Evidence map›Paper›PMID 35057108›Full record

ReviewPharmaceutics2022

BCR-ABL1 Tyrosine Kinase Complex Signaling Transduction: Challenges to Overcome Resistance in Chronic Myeloid Leukemia.

Gustavo P Amarante-Mendes, Aamir Rana, Tarcila Santos Datoguia, Nelson Hamerschlak, Gabriela Brumatti

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
13.5field-weighted citation impact, top 1% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

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9 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 3 countries.

Gustavo P Amarante-MendesDepartamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo 05508-000, Brazil.ORCID 0000-0002-7851-6205
Aamir RanaDepartamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo 05508-000, Brazil.
Tarcila Santos DatoguiaHospital Israelita Albert Einstein, São Paulo 05652-900, Brazil.
Nelson HamerschlakHospital Israelita Albert Einstein, São Paulo 05652-900, Brazil.ORCID 0000-0002-5140-5310
Gabriela BrumattiInflammation Division, Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia.
Hospital Israelita Albert Einstein · BRUniversidade de São Paulo · BRThe University of Melbourne · AU

Funding

Cancer Australia and Leukaemia Foundation Australia Priority Grant PdCCRS 1162023National Council for Scientific and Technological Development 303810/2018-1National Council for Scientific and Technological Development 308927/2019-2National Council for Scientific and Technological Development 408909/2018-8São Paulo Research Foundation 2015/09568-5São Paulo Research Foundation 2018/25395-1
6 · The paper itself

Abstract

The constitutively active BCR-ABL1 tyrosine kinase, found in t(9;22)(q34;q11) chromosomal translocation-derived leukemia, initiates an extremely complex signaling transduction cascade that induces a strong state of resistance to chemotherapy. Targeted therapies based on tyrosine kinase inhibitors (TKIs), such as imatinib, dasatinib, nilotinib, bosutinib, and ponatinib, have revolutionized the treatment of BCR-ABL1-driven leukemia, particularly chronic myeloid leukemia (CML). However, TKIs do not cure CML patients, as some develop TKI resistance and the majority relapse upon withdrawal from treatment. Importantly, although BCR-ABL1 tyrosine kinase is necessary to initiate and establish the malignant phenotype of Ph-related leukemia, in the later advanced phase of the disease, BCR-ABL1-independent mechanisms are also in place. Here, we present an overview of the signaling pathways initiated by BCR-ABL1 and discuss the major challenges regarding immunologic/pharmacologic combined therapies.

Indexed as

BCR-ABL1chronic myeloid leukemiatyrosine kinase inhibitors

Identifiers

PMID35057108
PMCPMC8780254
OpenAlexW4206269061

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.