For Patients and Caregivers

VENCLEXTA study designs

VEN+AZA Study Design

VIALE-A

Efficacy and safety data of VENCLEXTA (venetoclax tablets) + azacitidine (VEN+AZA) were evaluated in a pivotal phase 3 trial1,3

VIALE-A was a randomized (2:1), double-blind, placebo-controlled, multicenter, phase 3 clinical trial that evaluated the efficacy and safety of VEN+AZA vs placebo (PBO)+AZA in newly diagnosed patients with AML who were ≥75 years of age, or had comorbidities that precluded the use of intensive induction chemotherapy.

Comorbidities based on at least one of the following criteria1:

  • Baseline ECOG performance status of 2-3
  • Severe cardiac or pulmonary comorbidity
  • Moderate hepatic impairment
  • CLcr <45 mL/min
  • Other comorbidities

Select clinical endpoints1,3:

  • Primary endpoint: overall survival (OS)
  • Select secondary endpoints: CR, CR+CRh, CR+CRh by initiation of Cycle 2

Efficacy was based on OS, measured from the date of randomization to death from any cause1

Complete remission (CR) was defined as absolute neutrophil count (ANC) >1,000/microliter, platelets >100,000/microliter, RBC transfusion independence, and bone marrow with <5% blasts. Absence of circulating blasts and blasts with Auer rods; absence of extramedullary disease.

Complete remission with partial hematologic recovery (CRh) was defined as <5% of blasts in the bone marrow, no evidence of disease, and partial recovery of peripheral blood counts (platelets >50,000/microliter and ANC >500/microliter).

Baseline Characteristics

VIALE-A included patients with various comorbidities and different mutational and cytogenetic profiles1,3

Select baseline characteristics for patients treated in the VIALE-A trial

76 MEDIAN
AGE
~45% ECOG
2-3
100% INTERMEDIATE
OR POOR
CYTOGENETIC RISK
Baseline characteristics1
Characteristic VEN+AZA (N=286) AZA (N=145)
Age, years; median (range) 76 (49, 91) 76 (60, 90)
Race, %
White 76 75
Black or African American 1 1.4
Asian 23 23
Male, % 60 60
ECOG performance status, %
0-1 55 56
2 40 41
3 5.6 3.4
Bone marrow blast, %
<30% 30 28
≥30% to <50% 21 23
≥50% 49 49
Disease history, %
De novo AML  75 76
Secondary AML  25 24
Cytogenetic risk detected,* %
Intermediate 64 61
Poor 36 39
Mutation analyses detected, n/N† (%)
IDH1 or IDH2 61/245 (25) 28/127 (22)
IDH1 23/245 (9.4) 11/127 (8.7)
IDH2 40/245 (16) 18/127 (14)
FLT3 29/206 (14) 22/108 (20)
NPM1 27/163 (17) 17/86 (20)
TP53 38/163 (23) 14/86 (16)

*Cytogenetic risk grading from VIALE-A trial per the 2016 NCCN Guidelines®. 
†Number of evaluable bone marrow aspirate (BMA) specimens received at baseline.

AML=acute myeloid leukemia; AZA=azacitidine; CLcr=creatinine clearance; CRh=complete remission with partial hematologic recovery; ECOG=Eastern Cooperative Oncology Group; FLT=fms-like tyrosine kinase; IDH=isocitrate dehydrogenase; NCCN=National Comprehensive Cancer Network; NPM1=nucleophosmin 1; OS=overall survival; PBO=placebo; TP53=tumor protein 53; VEN=VENCLEXTA.

VEN+DEC Study Design

M14-3581

Study M14-358 was a non-randomized, open-label trial that evaluated the efficacy and safety of VENCLEXTA (venetoclax tablets) in combination with azacitidine (VEN+AZA; N=84) or decitabine (VEN+DEC; N=31) in patients with newly diagnosed acute myeloid leukemia (AML).

Of those patients, 67 who received AZA combination and 13 who received DEC combination were 75 years or older, or had comorbidities that precluded the use of intensive induction chemotherapy based on at least one of the following criteria:

  • Baseline ECOG performance status of 2-3
  • Severe cardiac or pulmonary comorbidity
  • Moderate hepatic impairment
  • CLcr <45 mL/min, or
  • Other comorbidity

Dosing:

  • Patients received VENCLEXTA 400 mg orally once daily following completion of the ramp-up dosing schedule in combination with azacitidine (75 mg/m2 either intravenously or subcutaneously on Days 1-7 of each 28-day cycle beginning on Cycle 1, Day 1) or decitabine (20 mg/m2 was administered intravenously on Days 1-5 of each 28-day cycle beginning on Cycle 1, Day 1)
  • During the ramp-up phase, patients received TLS prophylaxis and were hospitalized for monitoring
  • Treatment was continued until disease progression or unacceptable toxicity

Baseline characteristics1

The median age of patients treated with VEN+DEC was 75 years (range: 68-86 years). ECOG performance status at baseline was 0-1 for 92% of patients and 2 for 7.7% of patients.

Of the 13 patients in the VEN+DEC arm, those who had mutations identified were as follows:

  • 31% with TP53
  • 23% with FLT3
  • 15% with NPM1
  • No patients with IDH1 or IDH2

Intermediate or poor cytogenetic risk was present in 38% and 62% of patients, respectively.

Safety icon
Review a summary of safety data for patients treated with VEN+DEC from Study M14-358
Review safety data

DEC=decitabine; TLS=tumor lysis syndrome. 

VEN+LDAC Study Design

VIALE-C1

The efficacy and safety of VENCLEXTA (venetoclax tablets) in combination with low-dose cytarabine (VEN+LDAC; N=143) vs placebo with low-dose cytarabine (PBO+LDAC; N=68) were evaluated in VIALE C, a double-blind, randomized trial in patients with newly diagnosed AML.

At baseline, patients were ≥75 years of age, or had comorbidities that precluded the use of intensive induction chemotherapy based on at least one of the following criteria:

  • Baseline ECOG performance status of 2-3
  • Severe cardiac or pulmonary comorbidity
  • Moderate hepatic impairment
  • CLcr <45 mL/min, or
  • Other comorbidity

Dosing:

  • Patients received VENCLEXTA 600 mg orally once daily on Days 1-28 following completion of the ramp-up dosing schedule or placebo in combination with LDAC at 20 mg/m2 subcutaneously once daily on Days 1-10 of each 28-day cycle beginning on Cycle 1, Day 1
  • During the 4-day ramp-up phase, patients received TLS prophylaxis and were hospitalized for monitoring

Bone marrow assessment:

  • A bone marrow assessment was performed following Cycle 1 of treatment. If bone marrow assessment confirmed a remission, defined as less than 5% leukemia blasts with cytopenia, VENCLEXTA or placebo was interrupted up to 14 days or until ANC ≥500/microliter and platelet count ≥50 × 103/microliter
  • For patients with resistant disease at the end of Cycle 1, a bone marrow assessment was performed after Cycle 2 or 3 and was clinically indicated
  • LDAC was resumed on the same day as VENCLEXTA or placebo following interruption
  • Patients continued to receive treatment until disease progression or unacceptable toxicity

Baseline characteristics1

VEN+LDAC (N=143):

The median age of patients treated with VEN+LDAC was 76 years (range: 36-93 years). ECOG performance status at baseline was 0-1 for 52% of patients, 2 for 44% of patients, and 3 for 4.2% of patients.

Mutations identified were as follows:

  • 20% (22/112) with TP53
  • 19% (21/112) with IDH1 or IDH2
  • 18% (20/112) with FLT3
  • 16% (18/112) with NPM1

Intermediate or poor cytogenetic risk was present in 63% and 33% of patients, respectively.

LDAC (N=68):

The median age of patients treated with LDAC was 76 years (range: 41-88 years). ECOG performance status at baseline was 0-1 for 50% of patients, 2 for 37% of patients, and 3 for 13% of patients.

Mutations identified were as follows:

  • 23% (12/52) with IDH1 or IDH2
  • 17% (9/52) with FLT3
  • 17% (9/52) with TP53
  • 13% (7/52) with NPM1

Intermediate or poor cytogenetic risk was present in 63% and 29% of patients, respectively.

Safety icon
Review a summary of safety data for patients treated with VEN+LDAC from the VIALE-C trial
Review safety data

LDAC=low-dose cytarabine.

Safety icon
Safety Data

Review a summary of safety data for patients treated with VENCLEXTA across different regimens 

 

Review Safety Data
NEXT: Efficacy in VEN + AZA

US-VENA-250092

Important Safety Information & Indication

Indication

VENCLEXTA is indicated in combination with azacitidine, or decitabine, or low-dose cytarabine for the treatment of newly diagnosed acute myeloid leukemia (AML) in adults 75 years or older, or who have comorbidities that preclude use of intensive induction chemotherapy.

Important Safety Information

Tumor Lysis Syndrome
  • Tumor lysis syndrome (TLS), including fatal events and renal failure requiring dialysis, has occurred in patients treated with VENCLEXTA.
  • VENCLEXTA can cause rapid reduction in tumor and thus poses a risk for TLS at initiation and during the ramp-up phase in all patients. Changes in blood chemistries consistent with TLS that require prompt management can occur as early as 6 to 8 hours following the first dose of VENCLEXTA and at each dose increase.
  • In patients with AML who followed the current 3-day ramp-up dosing schedule and the TLS prophylaxis and monitoring measures, the rate of TLS was 1.1% in patients who received VENCLEXTA in combination with azacitidine. In patients with AML who followed a 4-day ramp-up dosing schedule and the TLS prophylaxis and monitoring measures, the rate of TLS was 5.6% and included deaths and renal failure in patients who received VENCLEXTA in combination with low-dose cytarabine.
  • The risk of TLS is a continuum based on multiple factors, particularly reduced renal function, tumor burden, and type of malignancy.
  • Assess all patients for risk and provide appropriate prophylaxis for TLS, including hydration and anti-hyperuricemics. Monitor blood chemistries and manage abnormalities promptly. Employ more intensive measures (IV hydration, frequent monitoring, hospitalization) as overall risk increases. Interrupt dosing if needed; when restarting VENCLEXTA follow dose modification guidance in the Prescribing Information.
  • Concomitant use of VENCLEXTA with P-gp inhibitors or strong or moderate CYP3A inhibitors increases venetoclax exposure, which may increase the risk of TLS at initiation and during the ramp-up phase, and requires VENCLEXTA dose reduction.
Neutropenia
  • In patients with AML, baseline neutrophil counts worsened in 95% to 100% of patients treated with VENCLEXTA in combination with azacitidine or decitabine or low-dose cytarabine. Neutropenia can recur with subsequent cycles.
  • Monitor complete blood counts. Interrupt dosing for severe neutropenia. Resume at same dose then reduce duration based on remission status and first or subsequent occurrence of neutropenia. Consider supportive measures including antimicrobials and growth factors (e.g., G-CSF).
Infections
  • Fatal and serious infections such as pneumonia and sepsis have occurred in patients treated with VENCLEXTA. Monitor patients for signs and symptoms of infection and treat promptly. Withhold VENCLEXTA for Grade 3 and 4 infection until resolution and resume at same dose.
Immunization
  • Do not administer live attenuated vaccines prior to, during, or after treatment with VENCLEXTA until B-cell recovery occurs. Advise patients that vaccinations may be less effective.
Embryo-Fetal Toxicity
  • VENCLEXTA may cause embryo-fetal harm when administered to a pregnant woman. Advise females of reproductive potential to use effective contraception during treatment with VENCLEXTA and for 30 days after the last dose.
Increased Mortality in Patients with Multiple Myeloma when VENCLEXTA is Added to Bortezomib and Dexamethasone
  • In a randomized trial (BELLINI; NCT02755597) in patients with relapsed or refractory multiple myeloma, the addition of VENCLEXTA to bortezomib plus dexamethasone, a use for which VENCLEXTA is not indicated, resulted in increased mortality. Treatment of patients with multiple myeloma with VENCLEXTA in combination with bortezomib plus dexamethasone is not recommended outside of controlled clinical trials.
Adverse Reactions
  • In patients with AML receiving combination therapy with azacitidine, the most frequent serious adverse reactions (≥5%) were febrile neutropenia (30%), pneumonia (22%), sepsis (excluding fungal; 19%), and hemorrhage (6%). The most common adverse reactions including hematological abnormalities (≥30%) of any grade were neutrophils decreased (98%), platelets decreased (94%), lymphocytes decreased (91%), hemoglobin decreased (61%), nausea (44%), diarrhea (43%), febrile neutropenia (42%), musculoskeletal pain (36%), pneumonia (33%), fatigue (31%), and vomiting (30%). Fatal adverse reactions occurred in 23% of patients who received VENCLEXTA in combination with azacitidine, with the most frequent (≥2%) being pneumonia (4%), sepsis (excluding fungal; 3%), and hemorrhage (2%).
  • In patients with AML receiving combination therapy with decitabine, the most frequent serious adverse reactions (≥10%) were sepsis (excluding fungal; 46%), febrile neutropenia (38%), and pneumonia (31%). The most common adverse reactions including hematological abnormalities (≥30%) of any grade were neutrophils decreased (100%), lymphocytes decreased (100%), white blood cells decreased (100%), platelets decreased (92%), hemoglobin decreased (69%), febrile neutropenia (69%), fatigue (62%), constipation (62%), musculoskeletal pain (54%), dizziness (54%), nausea (54%), abdominal pain (46%), diarrhea (46%), pneumonia (46%), sepsis (excluding fungal; 46%), cough (38%), pyrexia (31%), hypotension (31%), oropharyngeal pain (31%), edema (31%), and vomiting (31%). One (8%) fatal adverse reaction of bacteremia occurred within 30 days of starting treatment.
  • In patients with AML receiving combination therapy with low-dose cytarabine, the most frequent serious adverse reactions (≥10%) were pneumonia (17%), febrile neutropenia (16%), and sepsis (excluding fungal; 12%). The most common adverse reactions including hematological abnormalities (≥30%) of any grade were platelets decreased (97%), neutrophils decreased (95%), lymphocytes decreased (92%), hemoglobin decreased (63%), nausea (42%), and febrile neutropenia (32%). Fatal adverse reactions occurred in 23% of patients who received VENCLEXTA in combination with LDAC, with the most frequent (≥5%) being pneumonia (6%) and sepsis (excluding fungal; 7%).
Drug Interactions
  • Concomitant use with a P-gp inhibitor or a strong or moderate CYP3A inhibitor increases VENCLEXTA exposure, which may increase VENCLEXTA toxicities, including the risk of TLS. Consider alternative medications or adjust VENCLEXTA dosage and monitor more frequently for adverse reactions. Resume the VENCLEXTA dosage that was used prior to concomitant use of a P-gp inhibitor or a strong or moderate CYP3A inhibitor 2 to 3 days after discontinuation of the inhibitor.
  • Patients should avoid grapefruit products, Seville oranges, and starfruit during treatment as they contain inhibitors of CYP3A.
  • Avoid concomitant use of strong or moderate CYP3A inducers.
  • Monitor international normalized ratio (INR) more frequently in patients receiving warfarin.
  • Avoid concomitant use of VENCLEXTA with a P-gp substrate. If concomitant use is unavoidable, separate dosing of the P-gp substrate at least 6 hours before VENCLEXTA.
Lactation
  • Advise nursing women not to breastfeed during treatment with VENCLEXTA and for 1 week after the last dose.
Females and Males of Reproductive Potential
  • Advise females of reproductive potential to use effective contraception during treatment with VENCLEXTA and for 30 days after the last dose.
  • Based on findings in animals, VENCLEXTA may impair male fertility.
Hepatic Impairment
  • Reduce the dose of VENCLEXTA for patients with severe hepatic impairment (Child-Pugh C); monitor these patients more frequently for signs of adverse reactions. No dose adjustment is recommended for patients with mild (Child-Pugh A) or moderate (Child-Pugh B) hepatic impairment.

Please see full Prescribing Information.

VENCLEXTA® and its design are registered trademarks of AbbVie Inc.

    • VENCLEXTA Prescribing Information.

      VENCLEXTA Prescribing Information.

    • Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Acute Myeloid Leukemia V.3.2026. © National Comprehensive Cancer Network, Inc. 2026. All rights reserved. Accessed November 24, 2025. To view the most recent and complete version of the guideline, go online to NCCN.org. NCCN makes no warranties of any kind whatsoever regarding their content, use or application and disclaims any responsibility for their application or use in any way.

      Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Acute Myeloid Leukemia V.3.2026. © National Comprehensive Cancer Network, Inc. 2026. All rights reserved. Accessed November 24, 2025. To view the most recent and complete version of the guideline, go online to NCCN.org. NCCN makes no warranties of any kind whatsoever regarding their content, use or application and disclaims any responsibility for their application or use in any way.

    • DiNardo CD, Jonas BA, Pullarkat V, et al. Azacitidine and venetoclax in previously untreated acute myeloid leukemia. N Engl J Med. 2020;383(7):617-629.

      DiNardo CD, Jonas BA, Pullarkat V, et al. Azacitidine and venetoclax in previously untreated acute myeloid leukemia. N Engl J Med. 2020;383(7):617-629.

    • Data on file, AbbVie Inc. ABVRRTI71211.

      Data on file, AbbVie Inc. ABVRRTI71211.

    • Data on file, AbbVie Inc. ABVRRTI71272.

      Data on file, AbbVie Inc. ABVRRTI71272.

    • Data on file, AbbVie Inc. ABVRRTI67697.

      Data on file, AbbVie Inc. ABVRRTI67697.

    • Data on file, AbbVie Inc. ABVRRTI71500.

      Data on file, AbbVie Inc. ABVRRTI71500.

    • CRESEMBA Prescribing Information.

      CRESEMBA Prescribing Information.

    • US Food and Drug Administration. Drug development and drug interactions: table of substrates, inhibitors and inducers. US Food and Drug Administration website. https://www.fda.gov/drugs/drug-interactions-labeling/drug-development-and-drug-interactions-table-substrates-inhibitors-and-inducers. Updated June 5, 2023. Accessed May 1, 2024.

      US Food and Drug Administration. Drug development and drug interactions: table of substrates, inhibitors and inducers. US Food and Drug Administration website. https://www.fda.gov/drugs/drug-interactions-labeling/drug-development-and-drug-interactions-table-substrates-inhibitors-and-inducers. Updated June 5, 2023. Accessed May 1, 2024.

    • Perl AE. The role of targeted therapy in the management of patients with AML. Blood Adv. 2017;1(24):2281-2294.

      Perl AE. The role of targeted therapy in the management of patients with AML. Blood Adv. 2017;1(24):2281-2294.

    • Karakas T, Maurer U, Weidmann E, Miething CC, Hoelzer D, Bergmann L. High expression of bcl-2 mRNA as a determinant of poor prognosis in acute myeloid leukemia. Ann Oncol. 1998;9(2):159-165.

      Karakas T, Maurer U, Weidmann E, Miething CC, Hoelzer D, Bergmann L. High expression of bcl-2 mRNA as a determinant of poor prognosis in acute myeloid leukemia. Ann Oncol. 1998;9(2):159-165.

    • Mehta SV, Shukla SN, Vora HH. Overexpression of Bcl2 protein predicts chemoresistance in acute myeloid leukemia: its correlation with FLT3. Neoplasma. 2013;60(6):666-675.

      Mehta SV, Shukla SN, Vora HH. Overexpression of Bcl2 protein predicts chemoresistance in acute myeloid leukemia: its correlation with FLT3. Neoplasma. 2013;60(6):666-675.

    • Tzifi F, Economopoulou C, Gourgiotis D, Ardavanis A, Papageorgiou S, Scorilas A. The role of BCL2 family of apoptosis regulator proteins in acute and chronic leukemias. Adv Hematol. 2012;2012:524308.

      Tzifi F, Economopoulou C, Gourgiotis D, Ardavanis A, Papageorgiou S, Scorilas A. The role of BCL2 family of apoptosis regulator proteins in acute and chronic leukemias. Adv Hematol. 2012;2012:524308.

    • Banker DE, Groudine M, Norwood T, Appelbaum FR. Measurement of spontaneous and therapeutic agent-induced apoptosis with BCL-2 protein expression in acute myeloid leukemia. Blood. 1997;89(1):243-255.

      Banker DE, Groudine M, Norwood T, Appelbaum FR. Measurement of spontaneous and therapeutic agent-induced apoptosis with BCL-2 protein expression in acute myeloid leukemia. Blood. 1997;89(1):243-255.

    • Data on file, Genentech, Inc. August 2025.

      Data on file, Genentech, Inc. August 2025.

    • Data on file, AbbVie Inc. ABVRRTI73540.

      Data on file, AbbVie Inc. ABVRRTI73540.

    • Pratz KW, Jonas BA, Pullarkat V, et al. Long-term follow-up of VIALE-A: venetoclax and azacitidine in chemotherapy-ineligible untreated acute myeloid leukemia. Am J Hematol. 2024;99(4):615-624.

      Pratz KW, Jonas BA, Pullarkat V, et al. Long-term follow-up of VIALE-A: venetoclax and azacitidine in chemotherapy-ineligible untreated acute myeloid leukemia. Am J Hematol. 2024;99(4):615-624.

    • Data on file, AbbVie Inc. ABVRRTI74719.

      Data on file, AbbVie Inc. ABVRRTI74719.

    • Ferrara F, Barosi G, Venditti A, et al. Consensus-based definition of unfitness to intensive and non-intensive chemotherapy in acute myeloid leukemia: a project of SIE, SIES and GITMO group on a new tool for therapy decision making. Leukemia. 2013;27(5):997-999.

      Ferrara F, Barosi G, Venditti A, et al. Consensus-based definition of unfitness to intensive and non-intensive chemotherapy in acute myeloid leukemia: a project of SIE, SIES and GITMO group on a new tool for therapy decision making. Leukemia. 2013;27(5):997-999.

    • Pratz KW, Jonas BA, Pullarkat V, et al. Long-term follow-up of the phase 3 VIALE-A clinical trial of venetoclax plus azacitidine for patients with untreated acute myeloid leukemia ineligible for intensive chemotherapy. Oral abstract presented at: 64th ASH Annual Meeting and Exposition; December 10, 2022; New Orleans, Louisiana. https://clin.larvol.com/abstract-detail/ASH%202022/61249960

      Pratz KW, Jonas BA, Pullarkat V, et al. Long-term follow-up of the phase 3 VIALE-A clinical trial of venetoclax plus azacitidine for patients with untreated acute myeloid leukemia ineligible for intensive chemotherapy. Oral abstract presented at: 64th ASH Annual Meeting and Exposition; December 10, 2022; New Orleans, Louisiana. https://clin.larvol.com/abstract-detail/ASH%202022/61249960

    • Pratz KW, Panayiotidis P, Recher C, et al. Venetoclax combinations delay the time to deterioration of HRQoL in unfit patients with acute myeloid leukemia. Blood Cancer J. 2022;12(4):71.

      Pratz KW, Panayiotidis P, Recher C, et al. Venetoclax combinations delay the time to deterioration of HRQoL in unfit patients with acute myeloid leukemia. Blood Cancer J. 2022;12(4):71.

    • Questionnaires. EORTC Quality of Life. Accessed February 28, 2025. https://qol.eortc.org

      Questionnaires. EORTC Quality of Life. Accessed February 28, 2025. https://qol.eortc.org

    • Pratz KW, Lai C, Jones BA, et al. Venetoclax plus azacitidine delays deterioration of health-related quality of life in patients with acute myeloid leukemia: VIALE-A long-term follow up. Oral abstract presented at: European Hematology Association (EHA) 2023 Hybrid Congress; June 8-11 2023; Frankfurt, Germany.

      Pratz KW, Lai C, Jones BA, et al. Venetoclax plus azacitidine delays deterioration of health-related quality of life in patients with acute myeloid leukemia: VIALE-A long-term follow up. Oral abstract presented at: European Hematology Association (EHA) 2023 Hybrid Congress; June 8-11 2023; Frankfurt, Germany.

    • Osoba D, Rodrigues G, Myles J, Zee B, Pater J. Interpreting the significance of changes in health-related quality-of-life scores. J Clin Oneal. 1998;16(1):139-144.

      Osoba D, Rodrigues G, Myles J, Zee B, Pater J. Interpreting the significance of changes in health-related quality-of-life scores. J Clin Oneal. 1998;16(1):139-144.

    • PROMIS Cancer Fatigue Short Form. NIH HEAL Initiative. Accessed February 28, 2025. https://www.eortc.org/app/uploads/sites/2/2018/08/Specimen-QLQ-C30-English.pdf

      PROMIS Cancer Fatigue Short Form. NIH HEAL Initiative. Accessed February 28, 2025. https://www.eortc.org/app/uploads/sites/2/2018/08/Specimen-QLQ-C30-English.pdf

    • Yost KJ, Eton DT, Garcia SF, Cella D. Minimally important differences were estimated for six Patient-Reported Outcomes Measurement Information System-Cancer scales in advanced-stage cancer patients. J Clin Epidemiol. 2011;64(5):507-516.

      Yost KJ, Eton DT, Garcia SF, Cella D. Minimally important differences were estimated for six Patient-Reported Outcomes Measurement Information System-Cancer scales in advanced-stage cancer patients. J Clin Epidemiol. 2011;64(5):507-516.

    • Richard-Carpentier G, DiNardo CD. Venetoclax for the treatment of newly diagnosed acute myeloid leukemia in patients who are ineligible for intensive chemotherapy. Ther Adv Hematol. 2019;10:1-14.

      Richard-Carpentier G, DiNardo CD. Venetoclax for the treatment of newly diagnosed acute myeloid leukemia in patients who are ineligible for intensive chemotherapy. Ther Adv Hematol. 2019;10:1-14.

    • Percival ME, Lai C, Estey E, Hourigan CS. Bone marrow evaluation for diagnosis and monitoring of acute myeloid leukemia. Blood Rev. 2017;31(4):185-192.

      Percival ME, Lai C, Estey E, Hourigan CS. Bone marrow evaluation for diagnosis and monitoring of acute myeloid leukemia. Blood Rev. 2017;31(4):185-192.

    • van Eekelen L, Pinckaers H, van dien Brand M, Hebeda KM, Litjens G. Using deep learning for quantification of cellularity and cell lineages in bone marrow biopsies and comparison to normal age-related variation. Pathology. 2022;54(3):318-327.

      van Eekelen L, Pinckaers H, van dien Brand M, Hebeda KM, Litjens G. Using deep learning for quantification of cellularity and cell lineages in bone marrow biopsies and comparison to normal age-related variation. Pathology. 2022;54(3):318-327.

    • Jonas B, Wei A, Recher C, et al. Timing of response with venetoclax combination treatment in patients with newly diagnosed acute myeloid leukemia. Am J Hematol. 2022;97:E299–E303.

      Jonas B, Wei A, Recher C, et al. Timing of response with venetoclax combination treatment in patients with newly diagnosed acute myeloid leukemia. Am J Hematol. 2022;97:E299–E303.

    +