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Article ; Online: This CAR won't start: predicting nonresponse in ALL.

Webster, Jonathan A / Luznik, Leo

2023 Volume 7, Issue 15, Page(s) 4215–4217

MeSH term(s)	Child ; Humans ; Epigenome ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; T-Lymphocytes
Language	English
Publishing date	2023-08-08
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2023009776
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Article: Treatment of AML Relapse After Allo-HCT.

Webster, Jonathan A / Luznik, Leo / Gojo, Ivana

Frontiers in oncology

2021 Volume 11, Page(s) 812207

Abstract: With advances in allogeneic hematopoietic stem cell transplant (allo-HCT), disease relapse has replaced transplant-related mortality as the primary cause of treatment failure for patients with acute myeloid leukemia (AML). The efficacy of allo-HCT in AML ...

Abstract	With advances in allogeneic hematopoietic stem cell transplant (allo-HCT), disease relapse has replaced transplant-related mortality as the primary cause of treatment failure for patients with acute myeloid leukemia (AML). The efficacy of allo-HCT in AML is a consequence of a graft-versus-leukemia (GVL) effect that is mediated by T lymphocytes, and unique mechanisms of immune evasion underlying post-allo-HCT AML relapses have recently been characterized. Relapsed AML following allo-HCT presents a particularly vexing clinical challenge because transplant-related toxicities, such as graft-versus-host (GVHD) and infections, increase the risk of treatment-related morbidity and mortality. In general, the prognosis of relapsed AML following allo-HCT is poor with most patients failing to achieve a subsequent remission and 2-year survival consistently <15%. The two factors that have been found to predict a better prognosis are a longer duration of post-transplant remission prior to relapse and a lower disease burden at the time of relapse. When considered in combination with a patient's age; co-morbidities; and performance status, these factors can help to inform the appropriate therapy for the treatment of post-transplant relapse. This review discusses the options for the treatment of post-transplant AML relapse with a focus on the options to achieve a subsequent remission and consolidation with cellular immunotherapy, such as a second transplant or donor lymphocyte infusion (DLI). While intensive reinduction therapy and less intensive approaches with hypomethylating agents have long represented the two primary options for the initial treatment of post-transplant relapse, molecularly targeted therapies and immunotherapy are emerging as potential alternative options to achieve remission. Herein, we highlight response and survival outcomes achieved specifically in the post-transplant setting using each of these approaches and discuss how some therapies may overcome the immunologic mechanisms that have been implicated in post-transplant relapse. As long-term survival in post-transplant relapse necessarily involves consolidation with cellular immunotherapy, we present data on the efficacy and toxicity of both DLI and second allo-HCT including when such therapies are integrated with reinduction. Finally, we provide our general approach to the treatment of post-transplant relapse, integrating both novel therapies and our improved understanding of the mechanisms underlying post-transplant relapse.
Language	English
Publishing date	2021-12-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2021.812207
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Article ; Online: DNA methyltransferase inhibitor exposure-response: Challenges and opportunities.

Kagan, Amanda B / Garrison, Dominique A / Anders, Nicole M / Webster, Jonathan A / Baker, Sharyn D / Yegnasubramanian, Srinivasan / Rudek, Michelle A

Clinical and translational science

2023 Volume 16, Issue 8, Page(s) 1309–1322

Abstract: Although DNA methyltransferase inhibitors (DNMTis), such as azacitidine and decitabine, are used extensively in the treatment of myelodysplastic syndromes and acute myeloid leukemia, there remain unanswered questions about DNMTi's mechanism of action and ...

Abstract	Although DNA methyltransferase inhibitors (DNMTis), such as azacitidine and decitabine, are used extensively in the treatment of myelodysplastic syndromes and acute myeloid leukemia, there remain unanswered questions about DNMTi's mechanism of action and predictors of clinical response. Because patients often remain on single-agent DNMTis or DNMTi-containing regimens for several months before knowing whether clinical benefit can be achieved, the development and clinical validation of response-predictive biomarkers represents an important unmet need in oncology. In this review, we will summarize the clinical studies that led to the approval of azacitidine and decitabine, as well as the real-world experience with these drugs. We will then focus on biomarker development for DNMTis-specifically, efforts at determining exposure-response relationships and challenges that remain impacting the broader clinical translation of these methods. We will highlight recent progress in liquid-chromatography tandem mass spectrometry technology that has allowed for the simultaneous measurement of decitabine genomic incorporation and global DNA methylation, which has significant potential as a mechanism-of-action based biomarker in patients on DNMTis. Last, we will cover important research questions that need to be addressed in order to optimize this potential biomarker for clinical use.
MeSH term(s)	Humans ; Decitabine/therapeutic use ; Azacitidine/therapeutic use ; Azacitidine/pharmacology ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Leukemia, Myeloid, Acute/drug therapy ; DNA Methylation ; DNA ; Methyltransferases
Chemical Substances	Decitabine (776B62CQ27) ; Azacitidine (M801H13NRU) ; Enzyme Inhibitors ; DNA (9007-49-2) ; Methyltransferases (EC 2.1.1.-)
Language	English
Publishing date	2023-06-21
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2433157-0
ISSN	1752-8062 ; 1752-8054
ISSN (online)	1752-8062
ISSN	1752-8054
DOI	10.1111/cts.13548
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Article ; Online: Acute myeloid leukemia in the elderly: therapeutic options and choice.

Webster, Jonathan A / Pratz, Keith W

Leukemia & lymphoma

2017 Volume 59, Issue 2, Page(s) 274–287

Abstract: Acute myeloid leukemia (AML) therapies are rapidly evolving with novel targeted therapies showing high-level responses in a notoriously difficult to treat group of patients - the elderly and unfit. This review will examine the outcomes of older AML ... ...

Abstract	Acute myeloid leukemia (AML) therapies are rapidly evolving with novel targeted therapies showing high-level responses in a notoriously difficult to treat group of patients - the elderly and unfit. This review will examine the outcomes of older AML patients (>60 years old) with conventional induction strategies, and published literature on risks of pursuit of induction. Low-intensity combination therapy response rates appear to be approaching that of induction regimens, and with lower toxicity, low-intensity therapy likely represents the future standard approach in this age group. Lastly, allogeneic transplant appears to have a role in increasing durable remissions regardless of age and should be considered in patients with limited comorbidities.
MeSH term(s)	Age Factors ; Aged ; Aged, 80 and over ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Clinical Decision-Making ; Combined Modality Therapy ; Consolidation Chemotherapy ; Disease Management ; Humans ; Incidence ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/epidemiology ; Leukemia, Myeloid, Acute/therapy ; Maintenance Chemotherapy ; Molecular Targeted Therapy ; Mortality ; Remission Induction/methods ; Treatment Outcome
Language	English
Publishing date	2017-06-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1042374-6
ISSN	1029-2403 ; 1042-8194
ISSN (online)	1029-2403
ISSN	1042-8194
DOI	10.1080/10428194.2017.1330956
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Article ; Online: Mobile app validation: a digital health scorecard approach.

Sedhom, Ramy / McShea, Michael J / Cohen, Adam B / Webster, Jonathan A / Mathews, Simon C

NPJ digital medicine

2021 Volume 4, Issue 1, Page(s) 111

Abstract: While digital health solutions continue to grow in number and in complexity, the ability for stakeholders in healthcare to easily discern quality lags far behind. This challenge is in part due to the lack of a transparent and standardized approach to ... ...

Abstract	While digital health solutions continue to grow in number and in complexity, the ability for stakeholders in healthcare to easily discern quality lags far behind. This challenge is in part due to the lack of a transparent and standardized approach to validation. Evaluation of mobile health applications (apps) is further burdened by low barriers to development and direct-to-user marketing, leading to a crowded and confusing landscape. In this context, we investigated the pragmatic application of a previously described framework for digital health validation, the Digital Health Scorecard, in a cohort of 22 popular mobile health oncology apps. The apps evaluated using this framework performed poorly, scoring 49.4% across all evaluation criteria as a group. Performance across component domains varied considerably with cost scoring highest at 100%, usability at 56.7%, technical at 37.3%, and clinical at 15.9%. satisfaction of prospectively determined end-user requirements derived from patient, family, and clinician consensus scored 37.2%. While cost outperformed consistently and usability was adequate, the results also suggested that apps suffered from significant technical limitations, were of limited clinical value, and generally did not do what end users wanted. These large gaps further support the need for transparent and standardized evaluation to help all stakeholders in healthcare improve the quality of mobile health.
Language	English
Publishing date	2021-07-15
Publishing country	England
Document type	Journal Article
ISSN	2398-6352
ISSN (online)	2398-6352
DOI	10.1038/s41746-021-00476-7
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Article ; Online: Outcome heterogeneity of

Pasca, Sergiu / Haldar, Saurav D / Ambinder, Alexander / Webster, Jonathan A / Jain, Tania / Dalton, W Brian / Prince, Gabrielle T / Ghiaur, Gabriel / DeZern, Amy E / Gojo, Ivana / Smith, B Douglas / Karantanos, Theodoros / Schulz, Cory / Stokvis, Kristin / Levis, Mark J / Jones, Richard J / Gondek, Lukasz P

Haematologica

2024 Volume 109, Issue 3, Page(s) 948–952

MeSH term(s)	Humans ; Hematopoietic Stem Cell Transplantation ; Neoplasms ; Tumor Suppressor Protein p53/genetics
Chemical Substances	TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2024-03-01
Publishing country	Italy
Document type	Journal Article
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2023.283886
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Uh III Zs.76: Show issues

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Article ; Online: B-Lymphoid Blast Phase of Chronic Myeloid Leukemia: A Case Report and Review of the Literature.

Ware, Alisha D / Wake, Laura / Brown, Patrick / Webster, Jonathan A / Smith, B Douglas / Duffield, Amy S

AJSP: reviews & reports

2020 Volume 24, Issue 5, Page(s) 191–195

Abstract: Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disorder characterized by a reciprocal translocation, t(9;22) (q34.1;q11.2). This leads to fusion of ... ...

Abstract	Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disorder characterized by a reciprocal translocation, t(9;22) (q34.1;q11.2). This leads to fusion of the
Language	English
Publishing date	2020-07-14
Publishing country	United States
Document type	Journal Article
ISSN	2381-652X
ISSN (online)	2381-652X
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Article ; Online: AMPK inhibition sensitizes acute leukemia cells to BH3 mimetic-induced cell death.

Cell death and differentiation

2024 Volume 31, Issue 4, Page(s) 405–416

Abstract: BH3 mimetics, including the BCL2/ ... ...

Abstract	BH3 mimetics, including the BCL2/BCLX
MeSH term(s)	Humans ; Animals ; Aniline Compounds/pharmacology ; Sulfonamides/pharmacology ; AMP-Activated Protein Kinases/metabolism ; Mice ; bcl-X Protein/metabolism ; bcl-X Protein/antagonists & inhibitors ; Cell Line, Tumor ; Pyrimidines/pharmacology ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Myeloid Cell Leukemia Sequence 1 Protein/antagonists & inhibitors ; Pyrazoles/pharmacology ; bcl-Associated Death Protein/metabolism ; Apoptosis/drug effects ; Cell Death/drug effects ; Leukemia/drug therapy ; Leukemia/pathology ; Leukemia/metabolism ; Phosphorylation/drug effects ; Peptide Fragments/pharmacology ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins/antagonists & inhibitors ; Drug Synergism
Chemical Substances	Aniline Compounds ; Sulfonamides ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; bcl-X Protein ; Pyrimidines ; Myeloid Cell Leukemia Sequence 1 Protein ; navitoclax (XKJ5VVK2WD) ; Pyrazoles ; dorsomorphin (10K52CIC1Z) ; bcl-Associated Death Protein ; MCL1 protein, human ; Peptide Fragments ; BCL2L1 protein, human ; Proto-Oncogene Proteins ; BAD protein, human
Language	English
Publishing date	2024-03-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-024-01283-9
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Zs.A 4230: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Venetoclax in combination with hypomethylating agent for the treatment of advanced myeloproliferative neoplasms and acute myeloid leukemia with extramedullary disease.

Sanber, Khaled / Ye, Kevin / Tsai, Hua-Ling / Newman, Matthew / Webster, Jonathan A / Gojo, Ivana / Ghiaur, Gabriel / Prince, Gabrielle T / Gondek, Lukasz P / Smith, B Douglas / Levis, Mark J / DeZern, Amy E / Ambinder, Alexander J / Dalton, William B / Jain, Tania

Leukemia & lymphoma

2023 Volume 64, Issue 4, Page(s) 846–855

Abstract: The combination of venetoclax and hypomethylating agent (HMA/venetoclax) has emerged as a treatment option for patients with de novo acute myeloid leukemia (AML) who are unfit to receive intensive chemotherapy. In this single-center retrospective study, ... ...

Abstract	The combination of venetoclax and hypomethylating agent (HMA/venetoclax) has emerged as a treatment option for patients with de novo acute myeloid leukemia (AML) who are unfit to receive intensive chemotherapy. In this single-center retrospective study, we evaluated clinical outcomes following treatment with HMA/venetoclax in 35 patients with advanced myeloproliferative neoplasms, myelodysplastic syndrome/myeloproliferative neoplasm overlap syndromes or AML with extramedullary disease. The composite complete remission (CR) rate (including confirmed/presumed complete cytogenetic response, acute leukemia response-complete, CR and CR with incomplete hematologic recovery) was 42.9% with median overall survival (OS) of 9.7 months. Complex karyotype was associated with inferior median OS (3.7 versus 12.2 months;
MeSH term(s)	Humans ; Retrospective Studies ; Bridged Bicyclo Compounds, Heterocyclic/adverse effects ; Sulfonamides ; Myeloproliferative Disorders/diagnosis ; Myeloproliferative Disorders/drug therapy ; Myeloproliferative Disorders/genetics ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Azacitidine/therapeutic use
Chemical Substances	venetoclax (N54AIC43PW) ; Bridged Bicyclo Compounds, Heterocyclic ; Sulfonamides ; Azacitidine (M801H13NRU)
Language	English
Publishing date	2023-02-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	1042374-6
ISSN	1029-2403 ; 1042-8194
ISSN (online)	1029-2403
ISSN	1042-8194
DOI	10.1080/10428194.2023.2173523
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Article ; Online: A randomized, phase II trial of adjuvant immunotherapy with durable TKI-free survival in patients with chronic phase CML.

Webster, Jonathan A / Robinson, Tara M / Blackford, Amanda L / Warlick, Erica / Ferguson, Anna / Borrello, Ivan / Zahurak, Marianna / Jones, Richard J / Smith, B Douglas

Leukemia research

2021 Volume 111, Page(s) 106737

Abstract: Purpose: Chronic myeloid leukemia (CP-CML) patients can achieve undetectable minimal residual disease (UMRD) and discontinue tyrosine kinase inhibitors (TKIs). Cellular immunity plays an important role in CML disease control. We conducted a randomized, ... ...

Abstract	Purpose: Chronic myeloid leukemia (CP-CML) patients can achieve undetectable minimal residual disease (UMRD) and discontinue tyrosine kinase inhibitors (TKIs). Cellular immunity plays an important role in CML disease control. We conducted a randomized, non-blinded phase II trial of adjuvant immunotherapy with TKIs to facilitate TKI discontinuation. Methods: TKI-treated patients with CP-CML were randomized to receive the K562/GM-CSF vaccine (vaccine) OR Interferon-α + Sargramostim (IFN). If UMRD was achieved, then all treatment was stopped. Patients who did not achieve UMRD within one year, had a molecular relapse, or discontinued therapy for toxicity could crossover. Results: Thirty-four patients were randomized to IFN (n = 18) or vaccine (n = 16), and 21 patients crossed over (IFN⟶vaccine: n = 9, vaccine⟶IFN, n = 12). TKIs at enrollment included imatinib (n = 31), nilotinib (n = 2), and dasatinib (n = 1). No patients discontinued vaccine due to side effects, while 33 % of IFN-treated patients discontinued treatment. More patients randomized to IFN (47.4 %, 95 % CI: 16.7-66.7 %) versus vaccine (25.0 %, 95 % CI: 0.5-43.5 %) achieved UMRD within one year. Seven patients randomized to IFN discontinued treatment with 28.6 % (95 % CI: 8.9-92.2 %) sustaining treatment-free remission (TFR) at 1 year, while three patients randomized to vaccine discontinued treatment with none sustaining TFR. Including crossover, there was a cumulative discontinuation success rate of 36.4 % (95 % CI: 16.6 %-79.5 %) after adjuvant IFN. Patients who sustained TFR received a median of 29 months of imatinib prior to discontinuation. Conclusion: Adjuvant IFN led to durable TFRs with limited prior TKI exposure with comparable success to prior discontinuation trials, but many patients stopped IFN early.
MeSH term(s)	Adjuvants, Immunologic/administration & dosage ; Adult ; Aged ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Cancer Vaccines/administration & dosage ; Cross-Over Studies ; Dasatinib/administration & dosage ; Female ; Follow-Up Studies ; Humans ; Imatinib Mesylate/administration & dosage ; Immunotherapy/mortality ; Interferons/administration & dosage ; Leukemia, Myeloid, Chronic-Phase/drug therapy ; Leukemia, Myeloid, Chronic-Phase/immunology ; Leukemia, Myeloid, Chronic-Phase/mortality ; Leukemia, Myeloid, Chronic-Phase/pathology ; Male ; Middle Aged ; Prognosis ; Pyrimidines/administration & dosage ; Survival Rate ; Young Adult
Chemical Substances	Adjuvants, Immunologic ; Cancer Vaccines ; Pyrimidines ; Imatinib Mesylate (8A1O1M485B) ; Interferons (9008-11-1) ; nilotinib (F41401512X) ; Dasatinib (RBZ1571X5H)
Language	English
Publishing date	2021-11-02
Publishing country	England
Document type	Clinical Trial, Phase II ; Journal Article ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural
ZDB-ID	752396-8
ISSN	1873-5835 ; 0145-2126
ISSN (online)	1873-5835
ISSN	0145-2126
DOI	10.1016/j.leukres.2021.106737
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