Evidence map›Paper›PMID 12917625›Full record

ArticleOncogene2003

Loss of p53 function accelerates acquisition of telomerase activity in indefinite lifespan human mammary epithelial cell lines.

Martha R Stampfer, James Garbe, Tarlochan Nijjar, Don Wigington, Karen Swisshelm, Paul Yaswen

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.7field-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.

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

37 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
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  14. Functional role ofOncotarget · 2017
    Article
  15. 184AA3: a xenograft model of ER+ breast adenocarcinoma.Breast cancer research and treatment · 2016
    Article
  16. Article
  17. Article
  18. Article
  19. Exome-wide mutation profile in benzo[a]pyrene-derived post-stasis and immortal human mammary epithelial cells.Mutation research. Genetic toxicology and environmental mutagenesis · 2014
    Article
  20. 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

6 authors at 2 institutions in 1 country.

Martha R StampferLawrence Berkeley National Laboratory, Life Sciences Division, Berkeley, CA 94720, USA. mrstampfer@lbl.gov
James Garbe
Tarlochan Nijjar
Don Wigington
Karen Swisshelm
Paul Yaswen
Lawrence Berkeley National Laboratory · USUniversity of Washington · US

Funding

HUMAN MAMMARY CELLSR01CA024844 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI STAMPFER, MARTHA R · 1985 to 2002
$1.6M
MAMMARY CELLSR37CA024844 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI STAMPFER, MARTHA R · 1989 to 1997
–
NCI NIH HHS CA24844
6 · The paper itself

Abstract

We describe novel effects of p53 loss on immortal transformation, based upon comparison of immortally transformed human mammary epithelial cell (HMEC) lines lacking functional p53 with closely related p53(+) lines. Our previous studies of p53(+) immortal HMEC lines indicated that overcoming the stringent replicative senescence step associated with critically short telomeres (agonescence), produced indefinite lifespan lines that maintained growth without immediately expressing telomerase activity. These telomerase(-) 'conditionally immortal' HMEC underwent an additional step, termed conversion, to become fully immortal telomerase(+) lines with uniform good growth. The very gradual conversion process was associated with slow heterogeneous growth and high expression of the cyclin-dependent kinase inhibitor p57(Kip2). We now show that p53 suppresses telomerase activity and is necessary for the p57 expression in early passage p53(+) conditionally immortal HMEC lines, and that p53(-/-) lines exhibit telomerase reactivation and attain full immortality much more rapidly. A p53-inhibiting genetic suppressor element introduced into early passages of a conditionally immortal telomerase(-) p53(+) HMEC line led to rapid induction of hTERT mRNA, expression of telomerase activity, loss of p57 expression, and quick attainment of uniform good growth. These studies indicate that derangements in p53 function may impact malignant progression through direct effects on the conversion process, a potentially rate-limiting step in HMEC acquisition of uniform unlimited growth potential. These studies also provide evidence that the function of p53 in suppression of telomerase activity is separable from its cell cycle checkpoint function.

Indexed as

BreastBreast NeoplasmsCell Line, TransformedCell Transformation, NeoplasticFemaleGene DeletionHumansTelomeraseTumor Suppressor Protein p53TelomeraseTumor Suppressor Protein p53

Identifiers

PMID12917625
OpenAlexW1979401608

What OpenQuestion holds

Textmetadata
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.