Evidence map›Paper›PMID 26299805›Full record

ReviewOncotarget2015

Similar but different: distinct roles for KRAS and BRAF oncogenes in colorectal cancer development and therapy resistance.

Markus Morkel, Pamela Riemer, Hendrik Bläker, Christine Sers

Registry-linked trialOpen access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05438667 (A Prospective, One Arm Clinical Study on the Safety, Efficacy and Pharmacokinetics of KRAS Mutant Antigen Specific TCR-T Cells in the Treatment of Advanced Solid Tumors.), which is not on this map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% 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.

NCT05438667 early_phase1recruitingnot on this mapstarted 2023, after this paper: background citation

A Prospective, One Arm Clinical Study on the Safety, Efficacy and Pharmacokinetics of KRAS Mutant Antigen Specific TCR-T Cells in the Treatment of Advanced Solid Tumors.

TypeinterventionalSponsorSun Yat-Sen Memorial Hospital of Sun Yat-Sen UniversityRan2023 to 2028Enrolled18ConditionsPancreatic CancerArmsTCR-T therapy
3 · Its place in the literature

Who cites it

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Phase II Trial of Vemurafenib and Sorafenib Combination in AdvancedJournal of immunotherapy and precision oncology · 2026
    Article
  6. Article
  7. Article
  8. Colorectal cancer tumor phenotypes associated withWorld journal of gastrointestinal pathophysiology · 2025
    Article
  9. Article
  10. Gynecologic oncology reports · 2025
    Article
  11. Article
  12. Article
  13. Expert consensus on the optimal management of BRAFAsia-Pacific journal of clinical oncology · 2025
    Article
  14. UnravelingCancer drug resistance (Alhambra, Calif.) · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

21 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Markus MorkelCharité Universitätsmedizin Berlin, Institute of Pathology, Laboratory of Molecular Tumor Pathology and Systems Biology, Berlin 10117, Germany.
Pamela RiemerCharité Universitätsmedizin Berlin, Institute of Pathology, Laboratory of Molecular Tumor Pathology and Systems Biology, Berlin 10117, Germany.
Hendrik BläkerDKTK, German Consortium for Translational Cancer Research, Partner Site Berlin and DKFZ, German Cancer Research Center, D-63170 Heidelberg, Germany.
Christine SersCharité Universitätsmedizin Berlin, Institute of Pathology, Laboratory of Molecular Tumor Pathology and Systems Biology, Berlin 10117, Germany.
Charité - Universitätsmedizin Berlin · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is characterized by recurrent mutations deregulating key cell signaling cascades and providing the cancer cells with novel functional traits. Among the most frequent mutations in CRC are gain-of-function missense mutations in KRAS and BRAF. Oncogenic activation of KRAS and BRAF is mutually exclusive and occurs in approximately 40% and 10% of all CRCs, respectively. Here we summarize genetic alterations currently described in the literature and databases, indicating overlapping but also specific co-occurrences with either mutated BRAF or KRAS. We describe common and potentially specific biological functions of KRAS and BRAF oncoproteins in the intestinal epithelial cells and during initiation and progression of CRC. We discuss signal transduction networks, highlighting individual functions of oncogenic KRAS and BRAF in terms of feedback loops and their impact on treatment outcome. Finally, we give an update on current strategies of targeted therapeutic intervention in oncogenic RAS-RAF signaling networks for the treatment of metastatic CRC and outline future directions.

Indexed as

Drug Resistance, NeoplasmGene Expression Regulation, NeoplasticAnimalsColorectal NeoplasmsDisease ProgressionDNA Mutational AnalysisHumansMAP Kinase Signaling SystemMiceMutationMutation, MissenseProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)Signal TransductionStem CellsBRAF protein, humanKRAS protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)BRAFcolorectal cancerKRASsignalingtherapy

Identifiers

PMID26299805
PMCPMC4673229
OpenAlexW1942560962

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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 Socratic graph.