Evidence map›Paper›PMID 39118358›Full record

ReviewMolecular cancer therapeutics2024

KRAS-Driven Tumorigenesis and KRAS-Driven Therapy in Pancreatic Adenocarcinoma.

Minh T Than, Mark O'Hara, Ben Z Stanger, Kim A Reiss

Abstract readReview
In one paragraph

Review in Molecular cancer therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. KRAS Inhibitors in Pancreas Cancer: Facts and Hopes about the Immunotherapy We Have All Been Waiting for.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Review
  3. Review
  4. UnlockingCurrent oncology (Toronto, Ont.) · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Pancreatic cancer is feeling the heat.Journal for immunotherapy of cancer · 2024
    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

4 authors.

Minh T ThanDepartment of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.ORCID 0000-0002-3163-0510
Mark O'HaraDepartment of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.ORCID 0000-0003-2751-6122
Ben Z StangerDepartment of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.ORCID 0000-0003-0410-4037
Kim A ReissDepartment of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.ORCID 0000-0003-0774-9914

Funding

CANCER RESEARCH TRAINING PROGRAMT32CA009615 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Gregory L Beatty, MICHAEL D HOGARTY · 1988 to 2026
$10.4M
National Institutes of Health (NIH) CA009615NCI NIH HHS T32 CA009615
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is associated with significant morbidity and mortality and is projected to be the second leading cause of cancer-related deaths by 2030. Mutations in KRAS are found in the vast majority of PDAC cases and plays an important role in the development of the disease. KRAS drives tumor cell proliferation and survival through activating the MAPK pathway to drive cell cycle progression and to lead to MYC-driven cellular programs. Moreover, activated KRAS promotes a protumorigenic microenvironment through forming a desmoplastic stroma and by impairing antitumor immunity. Secretion of granulocyte-macrophage colony-stimulating factor and recruitment of myeloid-derived suppressor cells and protumorigenic macrophages results in an immunosuppressive environment while secretion of secrete sonic hedgehog and TGFβ drive fibroblastic features characteristic of PDAC. Recent development of several small molecules to directly target KRAS marks an important milestone in precision medicine. Many molecules show promise in preclinical models of PDAC and in early phase clinical trials. In this review, we discuss the underlying cell intrinsic and extrinsic roles of KRAS in PDAC tumorigenesis, the pharmacologic development of KRAS inhibition, and therapeutic strategies to target KRAS in PDAC.

Indexed as

Pancreatic NeoplasmsProto-Oncogene Proteins p21(ras)AdenocarcinomaAnimalsCarcinogenesisCarcinoma, Pancreatic DuctalHumansMolecular Targeted TherapyMutationTumor MicroenvironmentKRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID39118358
PMCPMC11444872

What Socratic 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 Socratic graph.