Evidence map›Paper›PMID 22270257›Full record

ArticleInvestigational new drugs2012

Combination of ATP-competitive mammalian target of rapamycin inhibitors with standard chemotherapy for colorectal cancer.

Chloe E Atreya, Gregory S Ducker, Morris E Feldman, Emily K Bergsland, Robert S Warren, Kevan M Shokat

Abstract read
PubMed Publisher
In one paragraph

Article in Investigational new drugs, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  4. Article
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  7. Article
  8. Targeting mTOR network in colorectal cancer therapy.World journal of gastroenterology · 2014
    Review
  9. 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

6 authors at 3 institutions in 1 country.

Chloe E AtreyaDivision of Hematology/Oncology, UCSF Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA. chloe.atreya@gmail.com
Gregory S Ducker
Morris E Feldman
Emily K Bergsland
Robert S Warren
Kevan M Shokat
UCSF Helen Diller Family Comprehensive Cancer Center · USUniversity of California, Berkeley · USUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ATP-competitive mammalian target of rapamycin (mTOR) inhibitors are in early phase clinical trials. These novel targeted agents, including PP242, are mechanistically distinct from the allosteric, partial mTOR inhibitor, rapamycin. The goal of this study was to evaluate how PP242 best combines with standard chemotherapies for colorectal cancer (CRC), and which subsets of patients are most likely to benefit. The combination index for PP242 plus 5-fluorouracil, oxaliplatin, or irinotecan was determined in CRC cell lines with different mutational backgrounds. In KRAS mutant CRC cell lines, sensitivity to PP242 increases with co-mutation of PIK3CA. Mutation of p53 predicts resistance to chemotherapy, but not PP242. Efficacy of PP242 was comparable to that of standard chemotherapies over the dose range tested. Sensitivity or resistance to PP242 dictates relative synergy or antagonism, respectively, when PP242 is combined with 5-fluorouracil. The same trend exists for PP242 + oxaliplatin, but with a narrower dynamic range. Conversely potency of PP242 and the combination index for PP242 + irinotecan were unrelated, but synergy exists across all dose levels in PP242 and irinotecan sensitive, p53 wild-type cell lines. Overall, our in vitro analysis predicts that mutational status can be used to rank sensitivity to PP242 and standard chemotherapies. Single agent potency can in turn be used to predict the combination index in a drug-specific manner. Our data suggest a clinical trial to determine whether ATP-competitive mTOR inhibitors provide benefit in combination with standard chemotherapies for patients with PIK3CA mutant metastatic CRC, stratified by the presence or absence of KRAS co-mutation.

Indexed as

Adenosine TriphosphateAntineoplastic AgentsCamptothecinCell Line, TumorCell ProliferationColorectal NeoplasmsDrug CombinationsFluorouracilHumansIndolesIrinotecanMutationNuclear ProteinsOrganoplatinum CompoundsOxaliplatinProto-Oncogene ProteinsAdenosine TriphosphateAntineoplastic AgentsCamptothecinDrug CombinationsFluorouracilIndolesIrinotecanKRAS protein, humanMTOR protein, humanNuclear ProteinsOrganoplatinum CompoundsOxaliplatinPI3KCA protein, humanPP242Proto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Purinesras ProteinsTOR Serine-Threonine KinasesTranscription Factors

Identifiers

PMID22270257
OpenAlexW1991613093

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.