Evidence map›Paper›PMID 36902436›Full record

ArticleInternational journal of molecular sciences2023

Venetoclax-Resistant T-ALL Cells Display Distinct Cancer Stem Cell Signatures and Enrichment of Cytokine Signaling.

Kinjal Shah, Lina Al Ashiri, Ahmad Nasimian, Mehreen Ahmed, Julhash U Kazi

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Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Notch Inhibitors and BH3 Mimetics in T-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Article
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.

Kinjal ShahDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, 22381 Lund, Sweden.
Lina Al AshiriDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, 22381 Lund, Sweden.
Ahmad NasimianDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, 22381 Lund, Sweden.
Mehreen AhmedDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, 22381 Lund, Sweden.
Julhash U KaziDivision of Translational Cancer Research, Department of Laboratory Medicine, Lund University, 22381 Lund, Sweden.ORCID 0000-0002-0719-5336

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapy resistance remains one of the major challenges for cancer treatment that largely limits treatment benefits and patient survival. The underlying mechanisms that lead to therapy resistance are highly complicated because of the specificity to the cancer subtype and therapy. The expression of the anti-apoptotic protein BCL2 has been shown to be deregulated in T-cell acute lymphoblastic leukemia (T-ALL), where different T-ALL cells display a differential response to the BCL2-specific inhibitor venetoclax. In this study, we observed that the expression of anti-apoptotic BCL2 family genes, such as

Indexed as

Antineoplastic AgentsPrecursor T-Cell Lymphoblastic Leukemia-LymphomaApoptosisbcl-X ProteinBridged Bicyclo Compounds, HeterocyclicCell Line, TumorCytokinesHumansMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2SulfonamidesAntineoplastic Agentsbcl-X ProteinBridged Bicyclo Compounds, HeterocyclicCytokinesMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2Sulfonamidesvenetoclaxapoptosis resistanceBCL2 inhibitionleukemianavitoclaxtargeted therapy

Identifiers

PMID36902436
PMCPMC10003524

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Registered trials

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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.