Evidence map›Paper›PMID 36190670›Full record

ReviewCurrent treatment options in oncology2022

Pathogenic Mechanisms in Acute Myeloid Leukemia.

Sohini Chakraborty, Christopher Y Park

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current treatment options in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. miR-330-3p Inhibits the Development of Acute Myeloid Leukemia by Targeting SYTL4.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026
    Article
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  10. A Relapsed AML Case Featuring MYC and MECOM Rearrangements.Diagnostics (Basel, Switzerland) · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Sohini ChakrabortyDepartment of Pathology, New York University Grossman School of Medicine, New York, USA. Sohini.chakraborty@nyulangone.org.ORCID 0000-0002-6339-7792
Christopher Y ParkDepartment of Pathology, New York University Grossman School of Medicine, New York, USA. christopher.park@nyulangone.org.
New York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

opinion statementAcute myeloid leukemia (AML) is the most common form of leukemia in adults, leading to the highest number of annual leukemia-associated deaths in the USA. Although most AML patients initially enter remission following induction therapy, most eventually relapse, underscoring the unmet need for more effective therapies. In recent years, novel high-throughput sequencing techniques, and mouse and human models of disease have increased our understanding of the molecular mechanisms that lead to AML. Leukemogenic mechanisms can be broadly classified into two types-cell-intrinsic and cell-extrinsic. Cell-intrinsic mechanisms include an array of genetic and epigenetic alterations that lead to dysregulated gene expression and function in hematopoietic stem/progenitor cells, leading to their increased fitness and ultimately, malignant transformation. Extrinsic mechanisms include both hematopoietic and non-hematopoietic stromal components of the leukemic microenvironment that interact with pre-leukemic and leukemic clones to promote their survival, self-renewal, and/or resistance to therapy. Through the individual and concerted action of these factors, pre-leukemic clones acquire the changes necessary for leukemic transformation. In addition, following therapy, specific leukemic clones are selected for that eventually re-initiate disease. Improving our understanding of these cell-intrinsic and cell-extrinsic mechanisms will provide novel opportunities to treat AML as well as prevent the development of disease.

Indexed as

Leukemia, Myeloid, AcuteAdultAnimalsCell Transformation, NeoplasticHematopoietic Stem CellsHumansMiceTumor MicroenvironmentAcute myeloid leukemia (AML)Bone marrow (BM) microenvironmentClonal hematopoiesis (CH)Epigenetic mechanismsGermline mutationsHematopoietic stem/progenitor cells (HSPCs)Leukemia stem cells (LSCs)Noncoding RNAsSomatic mutations

Identifiers

PMID36190670
OpenAlexW4300688433

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.