Evidence map›Paper›PMID 25162504›Full record

ArticlePloS one2014

Spontaneous genomic alterations in a chimeric model of colorectal cancer enable metastasis and guide effective combinatorial therapy.

Yinghui Zhou, William M Rideout, Angela Bressel, Sireesha Yalavarthi, Tong Zi, Darren Potz, Samuel Farlow, Joelle Brodeur, Anthony Monti, Shailaja Reddipalli and 6 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. MicroRNA-21 promotes cell proliferation by targeting tumor suppressor TET1 in colorectal cancer.International journal of clinical and experimental pathology · 2018
    Article
  6. Article
  7. 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

16 authors at 2 institutions in 1 country.

Yinghui ZhouDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
William M RideoutDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Angela BresselDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Sireesha YalavarthiDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Tong ZiDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Darren PotzDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Samuel FarlowDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Joelle BrodeurDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Anthony MontiDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Shailaja ReddipalliDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Qiurong XiaoDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Steve BottegaDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Bin FengDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
M Isabel ChiuDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
Marcus BosenbergDepartment of Dermatology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
Joerg HeyerDepartment of Research, AVEO Pharmaceuticals, Inc., Cambridge, Massachusetts, United States of America.
AVEO Oncology (United States) · USYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colon cancer is the second most common cause of cancer mortality in the Western world with metastasis commonly present at the time of diagnosis. Screening for propagation and metastatic behavior in a novel chimeric-mouse colon cancer model, driven by mutant p53 and β-Catenin, led to the identification of a unique, invasive adenocarcinoma. Comparison of the genome of this tumor, CB42, with genomes from non-propagating tumors by array CGH and sequencing revealed an amplicon on chromosome five containing CDK6 and CDK14, and a KRAS mutation, respectively. Single agent small molecule inhibition of either CDK6 or MEK, a kinase downstream of KRAS, led to tumor growth inhibition in vivo whereas combination therapy not only led to regression of the subcutaneous tumors, but also near complete inhibition of lung metastasis; thus, genomic analysis of this tumor led to effective, individualized treatment.

Indexed as

AdenocarcinomaColonic NeoplasmsLung NeoplasmsMutationNeoplasm ProteinsNeoplasms, ExperimentalAnimalsMiceNeoplasm MetastasisNeoplasm Proteins

Identifiers

PMID25162504
PMCPMC4146580
OpenAlexW2047533852

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.