Evidence map›Paper›PMID 36140400›Full record

ArticleBiomedicines2022

Consecutive Inhibition of Telomerase and Alternative Lengthening Pathway Promotes Hodgkin's Lymphoma Cell Death.

Matheus Fabiao de Lima, Monique Oliveira Freitas, Mohammad K Hamedani, Aline Rangel-Pozzo, Xu-Dong Zhu, Sabine Mai

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Cellular senescence in glioma.Journal of neuro-oncology · 2023
    Review
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

6 authors at 3 institutions in 2 countries.

Matheus Fabiao de LimaDepartment of Physiology and Pathophysiology, CancerCare Manitoba Research Institute, University of Manitoba, Winnipeg, MB R3E 0V9, Canada.
Monique Oliveira FreitasGenetic Service, Institute of Paediatrics and Puericulture Martagão Gesteira (IPPMG), Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro 21941-912, Brazil.
Mohammad K HamedaniDepartment of Physiology and Pathophysiology, CancerCare Manitoba Research Institute, University of Manitoba, Winnipeg, MB R3E 0V9, Canada.
Aline Rangel-PozzoDepartment of Physiology and Pathophysiology, CancerCare Manitoba Research Institute, University of Manitoba, Winnipeg, MB R3E 0V9, Canada.
Xu-Dong ZhuDepartment of Biology, Faculty of Science, McMaster University, Hamilton, ON L8S 4K1, Canada.ORCID 0000-0003-1859-3134
Sabine MaiDepartment of Physiology and Pathophysiology, CancerCare Manitoba Research Institute, University of Manitoba, Winnipeg, MB R3E 0V9, Canada.ORCID 0000-0002-5797-2201
CancerCare Manitoba · CAMcMaster University · CAUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Telomere maintenance is key during cancer development. Malignant cells can either use telomerase or an alternative lengthening of telomere (ALT) pathway to maintain their telomere length. In Hodgkin's Lymphoma (HL), the presence of telomerase activation is established. The activation of ALT has been reported recently. Our data confirm this notion describing co-localization of the phosphorylated form of telomeric repeat-binding factor 1 (pT371-TRF1) with ALT-associated promyelocytic leukemia bodies. Surprisingly, to our knowledge, there are no published studies targeting both telomere maintenance pathways in HL. Consequently, we investigated, for the first time, the effects of both telomerase and ALT inhibition on HL cell viability: We inhibited telomerase and/or ALT, given either individually, simultaneously, or consecutively. We report that the inhibition of telomerase using BIBR1532 followed by ALT inhibition, using trabectedin, caused a decrease of greater than 90% in cell viability in three patient-derived HL cell lines. Our results suggest that HL cells are most vulnerable to the consecutive inhibition of telomerase followed by ALT inhibition.

Indexed as

alternative lengthening of telomeres (ALT)BIBR 1532promyelocytic leukemia bodies (PML)telomerasetelomeric repeat-binding factor 1 (TRF1)trabectedin

Identifiers

PMID36140400
PMCPMC9496562
OpenAlexW4296280669

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.