17 | We don't know if this impacts prognosis |
| 232 | 7201 | - | b | Other KMT2A rearranged, TP53, Complex / monosomal modifier | Borrow from scenario 17 | 17 | We don't know if this impacts prognosis |
| 233 | 7203 | - | - | Other KMT2A rearranged, TP53, Therapy-related AML | Borrow from scenario 17 | 17 | We don't know if TP53 impacts prognosis |
| 234 | 7203 | - | b | Other KMT2A rearranged, TP53, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 17 | 17 | We don't know if TP53 impacts prognosis |
| 235 | 7233 | - | - | Other KMT2A rearranged, CEBPA bZIP | No direct text recorded | No case | Rare combination |
| 236 | 7297 | - | - | Other KMT2A rearranged, FLT3-TKD | Borrow from scenario 17 | 17 | FLT3-ITD or TKD and KMT2Ar – unclear if targeted therapy should be used. Not an independent adverse prognostic factor after accounting for other variables. |
| 237 | 7425 | - | - | Other KMT2A rearranged, FLT3-ITD | Borrow from scenario 17 | 17 | FLT3-ITD or TKD and KMT2Ar – unclear if targeted therapy should be used. Not an independent adverse prognostic factor after accounting for other variables. |
| 238 | 7553 | - | - | Other KMT2A rearranged, FLT3-ITD, FLT3-TKD | Borrow from scenario 17 | 17 | FLT3-ITD or TKD and KMT2Ar – unclear if targeted therapy should be used. Not an independent adverse prognostic factor after accounting for other variables. |
| 239 | 7681 | - | - | Other KMT2A rearranged, NPM1 | No direct text recorded | No case | This would be a rare combination. Suggest MDT discussion |
| 240 | 8193 | - | - | Other KMT2A rearranged, sAML mutation present | Borrow from scenario 17 | 17 | Probably doesn’t alter management. But sAML may confer worse prognosis see Harmony data |
| 241 | 8195 | - | - | Other KMT2A rearranged, sAML mutation present, Therapy-related AML | Borrow from scenario 17 | 17 | Probably doesn’t alter management. |
| 242 | 8197 | - | - | Other KMT2A rearranged, sAML mutation present, Prior MDS | Borrow from scenario 17 | 17 | Probably doesn’t alter management. But sAML may confer worse prognosis see Harmony data |
| 243 | 9219 | - | - | Other adverse / MECOM, Therapy-related AML | Borrow from scenario 27 | 27 | tAML is common in MECOM |
| 244 | 9221 | - | - | Other adverse / MECOM, Prior MDS | Borrow from scenario 27 | 27 | sAML is common in MECOM |
| 245 | 9233 | - | - | Other adverse / MECOM, DDX41 | Borrow from scenario 27 | 27 | Rare co-existence of DDX41 and this fusion. Might suggest that DDX41 is not the pathological driver variant. |
| 246 | 9281 | - | - | Other adverse / MECOM, CEBPA bZIP | Borrow from scenario 27 | 27 | Rare to have these two mutations together. Remains an adverse risk case |
| 247 | 9345 | - | - | Other adverse / MECOM, FLT3-TKD | Borrow from scenario 27 | 27 | Rare to have these two mutations together. Remains an adverse risk case |
| 248 | 9473 | - | - | Other adverse / MECOM, FLT3-ITD | Borrow from scenario 27 | 27 | Rare to have these two mutations together. Remains an adverse risk case |
| 249 | 9729 | - | - | Other adverse / MECOM, NPM1 | Borrow from scenario 27 | 27 | Rare to have these two mutations together. Remains an adverse risk case |
| 250 | 10241 | - | - | Other adverse / MECOM, sAML mutation present | Borrow from scenario 27 | 27 | sAML mutations are common in MECOM disease |
| 251 | 10243 | - | - | Other adverse / MECOM, sAML mutation present, Therapy-related AML | Borrow from scenario 27 | 27 | Therapy related disease is common in MECOM |
| 252 | 10245 | - | - | Other adverse / MECOM, sAML mutation present, Prior MDS | Borrow from scenario 27 | 27 | sAML mutations are common in MECOM disease |
| 253 | 13315 | - | - | Core binding factor AML, Therapy-related AML | Borrow from scenario 1 | 1 | Existence of therapy -related AML not thought to abolish the favourable risk prognosis. Definitely can co-occur together. |
| 254 | 13317 | - | - | Core binding factor AML, Prior MDS | No direct text recorded | No case | Rare to be CBF with pre-existing MDS. Suggest MDT discussion |
| 255 | 13329 | - | - | Core binding factor AML, DDX41 | Borrow from scenario 1 | 1 | Rare co-existence of DDX41 and this fusion. Might suggest that DDX41 is not the pathological driver variant. |
| 256 | 13377 | - | - | Core binding factor AML, CEBPA bZIP | Borrow from scenario 1 | 1 | Rare combination. Unlikely to change management of CBF leukaemia |
| 257 | 13441 | - | - | Core binding factor AML, FLT3-TKD | No direct text recorded | No case | FLT3 is a plausible co-operative mutation. FLT3-TKD not adverse. FLT3-ITD may be worse outcomes. Characteristics and outcome of patients with core-binding factor acute myeloid leukemia and FLT3-ITD: results from an international collaborative study | Haematologica. No data on use of FLT3-I in FLT3-ITD/CBF patients. |
| 258 | 13569 | - | - | Core binding factor AML, FLT3-ITD | No direct text recorded | No case | FLT3 is a plausible co-operative mutation. FLT3-TKD not adverse. FLT3-ITD may be worse outcomes. Characteristics and outcome of patients with core-binding factor acute myeloid leukemia and FLT3-ITD: results from an international collaborative study | Haematologica. No data on use of FLT3-I in FLT3-ITD/CBF patients. |
| 259 | 13697 | - | - | Core binding factor AML, FLT3-ITD, FLT3-TKD | No direct text recorded | No case | FLT3 is a plausible co-operative mutation. FLT3-TKD not adverse. FLT3-ITD may be worse outcomes. Characteristics and outcome of patients with core-binding factor acute myeloid leukemia and FLT3-ITD: results from an international collaborative study | Haematologica. No data on use of FLT3-I in FLT3-ITD/CBF patients. |
| 260 | 13825 | - | - | Core binding factor AML, NPM1 | No direct text recorded | No case | Rare combination. Suggest MDT discussion |
| 261 | 14337 | - | - | Core binding factor AML, sAML mutation present | Borrow from scenario 1 | 1 | Uncommon. Unlikely to over-ride biology of CBF. |
| 262 | 14339 | - | - | Core binding factor AML, sAML mutation present, Therapy-related AML | Borrow from scenario 1 | 1 | Uncommon. Unlikely to over-ride biology of CBF. |
| 263 | 14341 | - | - | Core binding factor AML, sAML mutation present, Prior MDS | Borrow from scenario 1 | 1 | Uncommon. Unlikely to over-ride biology of CBF. |
| 264 | 15361 | - | - | Core binding factor AML, Complex / monosomal modifier | Borrow from scenario 1 | 1 | CBF and CK is a recognised combination. Still retains favourable risk status. And treatment effective. Show scenario |
| 265 | 15361 | - | b | Core binding factor AML, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 1 | 1 | CBF and CK is a recognised combination. Still retains favourable risk status. And treatment effective. Show scenario |
| 266 | 15375 | - | - | KMT2A::MLLT3 t(9;11), Complex / monosomal modifier | Borrow from scenario 16 | 16 | Don’t know the impact of this combination. Univariate analysis was associated with worse OS. But not in multivariate. Harmony. Rare in Othman 6%. Suggest MDT discussion |
| 267 | 15376 | - | - | Other KMT2A rearranged, Complex / monosomal modifier | Borrow from scenario 17 | 17 | Don’t know the impact of this combination. Univariate analysis was associated with worse OS. But not in multivariate. Harmony. Rare in Othman 6%. Suggest MDT discussion |
| 268 | 15376 | - | b | Other KMT2A rearranged, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 17 | 17 | Don’t know the impact of this combination. Univariate analysis was associated with worse OS. But not in multivariate. Harmony. Rare in Othman 6%. Suggest MDT discussion |
| 269 | 15384 | - | - | Other adverse / MECOM, Complex / monosomal modifier | Borrow from scenario 27 | 27 | CK is common with inv(3)/t(3) so not likely to change prognosis / management |
| 270 | 15384 | - | b | Other adverse / MECOM, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 27 | 27 | CK is common with inv(3)/t(3) so not likely to change prognosis / management |
| 271 | 15384 | - | c | Other adverse / MECOM, Prior MDS, Complex / monosomal modifier | Borrow from scenario 27 | 27 | CK is common with inv(3)/t(3) so not likely to change prognosis / management |
| 272 | 23586 | - | - | Other adverse / MECOM, TP53, Complex / monosomal modifier | Borrow from scenario 19 | 19 | TP53 rare in inv(3)/t(3). Unclear impact prognosis but clearly remains a very poor prognosis disease. |
| 273 | 23586 | - | b | Other adverse / MECOM, TP53, Therapy-related AML, Complex / monosomal modifier | Borrow from scenario 19 | 19 | TP53 rare in inv(3)/t(3). Unclear impact prognosis but clearly remains a very poor prognosis disease. |
| 274 | 23586 | - | c | Other adverse / MECOM, TP53, Prior MDS, Complex / monosomal modifier | Borrow from scenario 19 | 19 | TP53 rare in inv(3)/t(3). Unclear impact prognosis but clearly remains a very poor prognosis disease. |
| 275 | 27681 | - | - | Core binding factor AML, TP53, Complex / monosomal modifier | No direct text recorded | No case | CBF and TP53 and complex karyotype = rare. No advice. |
| 276 | 27681 | - | b | Core binding factor AML, TP53, Therapy-related AML, Complex / monosomal modifier | No direct text recorded | No case | CBF and TP53 and complex karyotype = rare. No advice. |
| 277 | 2049 | - | b | MDS-associated adverse cytogenetics, Complex / monosomal modifier | Direct workbook text | CPX - moderate consensus | Presence of complex karyotype in absence of TP53 mutation not thought to change prognosis |
| 278 | 2817 | - | b | MDS-associated adverse cytogenetics, NPM1, Complex / monosomal modifier | Direct workbook text | No consensus on preferred treatment | Presence of complex karyotype in absence of TP53 mutation not thought to change prognosis |
| 279 | 2433 | - | b | MDS-associated adverse cytogenetics, FLT3-ITD, Complex / monosomal modifier | Direct workbook text | DA+ quizartinib - moderate consensus | Presence of complex karyotype in absence of TP53 mutation not thought to change prognosis |
| 280 | 2241 | - | b | MDS-associated adverse cytogenetics, FLT3-TKD, Complex / monosomal modifier | Direct workbook text | No consensus on preferred treatment | Presence of complex karyotype in absence of TP53 mutation not thought to change prognosis |