Evidence map›Paper›PMID 11139321›Full record

ArticleBritish journal of cancer2001

Evidence against apoptosis as a major mechanism for reproductive cell death following treatment of cell lines with anti-cancer drugs.

I F Tannock, C Lee

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
7.1field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 63 citations in OpenAlex.

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  9. Determine the effect of p53 on chemosensitivity.Methods in molecular biology (Clifton, N.J.) · 2013
    Article
  10. Article
  11. Article
  12. Apoptosis and survival.Indian journal of human genetics · 2011
    Article
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  15. Article
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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 2 institutions in 1 country.

I F TannockDept of Medical Oncology and Haematology and the Division of Experimental Therapy, Ontario Cancer Institute and Princess Margaret Hospital, University of Toronto, Toronto, Canada.
C Lee
Princess Margaret Cancer Centre · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An increase in apoptotic cells may be observed after treatment with chemotherapy, and many authors have assumed that anti-cancer drugs kill cells by inducing apoptosis. The most relevant endpoint of cell death following treatment of tumour cells is loss of reproductive ability as measured by a colony-forming assay, since cells with limited reproductive potential cannot regenerate a tumour. We have therefore investigated the relationship between apoptosis and reproductive cell death following in vitro treatment of mammalian cell lines with anti-cancer drugs. Markers of apoptosis (DNA ladders, TUNEL assay) were evaluated at various times after treatment of Chinese Hamster Ovary (CHO) cells, human bladder cancer MGH-U1 cells, and a murine T-lymphocytic cell line (CTLL-2) with several anti-cancer drugs. These markers were found infrequently, despite the use of doses that cause loss of colony-forming ability, except in CTLL-2 cells. We also transfected and expressed the human pro-apoptotic gene bax and the anti-apoptotic gene bcl-2 in MGH-U1 cells and compared cell survival after drug treatment with that of control cells transfected with the vector alone. Expression of these genes had at most small effects to influence cell survival. We conclude that apoptotic mechanisms had at most a minor role in leading to reproductive death of MGH-U1 and CHO cells after chemotherapy. When apoptosis is observed following treatment with anti-cancer drugs it may be a secondary event which occurs in lethally-damaged cells, leading to their lysis, rather than a primary event that leads to loss of reproductive integrity.

Indexed as

Proto-Oncogene Proteins c-bcl-2AnimalsAntineoplastic AgentsApoptosisbcl-2-Associated X ProteinCell DivisionCell SurvivalCHO CellsCisplatinCricetinaeCytarabineDeoxycytidineDoxorubicinEtoposideGemcitabineGenes, bcl-2Antineoplastic AgentsBAX protein, humanbcl-2-Associated X ProteinCisplatinCytarabineDeoxycytidineDoxorubicinEtoposideGemcitabineProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID11139321
PMCPMC2363623
OpenAlexW1966868760

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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.