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NCCN > AML > Flashcards

AML Flashcards

1
Q

Imaging if central nervous system (CNS) hemorrhage
suspected

A

Brain CT without contrast

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2
Q

Imaging if leukemic meningitis suspected

A

Brain MRI with and without contrast

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3
Q

Imaging in individuals with extramedullary disease

A

FDG-PET/CT

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4
Q

Imaging to evaluate myocardial function in patients
with a history or symptoms of cardiac disease or prior/planned exposure to cardiotoxic drugs or radiation therapy (RT) to thorax

A

Echocardiogram or MUGA scan

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5
Q

WBC count for Low risk APL

A

≤10 x 109/L

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6
Q

TRUE OR FALSE

FLT3 inhibitors are not recommended for FLT3-positive APL.

A

TRUE

FLT3 inhibitors are not recommended for FLT3-positive APL.

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7
Q

Used to manage high WBC count (>10 x 109/L) during induction with ATRA/arsenic trioxide

A

Hydroxyurea

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8
Q

Preferred Regimen for Low-Risk APL Induction

A

ATRA/arsenic trioxide

  • ATRA 45 mg/m2 in 2 divided doses daily + arsenic trioxide 0.15 mg/kg IV daily (category 1)
  • ATRA 45 mg/m2 in 2 divided doses daily + arsenic trioxide 0.3 mg/kg IV on days 1–5 of week 1 and 0.25 mg/kg twice weekly during weeks 2–8 (category 1)
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9
Q

Preferred Regimen for Low-Risk APL Consolidation

A

Arsenic trioxide/ATRA

  • Arsenic trioxideh 0.15 mg/kg/d IV 5 d/wk for 4 weeks every 8 weeks for a total of 4 cycles, and ATRA 45 mg/ m2/d for 2 weeks every 4 weeks for a total of 7 cycles (category 1)
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10
Q

Low-Risk APL

Useful in Certain Circumstances (if arsenic is not available or contraindicated)

A

Induction: ATRA/idarubicin;
Consolidation: ATRA/idarubicin, then ATRA/mitoxantrone, then ATRA/idarubicin

Induction: ATRA/gemtuzumab ozogamicin
Consolidation: ATRA/gemtuzumab ozogamicin

Induction:
* ATRA 45 mg/m2 in 2 divided doses daily + idarubicin 12 mg/
m2 on days 2, 4, 6, 8 (category 1) or on days 2, 4, 6 for aged >70 y
* ATRA 45 mg/m2 in 2 divided doses daily + a single dose of
gemtuzumab ozogamicin 9 mg/ m2 on day 5

Consolidation
ATRA 45 mg/m2 x 15 days + idarubicin 5 mg/m2 x 4 days x 1 cycle,
then ATRA x 15 days + mitoxantrone 10 mg/m2/d x 3 days x 1
cycle, then ATRA x 15 days + idarubicin 12 mg/m2 x 1 day x 1 cycle
(category 1)

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11
Q

Preferred Regimen for High-Risk APL Induction and Consolidation

A

Induction: ATRA/idarubicin/arsenic trioxide;
Consolidation: ATRA/arsenic trioxide

Induction: ATRA/arsenic trioxide/gemtuzumab ozogamicin;
Consolidation: Arsenic trioxide/ATRA

Induction: ATRA/arsenic trioxide/gemtuzumab ozogamicin;
Consolidation: Gemtuzumab ozogamicin (if ATRA/arsenic trioxide discontinued due to toxicity)

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12
Q

Regimen for High-Risk APL with Cardiac Issue: Low-Ejection Fraction

A

Induction: ATRA/arsenic trioxide/gemtuzumab ozogamicin;
Consolidation: Arsenic trioxide/ATRA

Induction: ATRA/arsenic trioxide/gemtuzumab ozogamicin;
Consolidation: Gemtuzumab ozogamicin (if ATRA/Arsenic trioxide discontinued due to toxicity)

No anthracyclibe

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13
Q

Regimen for High-Risk APL with Cardiac Issue: Prolonged QTc

A

Induction: ATRA/gemtuzumab ozogamicin;
Consolidation: ATRA/gemtuzumab ozogamicin

Induction: ATRA/daunorubicin/cytarabine;
Consolidation: Daunorubicin/cytarabine, then cytarabine/daunorubicin/IT chemotherapy

Induction: ATRA/idarubicin;
Consolidation: ATRA/idarubicin/cytarabine, then ATRA/mitoxantrone, then ATRA/idarubicin/cytarabine

No ATO

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14
Q

Test that should be performed on a blood sample at completion of consolidation to document molecular remission.

A

PCR

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15
Q

PCR monitoring

In patients receiving the ATRA/arsenic regimen,
consider earlier sampling at ______ months during consolidation.

A

3–4 months during consolidation

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16
Q

Prior practice guidelines have recommended monitoring blood by PCR every 3 mo for 2 y to
detect molecular relapse.

This is reccomended for patients with:

A
  • High-risk disease
  • Those >60 y of age
  • Had long interruptions during consolidation
  • Patients on regimens that use maintenance and are not able to tolerate maintenance
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17
Q

To confirm PCR positivity, a second blood sample should be done in ___ weeks in a reliable laboratory

A

2–4 weeks

  • If the second test is negative, frequent monitoring (every 3 mo for 2 y) is strongly recommended to confirm that the test remains negative.
  • The PCR testing lab should indicate the level of sensitivity of assay for positivity (most clinical labs have a sensitivity level of 10-4)
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18
Q

Management of clinical coagulopathy in APL

Targets

A
  • Platelets ≥50 x 109/L
  • Fibrinogen >150 mg/dL
  • PT and PTT close to normal values

Monitor daily until coagulopathy resolves.

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19
Q

TRUE OR FALSE

Leukapheresis is not routinely recommended in patients with a high WBC count in APL because of the difference in leukemia biology.

A

TRUE

Leukapheresis is not routinely recommended in patients with a high WBC count in APL because of the difference in leukemia biology.

However, in life-threatening cases with leukostasis that is not responsive to other modalities, leukapheresis can be considered with caution.

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20
Q

Syndrome associated with fever, often associated with increasing WBC count >10 x 109/L, usually
at initial diagnosis or relapse; shortness of breath; hypoxemia; pleural or pericardial effusions

A

Differentiation Syndrome

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21
Q

Management of Differentiation Syndrome

A
  • Close monitoring of volume overload and pulmonary status is indicated.
  • Initiate dexamethasone at first signs or symptoms of respiratory compromise (ie, hypoxemia, pulmonary infiltrates, pericardial or pleural effusions) (10 mg BID for 3–5 days with a taper over 2 weeks)
  • Consider interrupting ATRA therapy until hypoxia resolves.
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22
Q

Prophylaxis for Differentiation Syndrome

A

Prednisone 0.5 mg/kg day or
Dexamethasone 10 mg every 12 h

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23
Q

Treatment for leukocytosis associated with differentiation syndrome

A
  • Hydroxyurea
  • Anthracycline (daunorubicin or idarubicin) or Gemtuzumab ozogamicin
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24
Q

Diagnostics prior to starting ATO

A
  • ECG for prolonged QTc interval assessment
  • Serum electrolytes (Ca, K, Mg, phosphorus) and creatinine

During therapy (weekly during induction therapy and before each course of post-remission therapy)

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25
Q

Preferred Induction Regimen: Favorable-Risk AML by Cytogenetics (CBF-AML)

A

Cytarabine/Daunorubicin/Gemtuzumab ozogamicin

Cytarabine/Idarubicin/Gemtuzumab ozogamicin

Other recommended: 7 + 3 (mitoxantrone) - (for age ≥60 y)

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26
Q

Preferred Induction Regimen: Favorable-Risk AML by Mutation Profile (NPM1-mutated/FLT3 wild-type AML, in-frame bZIP mutation in CEBPA) and Intermediate-risk AML

A

Cytarabine/Daunorubicin

Cytarabine/Idarubicin

Cytarabine/Mitoxantrone (for age ≥60 y)

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27
Q

Induction Regimen: AML with FLT3 mutation

A

Cytarabine/Daunorubicin/Midostaurin
Cytarabine/Idarubicin/Midostaurin

Cytarabine/Daunorubicin/Quizartinib
Cytarabine/Idarubicin/Quizartinib

Walang preferred

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28
Q

Preferred Induction Regimen: Therapy-related AML other than CBF-AML; Antecedent MDS/CMML; AML-MRC

A

CPX-351/dual-drug liposomal cytarabine and daunorubicin (≥60 years of age)

Cytarabine/Daunorubicin (<60 years of age)

Cytarabine/Idarubicin (<60 years of age)

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29
Q

Induction Regimen: Poor-Risk AML without TP53 Mutation or del17p Abnormality

A

Cytarabine/Daunorubicin
Cytarabine/Idarubicin
CPX-351/dual-drug liposomal cytarabine and daunorubicin
FLAG-IDA
Decitabine (days 1–5)/Venetoclax
Azacitidine/Venetoclax
LDAC/Venetoclax

No regimens are considered preferred, clinical trial is recommended

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30
Q

Management of leukocytosis/leukostasis

A
  • Leukapheresis
  • Hydroxyurea
  • Single dose of cytarabine

Prompt institution of definitive therapy is essential.

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31
Q

Patients who receive transplant shortly following gemtuzumab ozogamicin administration may be at risk for developing ________________________.

A

Sinusoidal obstruction syndrome (SOS)

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32
Q

In times of fludarabine shortage, __________ can be substituted for fludarabine.

A

Cladribine

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33
Q

TRUE OR FALSE

Gemtuzumab ozogamicin may be beneficial in NPM1-mutated AML and CEBPA-mutated AML.

A

FALSE

Gemtuzumab ozogamicin may be beneficial in NPM1-mutated AML

The role of gemtuzumab ozogamicin in CEBPA-mutated AML is not established.

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34
Q

TRUE OR FALSE

While conventional induction chemotherapy regimens can be given in the setting of a TP53 mutation, less intensive chemotherapy is preferred for patients not enrolled in clinical trials.

A

TRUE

While conventional induction chemotherapy regimens can be given in the setting of a TP53 mutation, less intensive chemotherapy is preferred for patients not enrolled in clinical trials.

Outcomes for patients with poor-risk AML with TP53 mutation remain poor with conventional induction chemotherapy.

The panel prioritizes clinical trial enrollment in this setting.

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35
Q

When to perform follow-up BM aspirate and biopsy post induction

A

14–21 days after start
of therapy

When using a cytarabine-based induction regimen with doses of cytarabine >100 to 200 mg/m2, consider delaying BM aspirate and biopsy to D21.

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36
Q

If there is ambiguous resut, repeat BM biopsy within ____ days before proceeding with therapy

A

7 days

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37
Q

Hypoplasia is defined as:

A

Cellularity less than 20% of which the residual blasts are less than 5% (ie, blast percentage of residual cellularity).

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38
Q

When to perform follow-up BM aspirate and biopsy post re-induction

A
  • Upon count recovery, or
  • By day 42 at the latest in the setting of
    delayed count recovery

When performed, BM aspirate and biopsy should include cytogenetic and molecular studies, as appropriate.

For measurable (minimal) residual disease (MRD) assessment

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39
Q

Preferred Regimen: LOWER INTENSITY THERAPY (INTENSIVE INDUCTION INELIGIBLE OR DECLINES)

AML without IDH1 mutation

A
  • Azacitidine + venetoclax (category 1)
  • Decitabine + venetoclax
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40
Q

Preferred Regimen: LOWER INTENSITY THERAPY (INTENSIVE INDUCTION INELIGIBLE OR DECLINES)

AML with IDH1 mutation

A
  • Azacitidine + venetoclax (category 1)
  • Azacitidine + ivosidenib (category 1)
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41
Q

For patients who decline induction chemotherapy and/or targeted therapy, best supportive care may include:

A

Hydroxyurea and/or transfusion support

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42
Q

Response to treatment with enasidenib or ivosidenib may take ____ months

A

3–5 months

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43
Q

Criteria for patients eligible for the regimen Azacitidine + ivosidenib (IDH1-positive):

A

At least one of the following criteria:
* Aged >75 years
* Baseline ECOG performance status of 2
* Severe cardiac or pulmonary disease
* Hepatic impairment with bilirubin >1.5 times the upper limit of normal
* Creatinine clearance (CrCl) <45 mL/min, or
* Other comorbidity

44
Q

Criteria for patients eligible for the regimen LDAC + glasdegib

A
  • ≥75 years of age
  • Who have significant comorbid conditions (ie, severe cardiac disease, ECOG performance status ≥2, baseline creatinine >1.3 mg/dL)

has been associated with an improved OS in a randomized trial

45
Q

Allogeneic transplant is recommended for patients with favorable-risk disease who are:

A
  • Unable to complete consolidation
  • Who have high-risk features such as MRD-positivity or KIT mutation
46
Q

Who are eligible for maintenence therapy

A

Patient with non-CBF-AML:
* Who received prior intensive chemotherapy and
whose disease is now in remission
* Completed no consolidation, some consolidation or a recommended course of consolidation
* No allogeneic HCT is planned

Post allogeneic HCT, in remission, and history of FLT3 mutation

Patient with history of FLT3-ITD mutation:
* Previously received quizartinib
* No allogeneic HCT is planned

47
Q

Maintenence Therapy: Patient with non-CBF-AML

A
  • Oral azacitidine until progression or unacceptable toxicity (category 1, preferred for age ≥55 y)
  • HMA until progression or unacceptable toxicity
48
Q

Maintenence Therapy: Post allogeneic HCT, in remission, and history of FLT3 mutation

A
  • Sorafenib (FLT3-ITD only)
  • Midostaurin (FLT3-ITD or TKD) (category 2B)
  • Gilteritinib (FLT3-ITD or TKD) (category 2B)
  • Quizartinib (FLT3-ITD only) (category 2B)
49
Q

Maintenence Therapy: Patient with history of FLT3-ITD mutation

A

Quizartinib (FLT3-ITD only)

50
Q

AML Surveillance

CBC:
BMA:

A

CBC: every 1–3 mo for 2 y, then every 3-6 mo up to 5 y

BMA:only if peripheral smear is abnormal or cytopenias develop

51
Q

Initial successful induction regimen can be repeated if ______ months since induction regimen.

A

≥12 months

52
Q

Favorable Genetic Abnormality

A
  • t(8;21)(q22;q22.1)/RUNX1::RUNX1T1
  • inv(16)(p13.1q22) or t(16;16) (p13.1;q22) /CBFB::MYH11
  • Mutated NPM1 without FLT3-ITD
  • bZIP in-frame mutated CEBPAe
53
Q

Intermediate Genetic Abnormality

A
  • Mutated NPM1 with FLT3-ITD
  • Wild-type NPM1 with FLT3-ITD (without adverse-risk genetic lesions)
  • t(9;11)(p21.3;q23.3)/MLLT3::KMT2A
  • Cytogenetic and/or molecular abnormalities not classified as favorable or adverse
54
Q

Poor/Adverse Genetic Abnormality

A
  • t(6;9)(p23.3;q34.1)/DEK::NUP214
  • t(v;11q23.3)/KMT2A-rearranged
  • t(9;22)(q34.1;q11.2)/BCR::ABL1
  • t(8;16)(p11.2;p13.3)/KAT6A::CREBBP
  • inv(3)(q21.3q26.2) or t(3;3)(q21.3;q26.2)/GATA2, MECOM(EVI1)
  • t(3q26.2;v)/MECOM(EVI1)-rearranged
  • -5 or del(5q); -7; -17/abn(17p)
  • Complex karyotype, monosomal karyotype
  • Mutated ASXL1, BCOR, EZH2, RUNX1, SF3B1, SRSF2, STAG2, U2AF1, and/or ZRSR2
  • Mutated TP53

While ELN requires a variant allele fraction of at least 10% to categorize TP53 mutation as poor/ adverse risk, NCCN considers TP53 mutation as poor/adverse risk, regardless of variant allele
fraction.

55
Q

The next step if there is positive mass effect or increased intracranial pressure on imaging

A

Consider fine-needle aspiration (FNA) or biopsy

Do not perform LP

56
Q

Management if LP positive by morphology or immunotype by flow cytometry

A

IT chemotherapy 2x/wk until clear,
then weekly x 4–6 wks

Induction chemotherapy should be started concurrently.

However, for patients receiving HiDAC, since this agent crosses the blood brain barrier, IT therapy can be deferred until induction is completed.

IT chemotherapy may consist of methotrexate, cytarabine, or a combination of these agents.

57
Q

Management if positive mass effect or increased intracranial pressure

A
  • RT followed by IT chemotherapyf 2x/wk until clear, then weekly x 4–6 wks or
  • HiDAC-based therapy + dexamethasone to reduce intracranial pressure

Concurrent use of CNS RT with HiDAC or IT methotrexate may increase risk of neurotoxicity

58
Q

Screening LP should be considered at first remission before first consolidation for patients with:

A
  • Monocytic differentiation
  • MPAL
  • WBC count >40 x 109/L at diagnosis
  • Extramedullary disease
  • High-risk APL
  • FLT3 mutations
59
Q

Management of patients who present with isolated extramedullary disease (myeloid sarcoma)

A

Systemic therapy

Local therapy (RT or surgery [rare cases]) may be used for residual disease or for symptomatic disease.

60
Q

Transfusion thresholds:

Hemoglobin:

Platelets:

A

Hemoglobin: ≤7 to 8 g/dL or per institutional guidelines or symptoms of anemia

Platelets: < 10,000/mcL or with any signs of bleeding

  • Leukocyte-depleted products should be used for transfusion
  • Patients who are alloimmunized should receive cross-match–compatible and/or HLA-specific blood products
61
Q

Tumor lysis prophylaxis:

A
  • Hydration with diuresis
  • Allopurinol or rasburicase
62
Q

Should be considered as initial treatment in patients with rapidly increasing blast counts, high uric acid, or evidence of impaired renal function

A

Rasburicase

Glucose-6-phosphate dehydrogenase (G6PD) deficiency should be checked

63
Q

Neurologic assessment, including tests for nystagmus, slurred speech, and dysmetria, should be performed before each dose of cytarabine especially on:

A
  • Patients receiving HiDAC therapy (particularly those with impaired renal function), or
  • Intermediate-dose cytarabine in patients >60 years of age
64
Q

TRUE OR FALSE

In patients who develop cerebellar toxicity, cytarabine should be stopped and rechallenged thereafter.

A

FALSE

In patients who develop cerebellar toxicity, cytarabine should be stopped.

Rechallenge with HiDAC in future treatment cycles should not be attempted.

65
Q

Steroid eye drops should be administered to both eyes 4 times daily for all patients undergoing HiDAC therapy until _____ hours post completion of cytarabine.

A

24 hours

66
Q

Patients should be off granulocyte-macrophage colony-stimulating factor (GM-CSF) or G-CSF for a minimum of ____ days before obtaining BM to document remission.

A

7 days

67
Q

________________ has been shown to significantly decrease fungal infections when compared to fluconazole and itraconazole.

A

Posaconazole

68
Q

Monitoring during Induction therapy

CBC:

A
  • Daily or as clinically indicated during chemotherapy and
  • Every other day after recovery of ANC >0.5 x 109/L until either normal differential or persistent leukemia is documented
69
Q

Monitoring during Induction therapy

Platelet:

A

Daily while in the hospital until platelet-transfusion independent

70
Q

Monitoring during Induction therapy

Chemistry profile, including electrolytes, liver function tests (LFTs), blood urea nitrogen (BUN), creatinine, uric acid, and phosphorous:

A

Daily during active treatment until risk of tumor lysis is past

71
Q

Monitoring during Induction therapy

LFTs:

A

1–2 x/wk

72
Q

Monitoring during Induction therapy

Coagulation panel:

A

1–2 x/wk

DIC: daily

73
Q

Monitoring Post-Remission Therapy

During chemotherapy:
CBC, platelets:
Chemistry profile:

A

During chemotherapy:
CBC, platelets: 2x/wk
Chemistry profile: daily

74
Q

Monitoring Post-Remission Therapy

Outpatient monitoring post chemotherapy:

CBC, platelets, differential, and electrolytes:

A

Outpatient monitoring post chemotherapy:

CBC, platelets, differential, and electrolytes: 2–3 x/wk until recovery

75
Q

The most frequently employed methods for MRD assessment

A

Real-time quantitative PCR (RQ-PCR) assays (ie, NPM1,2 CBFB::MYH11, RUNX1::RUNX1T13) and
Multicolor flow cytometry (MFC) assays

NGS–based assays to detect mutated genes (targeted sequencing, 20–50 genes per panel) is not routinely used, as the sensitivity of PCR-based assays and flow cytometry is superior to what is achieved by conventional NGS.

76
Q

Timing of MRD assessment:

A
  • Upon completion of initial induction
  • Before allogeneic HCT

Additional time points should be guided by the regimen used

77
Q

RESPONSE CRITERIA DEFINITIONS

Morphologic leukemia-free state (MLFS)

A
  • BM <5% blasts in an aspirate with spicules; at least 200 cells must be enumerated
  • No blasts with Auer rods or persistence of extramedullary disease

  • If there is a question of residual leukemia, a BM aspirate/biopsy should be repeated in one week.
  • A BM biopsy/aspirate should be performed.
78
Q

RESPONSE CRITERIA DEFINITIONS

Complete response (CR)

A
  • Morphologic CR – transfusion independence
  • ANC ≥1 x 109/L (blasts <5%)
  • Platelets ≥100 x 109/L (blasts <5%)
79
Q

RESPONSE CRITERIA DEFINITIONS

CR with partial hematologic recovery (CRh)

A
  • <5% blasts in the BM, no evidence of disease (NED)
  • Partial recovery of peripheral blood counts (platelets >50 × 109/L and ANC ≥0.5 × 109/L)
80
Q

RESPONSE CRITERIA DEFINITIONS

CR with incomplete hematologic recovery (CRi)

A

All CR criteria and transfusion independence but with persistence of neutropenia (<1 x 109/L) or thrombocytopenia (<100 x 109/L)

81
Q

RESPONSE CRITERIA DEFINITIONS

Partial remission (PR)

A

Decrease of at least 50% in the percentage of blasts to 5% to 25% in the BM aspirate and the normalization of blood counts

82
Q

RESPONSE CRITERIA DEFINITIONS

Relapse following CR

A
  • Reappearance of leukemic blasts in the peripheral blood or
  • Finding of more than 5% blasts in the BM, not attributable to another cause (eg, BM regeneration after consolidation therapy) or
  • Extramedullary relapse
83
Q

RESPONSE CRITERIA DEFINITIONS

Lack of response to induction

A

Inability to attain CR or CRi following exposure to at least 2 courses of intensive induction therapy

84
Q

THERAPY FOR RELAPSED/REFRACTORY DISEASE

Targeted therapy:
Therapy for AML with FLT3-ITD mutation

Therapy for AML with FLT3-TKD mutation

Therapy for AML with IDH2 mutation

Therapy for AML with IDH1 mutation

Therapy for CD33-positive AML

A

Targeted therapy:
Therapy for AML with FLT3-ITD mutation
* Gilteritinib (category 1)
* HMAs (azacitidine or decitabine) + sorafenib
* Quizartinib4 (category 2B)

Therapy for AML with FLT3-TKD mutation
* Gilteritinib (category 1)

Therapy for AML with IDH2 mutation
* Enasidenib

Therapy for AML with IDH1 mutation
* Ivosidenib
* Olutasidenib

Therapy for CD33-positive AML
* Gemtuzumab ozogamicin

85
Q

THERAPY FOR RELAPSED/REFRACTORY DISEASE

Aggressive therapy for appropriate patients:

A
  • Cladribine + cytarabine + G-CSF ± mitoxantrone or idarubicin
  • Cytarabine ± (idarubicin or daunorubicin or mitoxantrone)
  • Fludarabine + cytarabine + G-CSF ± idarubicin
  • Etoposide + cytarabine ± mitoxantrone
  • Clofarabine ± cytarabine ± idarubicin
86
Q

THERAPY FOR RELAPSED/REFRACTORY DISEASE

Less aggressive therapy:

A
  • HMAs (azacitidine or decitabine)
  • LDAC (category 2B)
  • (HMA or LDAC) + venetoclax
87
Q

Potential drug interactions with Venetoclax

A
  • Strong CYP3A4 inhibitors (especially posaconazole) require significant dose reductions during initiation and ramp-up phase followed by a reduced daily dose.
  • The use of strong or moderate CYP3A4 inducers (eg, carbamazepine, phenytoin, rifampin) should be avoided.
88
Q

Prior to Venetoclax therapy it is important to decrease the risk of severe tumor lysis syndrome (TLS), aim to achieve WBC count of ___________ x 109/L with hydroxyurea/leukapheresis if necessary.

A

WBC count of <25 x 109/L

89
Q

Intrapatient dose escalation for venetoclax with HMA:

Intrapatient dose escalation for venetoclax with LDAC:

A

Intrapatient dose escalation for venetoclax with HMA: 100 mg, 200 mg, and 400 mg daily on days 1–3

Intrapatient dose escalation for venetoclax with LDAC: 100 mg, 200 mg, 400 mg, and 600 mg daily on days 1–4

  • Recommend treatment with allopurinol or other uric acid lowering agent until no further risk of TLS.
  • For patients with proliferative disease, monitor blood chemistries every 6–8 hours after initiation; if within normal limits, recheck once daily and continue monitoring until no further risk of TLS.
  • Aggressively monitor and manage electrolyte imbalances.
90
Q

TRUE OR FALSE

In Venetoclax use with HMA or LDAC

Continue treatment regardless of cytopenias; transfuse as needed and no growth factors until treatment cycle is complete.

A

TRUE

In Venetoclax use with HMA or LDAC

Continue treatment regardless of cytopenias; transfuse as needed and no growth factors until treatment cycle is complete.

91
Q

BM biopsy for response assessment on days _______

A

Days 21–28

  • If no morphologic remission (persistent BM blasts above 5%) but evidence of efficacy exists, proceed with a second cycle without interruption with the goal of achieving morphologic remission, and repeat BM biopsy on days 21–28 of this cycle.
92
Q

A disorder of immature dendritic cells that regulate effector T-cell function

Most commonly presents as asymptomatic skin lesions, cytopenias, circulating peripheral blasts (leukemic phase), lymphadenopathy, and CNS manifestations.

It constitutes only 0.44% of hematologic malignancies and < 1% of acute leukemia presentations

Median age, 65–67 years

Male-to-female ratio of 3:1

A

Blastic Plasmacytoid Dendritic Cell Neoplasm

93
Q

Prognosis for BPDCN is poor and the median OS is approximately ________ months when patients are treated with chemotherapy.

A

8–12 months

94
Q

BPDCN diagnosis requires at least 4 of 6 BPDCN antigens:

A
  • CD123
  • CD4
  • CD56
  • TCL-1
  • CD2AP
  • CD303/BDCA-2

Without myeloid T or B lineage expression markers

95
Q

Preferred Induction Regimen for BPDCN

A CD123-targeted therapy

A

Tagraxofusp-erzs (formerly SL-401)

12 mcg/kg IV over 15 minutes once daily on days 1–5 of a 21-day cycle7

Alternately, 5 doses can be administered over a 10-day period, if needed for dose delays.

IT chemotherapy in patients with documented CNS disease at diagnosis/
if clinically indicated (methotrexate, cytarabine)

96
Q

Patients with low performance and/or nutritional status

Options for Localized/isolated cutaneous disease

A
  • Surgical excision
  • Focal RT
97
Q

Patients with low performance and/or nutritional status

Options for Systemic disease (palliative intent)

A
  • Venetoclax-based therapy
  • Systemic steroids
  • Supportive Care
98
Q

Potentially serious adverse events associated with tagraxofusp-erzs treatment

A

Hypoalbuminemia and capillary leak syndrome

A decrease in serum albumin during the first days of treatment seems to be the most consistent predictor of capillary leak syndrome.

99
Q

Patients must have a baseline serum albumin of __________ to be able to start tagraxofusp-erzs.

A

3.2 g/dL or higher

Replace serum albumin if <3.5 g/dL or if there is a reduction of ≥0.5 from baseline.

100
Q

Hold Tagraxofusp-erzs Dosing for the Following Reasons:

A
  • Serum albumin <3.5 g/dL or a reduction from baseline of ≥0.5
  • Body weight ≥1.5 kg over prior day
  • Edema, fluid overload, and/or hypotension
  • Alanine aminotransferase (ALT)/aspartate aminotransferase (AST) increase >5 times the upper limit of normal
  • Serum creatinine >1.8 or CrCl ≤60 mL/min
  • Systolic blood pressure (SBP) ≥160 or ≤80 mmHg
  • Heart rate (HR) ≥130 bpm or ≤40 bpm
  • Temperature ≥38°C
  • Mild to severe hypersensitivity reaction
101
Q

The rate of therapy-related MDS/AML is higher among patients with certain primary tumors:

A
  • Breast cancer
  • Gynecologic cancers
  • Lymphomas (both non-Hodgkin lymphoma and Hodgkin lymphoma)
102
Q

Two well-documented categories of cytotoxic agents associated with the development of therapy-related MDS/AML:

A
  • Alkylating agents
  • Topoisomerase inhibitors
103
Q

Clinical outcomes in patients with therapy-related AML have been shown to be significantly inferior (both in terms of relapse-free survival [RFS] and overall survival [OS]) compared with patients with de novo cases except those with:

A
  • Therapy-related acute promyelocytic leukemia (APL) subtype or
  • The favorable-risk core binding factor (CBF) translocations
104
Q

Attributes of therapy-related APL (t-APL)

A
  • 1) the average age of diagnosis is 47 years with a higher incidence in females
  • 2) the risk significantly declines 2 years after completion of treatment for the primary antecedent disease;
  • 3) breast cancer, hematologic malignancy, multiple sclerosis, and genitourinary malignancy are the most common antecedent diseases;
  • 4) topoisomerase II inhibitors and RT have the highest risk associated with developing t-APL;
  • 5) the clinicopathology of t-APL is not different from de novo APL;
  • 6) the single mutation t(15;17) is most common; and
  • 7) the remission rate of t-APL is 80%, which is comparable to de novo APL

Therefore, t-APL and de novo APL are treated similarly.

105
Q

Anthracycline with longer intracellular retention time

A

Idarubicin

106
Q

A humanized anti-CD33 monoclonal antibody conjugated with the cytotoxic agent calicheamicin

A

GO

NCCN (11 decks)

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