Evidence map›Paper›PMID 36902139›Full record

ReviewInternational journal of molecular sciences2023

The Role of BCL-2 and PD-1/PD-L1 Pathway in Pathogenesis of Myelodysplastic Syndromes.

Bartłomiej Kuszczak, Tomasz Wróbel, Katarzyna Wicherska-Pawłowska, Justyna Rybka

Registry-linked trialOpen access · goldFull text readReview
In one paragraph

Review 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. It is linked to trial NCT03969446 (Phase 1b Study of Pembrolizumab, Decitabine +/- Venetoclax Combination Therapy in Patients With Relapsed or Refractory Acute Myeloid Leukemia or Myelodysplastic Syndrome), which is not on this map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.8field-weighted citation impact, top 7% 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.

NCT03969446 phase1suspendednot on this map

Phase 1b Study of Pembrolizumab, Decitabine +/- Venetoclax Combination Therapy in Patients With Relapsed or Refractory Acute Myeloid Leukemia or Myelodysplastic Syndrome

TypeinterventionalSponsorCity of Hope Medical CenterRan2020 to 2027Enrolled54ConditionsAcute Myeloid Leukemia, Myelodysplastic Syndrome, Recurrent Acute Myeloid Leukemia, Recurrent Myelodysplastic SyndromeArmsDecitabine, Pembrolizumab, Venetoclax
3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Observational
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
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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

4 authors at 1 institution in 1 country.

Bartłomiej KuszczakDepartment and Clinic of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Ludwika Pasteura 4 Street, 50-367 Wroclaw, Poland.ORCID 0000-0002-8036-073X
Tomasz WróbelDepartment and Clinic of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Ludwika Pasteura 4 Street, 50-367 Wroclaw, Poland.
Katarzyna Wicherska-PawłowskaDepartment and Clinic of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Ludwika Pasteura 4 Street, 50-367 Wroclaw, Poland.ORCID 0000-0001-6021-1123
Justyna RybkaDepartment and Clinic of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Ludwika Pasteura 4 Street, 50-367 Wroclaw, Poland.
Wroclaw Medical University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelodysplastic syndromes (MDSs) belong to a group of clonal bone marrow malignancies. In light of the emergence of new molecules, a significant contribution to the understanding of the pathogenesis of the disease is the study of the B-cell CLL/lymphoma 2 (BCL-2) and the programmed cell death receptor 1 (PD-1) protein and its ligands. BCL-2-family proteins are involved in the regulation of the intrinsic apoptosis pathway. Disruptions in their interactions promote the progression and resistance of MDSs. They have become an important target for specific drugs. Bone marrow cytoarchitecture may prove to be a predictor of response to its use. The challenge is the observed resistance to venetoclax, for which the MCL-1 protein may be largely responsible. Molecules with the potential to break the associated resistance include S63845, S64315, chidamide and arsenic trioxide (ATO). Despite promising in vitro studies, the role of PD-1/PD-L1 pathway inhibitors has not yet been established. Knockdown of the PD-L1 gene in preclinical studies was associated with increased levels of BCL-2 and MCL-1 in lymphocytes T, which could increase their survival and promote tumor apoptosis. A trial (NCT03969446) is currently underway to combine inhibitors from both groups.

Indexed as

B7-H1 AntigenMyelodysplastic SyndromesProgrammed Cell Death 1 ReceptorProto-Oncogene Proteins c-bcl-2Antineoplastic AgentsApoptosisCell Line, TumorHumansMyeloid Cell Leukemia Sequence 1 ProteinPyrimidinesThiophenesAntineoplastic AgentsB7-H1 AntigenBCL2 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinProgrammed Cell Death 1 ReceptorProto-Oncogene Proteins c-bcl-2PyrimidinesS63845ThiophenesBCL-2BH3-mimeticsMCL-1myelodysplastic syndromesPD-1PD-L1

Identifiers

PMID36902139
PMCPMC10003626
OpenAlexW4322743106

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read57
identifiers read10
Read underepoch 390

Registered trials

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.