Evidence map›Paper›PMID 38687597›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2024

Clinical and Genomic Landscape of RAS Mutations in Gynecologic Cancers.

Ji Son, Yingao Zhang, Heather Lin, Oriol Mirallas, Pablo Alvarez Ballesteros, Mirella Nardo, Natalie Clark, R Tyler Hillman, Erick Campbell, Vijaykumar Holla and 14 more

Abstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Mesonephric-like Adenocarcinoma (MLA) Diagnostic Criteria and Controversies: Perspectives and Guidance From Pathologists in the MLA Consortium.International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Clinical and Genomic Landscape of RAS Mutations in Gynecologic Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  9. Review
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

24 authors.

Ji SonDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-5130-4763
Yingao ZhangDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-8589-8638
Heather LinDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-1779-7007
Oriol MirallasDepartment of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-8492-5195
Pablo Alvarez BallesterosDepartment of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-5105-6037
Mirella NardoDepartment of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-9396-7864
Natalie ClarkDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0009-0007-6798-4111
R Tyler HillmanDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-9832-9925
Erick CampbellDepartment of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-4395-224X
Vijaykumar HollaKhalifa Institute for Personalized Cancer Therapy, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-2824-3202
Amber M JohnsonKhalifa Institute for Personalized Cancer Therapy, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-6202-6113
Amadeo B BiterDepartment of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-8794-4394
Ying YuanDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-3163-480X
Lauren P CobbDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-0778-7366
David M GershensonDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-9712-2140
Amir A JazaeriDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-4335-4151
Karen H LuDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-5317-9927
Pamela T SolimanDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-8784-9212
Shannon N WestinDepartment of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-1922-0156
Elizabeth D EuscherDepartment of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-0534-7340
Barrett C LawsonDepartment of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-2485-7087
Richard K YangDepartment of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-0433-8626
Funda Meric-BernstamDepartment of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-6816-6072
David S HongDepartment of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-8721-1609

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Training of Academic Gynecologic OncologistsT32CA101642 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ANIL K SOOD, Kathleen Schmeler · 2005 to 2026
$9.2M
Cancer Prevention and Research Institute of Texas (CPRIT) RP150535National Cancer Institute (NCI) CA101642National Cancer Institute (NCI) P30CA016672NCI NIH HHS P30 CA016672NCI NIH HHS T32 CA101642
6 · The paper itself

Abstract

purposeWe aimed to describe RAS mutations in gynecologic cancers as they relate to clinicopathologic and genomic features, survival, and therapeutic implications. EXPERIMENTAL

designGynecologic cancers with available somatic molecular profiling data at our institution between February 2010 and August 2022 were included and grouped by RAS mutation status. Overall survival was estimated by the Kaplan-Meier method, and multivariable analysis was performed using the Cox proportional hazard model.

resultsOf 3,328 gynecologic cancers, 523 (15.7%) showed any RAS mutation. Patients with RAS-mutated tumors were younger (57 vs. 60 years nonmutated), had a higher prevalence of endometriosis (27.3% vs. 16.9%), and lower grades (grade 1/2, 43.2% vs. 8.1%, all P < 0.0001). The highest prevalence of KRAS mutation was in mesonephric-like endometrial (100%, n = 9/9), mesonephric-like ovarian (83.3%, n = 5/6), mucinous ovarian (60.4%), and low-grade serous ovarian (44.4%) cancers. After adjustment for age, cancer type, and grade, RAS mutation was associated with worse overall survival [hazard ratio (HR) = 1.3; P = 0.001]. Specific mutations were in KRAS (13.5%), NRAS (2.0%), and HRAS (0.51%), most commonly KRAS G12D (28.4%) and G12V (26.1%). Common co-mutations were PIK3CA (30.9%), PTEN (28.8%), ARID1A (28.0%), and TP53 (27.9%), of which 64.7% were actionable. RAS + MAPK pathway-targeted therapies were administered to 62 patients with RAS-mutated cancers. While overall survival was significantly higher with therapy [8.4 years [(95% confidence interval (CI), 5.5-12.0) vs. 5.5 years (95% CI, 4.6-6.6); HR = 0.67; P = 0.031], this effect did not persist in multivariable analysis.

conclusionsRAS mutations in gynecologic cancers have a distinct histopathologic distribution and may impact overall survival. PIK3CA, PTEN, and ARID1A are potentially actionable co-alterations. RAS pathway-targeted therapy should be considered.

Indexed as

Genital Neoplasms, FemaleMutationAdultAgedBiomarkers, TumorDNA-Binding ProteinsFemaleGenomicsHumansMiddle AgedPrognosisProto-Oncogene Proteins p21(ras)ras ProteinsTranscription FactorsARID1A protein, humanBiomarkers, TumorDNA-Binding ProteinsKRAS protein, humanProto-Oncogene Proteins p21(ras)ras ProteinsTranscription Factors

Identifiers

PMID38687597
PMCPMC11250057

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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.