Evidence map›Paper›PMID 27081524›Full record

ArticleHuman genome variation2015

Pathway activation strength is a novel independent prognostic biomarker for cetuximab sensitivity in colorectal cancer patients.

Qingsong Zhu, Evgeny Izumchenko, Alexander M Aliper, Evgeny Makarev, Keren Paz, Anton A Buzdin, Alex A Zhavoronkov, David Sidransky

Abstract read
In one paragraph

Article in Human genome variation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

32 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Observational
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

8 authors.

Qingsong ZhuInSilico Medicine, Inc. , Baltimore, MD, USA.
Evgeny IzumchenkoDepartment of Otolaryngology-Head & Neck Surgery, Johns Hopkins University School of Medicine , Baltimore, MD, USA.
Alexander M AliperInSilico Medicine, Inc., Baltimore, MD, USA; Laboratory of Bioinformatics, D. Rogachyov Federal Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia; Pathway Pharmaceuticals, Wan Chai, Hong Kong, Hong Kong SAR.
Evgeny MakarevInSilico Medicine, Inc. , Baltimore, MD, USA.
Keren PazChampions Oncology, Inc. , Baltimore, MD, USA.
Anton A BuzdinLaboratory of Bioinformatics, D. Rogachyov Federal Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia; Pathway Pharmaceuticals, Wan Chai, Hong Kong, Hong Kong SAR; Group for Genomic Regulation of Cell Signaling Systems, Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Moscow, Russia.
Alex A ZhavoronkovInSilico Medicine, Inc., Baltimore, MD, USA; Laboratory of Bioinformatics, D. Rogachyov Federal Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia; Pathway Pharmaceuticals, Wan Chai, Hong Kong, Hong Kong SAR.
David SidranskyDepartment of Otolaryngology-Head & Neck Surgery, Johns Hopkins University School of Medicine , Baltimore, MD, USA.

Funding

TUMOR SUPPRESOR GENE PROMOTER HYPERMETHYLATION FOR DETECTION OF HEAD AND NECKP50DE019032 · NIDCR · JOHNS HOPKINS UNIVERSITY · PI SIDRANSKY, DAVID · 2007 to 2016
$27.1M
NIDCR NIH HHS P50 DE019032
6 · The paper itself

Abstract

Cetuximab, a monoclonal antibody against epidermal growth factor receptor (EGFR), was shown to be active in colorectal cancer. Although some patients who harbor K-ras wild-type tumors benefit from cetuximab treatment, 40 to 60% of patients with wild-type K-ras tumors do not respond to cetuximab. Currently, there is no universal marker or method of clinical utility that could guide the treatment of cetuximab in colorectal cancer. Here, we demonstrate a method to predict response to cetuximab in patients with colorectal cancer using OncoFinder pathway activation strength (PAS), based on the transcriptomic data of the tumors. We first evaluated our OncoFinder pathway activation strength model in a set of transcriptomic data obtained from patient-derived xenograft (PDx) models established from colorectal cancer biopsies. Then, the approach and models were validated using a clinical trial data set. PAS could efficiently predict patients' response to cetuximab, and thus holds promise as a selection criterion for cetuximab treatment in metastatic colorectal cancer.

Identifiers

PMID27081524
PMCPMC4785572

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.