Evidence map›Paper›PMID 25616942›Full record

ArticleSurgery2015

Survival in ampullary cancer: potential role of different KRAS mutations.

Nakul P Valsangkar, Thun Ingkakul, Camilo Correa-Gallego, Mari Mino-Kenudson, Ricard Masia, Keith D Lillemoe, Carlos Fernández-del Castillo, Andrew L Warshaw, Andrew S Liss, Sarah P Thayer

Abstract read
In one paragraph

Article in Surgery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

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

  1. Pooled it
  2. Extrahepatic biliary obstruction due to ampullary carcinoma in a dog.The Journal of veterinary medical science · 2026
    Article
  3. Rare, Yet Targetable: New Perspectives on Ampullary Carcinomas.International journal of molecular sciences · 2026
    Review
  4. Recent Anti-KRASCancers · 2025
    Review
  5. Article
  6. Expression Profile of KRAS and p16 in Periampullary Cancer.Indian journal of surgical oncology · 2024
    Article
  7. [Treatment of Ampullary Adenocarcinoma].The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi · 2023
    Review
  8. Frontiers in cell and developmental biology · 2023
    Review
  9. Review
  10. Article
  11. Targeting Mutated KRAS Genes to Treat Solid Tumours.Molecular diagnosis & therapy · 2022
    Review
  12. Article
  13. Article
  14. Ampullary and pancreatic adenocarcinoma-a comparative study.Journal of gastrointestinal oncology · 2019
    Article
  15. Article
  16. Article
  17. Primary small bowel adenomas and adenocarcinomas-recent advances.Virchows Archiv : an international journal of pathology · 2018
    Review
  18. Article
  19. Article
  20. 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

10 authors.

Nakul P ValsangkarDepartment of Surgery, Andrew L. Warshaw, M.D. Institute for Pancreatic Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Thun IngkakulDepartment of Surgery, Andrew L. Warshaw, M.D. Institute for Pancreatic Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Camilo Correa-GallegoDepartment of Surgery, Andrew L. Warshaw, M.D. Institute for Pancreatic Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Mari Mino-KenudsonDepartment of Pathology, Andrew L. Warshaw, M.D. Institute for Pancreatic Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Ricard MasiaDepartment of Pathology, Andrew L. Warshaw, M.D. Institute for Pancreatic Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Keith D LillemoeDepartment of Surgery, Andrew L. Warshaw, M.D. Institute for Pancreatic Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Carlos Fernández-del CastilloDepartment of Surgery, Andrew L. Warshaw, M.D. Institute for Pancreatic Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Andrew L WarshawDepartment of Surgery, Andrew L. Warshaw, M.D. Institute for Pancreatic Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Andrew S LissDepartment of Surgery, Andrew L. Warshaw, M.D. Institute for Pancreatic Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Sarah P ThayerDepartment of Surgery, Andrew L. Warshaw, M.D. Institute for Pancreatic Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA. Electronic address: sarah.thayer@unmc.edu.

Funding

The RAS and P13K Pathways in Pancreatic AdenocarcinomaP01CA117969 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DEPINHO, RONALD ANTHONY · 2006 to 2025
$41.7M
Tissue and Pathology ResourcesP50CA127003 · NCI · DANA-FARBER CANCER INST · PI EL-BARDEESY, NABEEL, SELLERS, WILLIAM R · 2007 to 2023
$33.2M
NCI NIH HHS CA117969NCI NIH HHS CA127003NCI NIH HHS P01 CA117969NCI NIH HHS P50 CA127003
6 · The paper itself

Abstract

objectiveThe prognosis of ampullary adenocarcinoma (AA) usually is favorable; however, a subset of AA have poor biology and outcomes similar to pancreatic cancer. Patients in this subset will have early recurrence and death usually within 2 years. To date, there are no genetic markers to identify these patients. This study identifies the high-risk subset of AA and evaluates the mutational status of KRAS in predicting poor outcome.

methodsThe tumor registry of an academic center was reviewed for data on patients managed operatively with AA. KRAS genotypes were determined for these patients using a polymerase chain reaction-based assay on clinical specimens. Analysis of variance and χ(2) tests was used to categorize continuous and categorical variables. Univariate and multivariate survival analyses were performed using Kaplan-Meier and Cox methods, respectively.

resultsA total of 146 patients were identified with AA between 1982 and 2008. After stringent pathologic review, 97 patients were confirmed with AA, of whom 75 had tissue specimens available for analysis. Genotyping revealed 67% were wild-type (KRAS(WT)), and 33% were mutant for KRAS. Patients with KRAS(G12D) (n = 9), the most common mutational genotype, had poorer median survival (62 months) compared with those with KRAS(non-G12D) mutants (median survival not reached, mean 145 months) and KRAS(WT) patients (155 months, P = .05). Patients with survival ≤30 months were labeled "high-risk." Of the 9 patients with KRAS(G12D), 56% were in this high-risk subset, compared with 18% of KRAS(WT) (P = .02) and 31% of KRAS(non-G12D) (P > .05) populations. Patients with KRAS(G12D) also were more likely to present with advanced T stage.

conclusionThe KRAS(G12D) mutation identifies a subset of AA patients with poor prognoses and may be used to identify patients at risk of early recurrence and poorer survival who may benefit from adjuvant therapy.

Indexed as

Ampulla of VaterMutationAdenocarcinomaAdultAgedAged, 80 and overAmino Acid SubstitutionBiomarkers, TumorCommon Bile Duct NeoplasmsFemaleHumansKaplan-Meier EstimateMaleMiddle AgedPoint MutationPrognosisBiomarkers, TumorKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID25616942
PMCPMC4451831

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.