Evidence map›Paper›PMID 37310170›Full record

ArticleMolecular cancer therapeutics2023

Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer.

Susmita Ghosh, Fan Fan, Reid T Powell, Jason Roszik, Yong Sung Park, Clifford Stephan, Manu Sebastian, Lin Tan, Alexey V Sorokin, Philip L Lorenzi and 3 more

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Enhancing efficacy of the MEK inhibitor trametinib with paclitaxel inTherapeutic advances in medical oncology · 2024
    Article
  5. 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

13 authors at 1 institution in 1 country.

Susmita GhoshDepartment of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-6591-9147
Fan FanDepartment of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-6708-5430
Reid T PowellCenter for Translational Cancer Research, Texas A&M University, Houston, Texas.ORCID 0000-0002-6242-8315
Jason RoszikDepartment of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-4561-6170
Yong Sung ParkCenter for Translational Cancer Research, Texas A&M University, Houston, Texas.ORCID 0000-0001-6642-7777
Clifford StephanCenter for Translational Cancer Research, Texas A&M University, Houston, Texas.ORCID 0000-0003-0657-6484
Manu SebastianDepartment of Veterinary Medicine and Surgery, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-9229-8750
Lin TanMetabolomics Core Facility, Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-5156-7814
Alexey V SorokinDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0009-0000-7195-6868
Philip L LorenziMetabolomics Core Facility, Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-0385-7774
Scott KopetzDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-9647-3416
Lee M EllisDepartment of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-8082-4904
Rajat BhattacharyaDepartment of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-5693-6754
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DIANE BODURKA · 1985 to 2026
$290.8M
Tyrosine Kinase Signaling in Cancer Cell MetabolismR01CA140515 · NCI · UNIVERSITY OF CHICAGO · PI Jing Chen · 2010 to 2026
$5.4M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA140515
6 · The paper itself

Abstract

Mutations in KRAS are found in more than 50% of tumors from patients with metastatic colorectal cancer (mCRC). However, direct targeting of most KRAS mutations is difficult; even the recently developed KRASG12C inhibitors failed to show significant benefit in patients with mCRC. Single agents targeting mitogen-activated protein kinase kinase (MEK), a downstream mediator of RAS, have also been ineffective in colorectal cancer. To identify drugs that can enhance the efficacy of MEK inhibitors, we performed unbiased high-throughput screening using colorectal cancer spheroids. We used trametinib as the anchor drug and examined combinations of trametinib with the NCI-approved Oncology Library version 5. The initial screen, and following focused validation screens, identified vincristine as being strongly synergistic with trametinib. In vitro, the combination strongly inhibited cell growth, reduced clonogenic survival, and enhanced apoptosis compared with monotherapies in multiple KRAS-mutant colorectal cancer cell lines. Furthermore, this combination significantly inhibited tumor growth, reduced cell proliferation, and increased apoptosis in multiple KRAS-mutant patient-derived xenograft mouse models. In vivo studies using drug doses that reflect clinically achievable doses demonstrated that the combination was well tolerated by mice. We further determined that the mechanism underlying the synergistic effect of the combination was due to enhanced intracellular accumulation of vincristine associated with MEK inhibition. The combination also significantly decreased p-mTOR levels in vitro, indicating that it inhibits both RAS-RAF-MEK and PI3K-AKT-mTOR survival pathways. Our data thus provide strong evidence that the combination of trametinib and vincristine represents a novel therapeutic option to be studied in clinical trials for patients with KRAS-mutant mCRC. SIGNIFICANCE: Our unbiased preclinical studies have identified vincristine as an effective combination partner for the MEK inhibitor trametinib and provide a novel therapeutic option to be studied in patients with KRAS-mutant colorectal cancer.

Indexed as

Colonic NeoplasmsColorectal NeoplasmsMitogen-Activated Protein Kinase KinasesVincristineAnimalsCell Line, TumorHumansMiceMutationPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)TOR Serine-Threonine KinasesKRAS protein, humanMitogen-Activated Protein Kinase KinasesPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)TOR Serine-Threonine KinasesVincristine

Identifiers

PMID37310170
PMCPMC11991686
OpenAlexW4380422244

What OpenQuestion holds

Textmetadata
LicenceTDM
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.