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Article ; Online: Pediatric Acute Myeloid Leukemia Enters the Molecularly Targeted Era Via FLT3 Inhibition.

Perl, Alexander E

Journal of clinical oncology : official journal of the American Society of Clinical Oncology

2022 Volume 40, Issue 18, Page(s) 2058–2060

MeSH term(s)	Child ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Mutation ; fms-Like Tyrosine Kinase 3/genetics
Chemical Substances	FLT3 protein, human (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1)
Language	English
Publishing date	2022-04-18
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	604914-x
ISSN	1527-7755 ; 0732-183X
ISSN (online)	1527-7755
ISSN	0732-183X
DOI	10.1200/JCO.22.00499
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Article ; Online: Which novel agents will have a clinically meaningful impact in AML at diagnosis?

Perl, Alexander E

Best practice & research. Clinical haematology

2021 Volume 34, Issue 1, Page(s) 101257

Abstract: New drug approvals now afford AML physicians a wider choice of initial treatment options than ever before. Although chemotherapy for AML is by no means ready to be replaced entirely by novel agents, the role of traditional cytotoxics in AML therapy is ... ...

Abstract	New drug approvals now afford AML physicians a wider choice of initial treatment options than ever before. Although chemotherapy for AML is by no means ready to be replaced entirely by novel agents, the role of traditional cytotoxics in AML therapy is rapidly changing. In particular, biologically targeted agents such as the BCL2 inhibitor venetoclax and inhibitors of FLT3 and IDH mutations stand out as drugs likely to take AML therapy in important new directions. Maximum response and survival benefits likely require combinations of novel agents and chemotherapy or multiple novel agents together. The recently-published phase 3 VIALE-A study demonstrates a very successful example of a new combination approach, which led to venetoclax plus azacitidine establishing itself as the new standard of care for patients unfit for intensive chemotherapy. One could reasonably expect other subsets of AML to benefit from this regimen or other applications of venetoclax combinations. Building on this experience, venetoclax-based regimens also have the potential to replace standard intensive cytarabine/anthracycline "7&3" induction approach for some if not many patients who are fit for induction. This review will describe novel agents with the greatest potential for impactful frontline applications that will change the AML treatment paradigm.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Azacitidine/therapeutic use ; Cytarabine/therapeutic use ; Humans ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/drug therapy
Chemical Substances	Antineoplastic Agents ; Cytarabine (04079A1RDZ) ; Azacitidine (M801H13NRU)
Language	English
Publishing date	2021-02-13
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2048027-1
ISSN	1532-1924 ; 1521-6926
ISSN (online)	1532-1924
ISSN	1521-6926
DOI	10.1016/j.beha.2021.101257
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Article ; Online: MLL-menin and FLT3 inhibitors team up for AML.

Perl, Alexander E

Blood

2020 Volume 136, Issue 21, Page(s) 2369–2370

MeSH term(s)	Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Myeloid-Lymphoid Leukemia Protein/genetics ; Transcription Factors ; fms-Like Tyrosine Kinase 3/genetics
Chemical Substances	Transcription Factors ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; FLT3 protein, human (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1)
Language	English
Publishing date	2020-11-19
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2020007671
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Article ; Online: Incorporation of FLT3 Inhibitors Into the Treatment Regimens for FLT3 Mutated Acute Myeloid Leukemia: The Case for Total Therapy.

Perl, Alexander E / Pratz, Keith W

Cancer journal (Sudbury, Mass.)

2022 Volume 28, Issue 1, Page(s) 14–20

Abstract: Abstract: Therapeutic outcomes for acute myeloid leukemia patients with Fms-like tyrosine kinase 3 (FLT3) mutations have improved substantially since the discovery of small molecule tyrosine kinase inhibitors. Today, use of FLT3 inhibitors is standard ... ...

Abstract	Abstract: Therapeutic outcomes for acute myeloid leukemia patients with Fms-like tyrosine kinase 3 (FLT3) mutations have improved substantially since the discovery of small molecule tyrosine kinase inhibitors. Today, use of FLT3 inhibitors is standard in frontline intensive chemotherapy as well as patients with relapsed or refractory acute myeloid leukemia and FLT3 mutations and increasingly used as for prolonged remission maintenance posttransplant and/or postconsolidation. Yet, FLT3 inhibitors alone are not curative, and best outcomes are seen when the drugs are used as part of combination regimens. Optimizing therapy for patients with FLT3 mutations remains a work in progress. Overall, modern therapeutic approaches generate cure rates for this group at levels that argue against considering these mutations adverse risk. Still, such survivals require intensive therapy and often transplant. Therefore, efforts are underway to determine if lower toxicity regimens can attain comparable outcomes, at least for patients responding optimally. This review will review the various FLT3 inhibitors that are approved or in development, highlight the areas where they have been shown to add value, and identify areas where their use remains controversial.
MeSH term(s)	Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Protein Kinase Inhibitors/therapeutic use ; fms-Like Tyrosine Kinase 3/genetics
Chemical Substances	Protein Kinase Inhibitors ; FLT3 protein, human (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1)
Language	English
Publishing date	2022-01-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2018400-1
ISSN	1540-336X ; 1528-9117 ; 1081-4442
ISSN (online)	1540-336X
ISSN	1528-9117 ; 1081-4442
DOI	10.1097/PPO.0000000000000576
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Zs.A 4470: 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: Shall We Dance: Evolving Partnerships of Targeted Therapies for AML.

Perl, Alexander E / Vyas, Paresh

Clinical cancer research : an official journal of the American Association for Cancer Research

2022 Volume 28, Issue 13, Page(s) 2719–2721

Abstract: Two publications detailing the clinical outcomes of patients with acute myeloid leukemia and mutations in IDH1, IDH2, or FLT3 who received initial therapy with venetoclax and azacitidine provide new insights into risk stratification and set the stage for ...

Abstract	Two publications detailing the clinical outcomes of patients with acute myeloid leukemia and mutations in IDH1, IDH2, or FLT3 who received initial therapy with venetoclax and azacitidine provide new insights into risk stratification and set the stage for future trials integrating molecularly targeted therapy with this new standard regimen. See related articles by Konopleva et al., p. 2744 and Pollyea et al., p. 2753.
MeSH term(s)	Azacitidine/therapeutic use ; Bridged Bicyclo Compounds, Heterocyclic ; Dancing ; Humans ; Isocitrate Dehydrogenase/genetics ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Sulfonamides
Chemical Substances	Bridged Bicyclo Compounds, Heterocyclic ; Sulfonamides ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; IDH1 protein, human (EC 1.1.1.42.) ; Azacitidine (M801H13NRU) ; venetoclax (N54AIC43PW)
Language	English
Publishing date	2022-04-22
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-22-0279
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Zs.A 4223: Show issues

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Article: Improving Response to FLT3 Inhibitors-BCL2 the Rescue?

Perl, Alexander E

Clinical cancer research : an official journal of the American Association for Cancer Research

2019 Volume 25, Issue 22, Page(s) 6567–6569

Abstract: As single agents, FLT3 inhibitors are active in FLT3-mutated acute myeloid leukemia (AML) therapy but not curative. The BCL2 inhibitor, venetoclax, enhances responses to low intensity AML chemotherapy but its activity is limited by MCL1 upregulation. ... ...

Abstract	As single agents, FLT3 inhibitors are active in FLT3-mutated acute myeloid leukemia (AML) therapy but not curative. The BCL2 inhibitor, venetoclax, enhances responses to low intensity AML chemotherapy but its activity is limited by MCL1 upregulation. FLT3 inhibitors downregulate MCL1 and synergize with venetoclax in preclinical AML models.
MeSH term(s)	Aniline Compounds ; Humans ; Leukemia, Myeloid, Acute ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins c-bcl-2 ; Pyrazines ; Staurosporine/analogs & derivatives ; fms-Like Tyrosine Kinase 3
Chemical Substances	Aniline Compounds ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins c-bcl-2 ; Pyrazines ; gilteritinib ; FLT3 protein, human (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1) ; Staurosporine (H88EPA0A3N) ; midostaurin (ID912S5VON)
Language	English
Publishing date	2019-09-12
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-19-2339
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Article ; Online: Availability of FLT3 inhibitors: how do we use them?

Perl, Alexander E

Blood

2019 Volume 134, Issue 9, Page(s) 741–745

Abstract: The natural history of FLT3-mutated AML is changing after the approval of midostaurin for frontline therapy and gilteritinib for relapsed or refractory patients. Recently reported, positive randomized trials of the drugs gilteritinib, quizartinib, and ... ...

Abstract	The natural history of FLT3-mutated AML is changing after the approval of midostaurin for frontline therapy and gilteritinib for relapsed or refractory patients. Recently reported, positive randomized trials of the drugs gilteritinib, quizartinib, and sorafenib predict even wider use of FLT3 inhibitors going forward. FLT3 inhibitors now emerge as an important, if not indispensable, part of therapy for a large subset of high-risk patients.
MeSH term(s)	Aniline Compounds/pharmacology ; Aniline Compounds/therapeutic use ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Benzothiazoles/pharmacology ; Benzothiazoles/therapeutic use ; Clinical Trials as Topic ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Phenylurea Compounds/pharmacology ; Phenylurea Compounds/therapeutic use ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Pyrazines/pharmacology ; Pyrazines/therapeutic use ; Sorafenib/pharmacology ; Sorafenib/therapeutic use ; Staurosporine/analogs & derivatives ; Staurosporine/pharmacology ; Staurosporine/therapeutic use ; fms-Like Tyrosine Kinase 3/antagonists & inhibitors
Chemical Substances	Aniline Compounds ; Antineoplastic Agents ; Benzothiazoles ; Phenylurea Compounds ; Protein Kinase Inhibitors ; Pyrazines ; gilteritinib ; quizartinib (7LA4O6Q0D3) ; Sorafenib (9ZOQ3TZI87) ; FLT3 protein, human (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1) ; Staurosporine (H88EPA0A3N) ; midostaurin (ID912S5VON)
Language	English
Publishing date	2019-06-26
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2019876821
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Article ; Online: The most novel of the novel agents for acute myeloid leukemia.

Perl, Alexander E

Current opinion in hematology

2018 Volume 25, Issue 2, Page(s) 81–89

Abstract: Purpose of review: Precious few drugs were successfully developed for acute myeloid leukemia (AML) over the past decades, despite a dramatic expansion of our understanding of its molecular underpinnings during this time. Then in 2017, a wave of new ... ...

Abstract	Purpose of review: Precious few drugs were successfully developed for acute myeloid leukemia (AML) over the past decades, despite a dramatic expansion of our understanding of its molecular underpinnings during this time. Then in 2017, a wave of new drugs suddenly became approved. This review serves to introduce the newly available drugs, discuss their impact upon therapy, and highlight additional novel agents that are waiting in the wings. Recent findings: Newly approved agents in AML include a tyrosine kinase inhibitor for patients with FMS-like tyrosine kinase 3 (FLT3) mutations, an inhibitor of mutant isocitrate dehydrogenase (IDH2), and two novel agents using antibody-delivered or liposome-delivered cytotoxics. All of these new agents have demonstrable activity in AML and several have improved survival in randomized studies. In addition to these agents, promising data from other inhibitors of FLT3, IDH1, and B-cell lymphoma 2 (BCL2) will be discussed. Summary: Response, survival, and symptom burden of AML therapy are all improving through novel agents. As many of the newly approved drugs benefit-specific genetic subsets, a new priority has emerged to increase the speed of diagnostic genomic studies as a means to guide frontline therapy. This will ensure patients are optimally categorized and treated with to the most rational agents.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Cytotoxins/therapeutic use ; Humans ; Isocitrate Dehydrogenase/antagonists & inhibitors ; Isocitrate Dehydrogenase/genetics ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/enzymology ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/pathology ; Mutation ; Protein Kinase Inhibitors/therapeutic use ; fms-Like Tyrosine Kinase 3/antagonists & inhibitors ; fms-Like Tyrosine Kinase 3/genetics
Chemical Substances	Antineoplastic Agents ; Cytotoxins ; Protein Kinase Inhibitors ; IDH2 protein, human (EC 1.1.1.41) ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; FLT3 protein, human (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1)
Language	English
Publishing date	2018-01-25
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000411
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Article ; Online: The role of targeted therapy in the management of patients with AML.

Perl, Alexander E

Hematology. American Society of Hematology. Education Program

2017 Volume 2017, Issue 1, Page(s) 54–65

Abstract: Drug therapy for acute myeloid leukemia (AML) is finally undergoing major changes in 2017. This is due to the US Food and Drug Administration's approval of several new, targeted agents (midostaurin, enasidenib, and gemtuzumab ozogamicin). Paired with the ...

Abstract	Drug therapy for acute myeloid leukemia (AML) is finally undergoing major changes in 2017. This is due to the US Food and Drug Administration's approval of several new, targeted agents (midostaurin, enasidenib, and gemtuzumab ozogamicin). Paired with the recent approval of a novel liposomal formulation of daunorubicin/cytarabine (CPX-351/Vyxeos), the standard of care is changing rapidly in AML for subgroups. This review will focus on currently approved agents and promising novel agents in development and will highlight controversial areas in targeted treatment.
MeSH term(s)	Cytarabine/therapeutic use ; Daunorubicin/therapeutic use ; Drug Delivery Systems/methods ; Humans ; Leukemia, Myeloid, Acute/drug therapy
Chemical Substances	Cytarabine (04079A1RDZ) ; Daunorubicin (ZS7284E0ZP)
Language	English
Publishing date	2017-12-06
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1520-4383
ISSN (online)	1520-4383
DOI	10.1182/asheducation-2017.1.54
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Article: The role of targeted therapy in the management of patients with AML.

Perl, Alexander E

Blood advances

2017 Volume 1, Issue 24, Page(s) 2281–2294

Abstract	Drug therapy for acute myeloid leukemia (AML) is finally undergoing major changes in 2017. This is due to the US Food and Drug Administration's approval of several new, targeted agents (midostaurin, enasidenib, and gemtuzumab ozogamicin). Paired with the recent approval of a novel liposomal formulation of daunorubicin/cytarabine (CPX-351/Vyxeos), the standard of care is changing rapidly in AML for subgroups. This review will focus on currently approved agents and promising novel agents in development and will highlight controversial areas in targeted treatment.
Language	English
Publishing date	2017-11-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2876449-3
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2017009829
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