Cited by 1,982Pancreatic and Hepatic Oncology ResearchPancreatitis Pathology and TreatmentCancer, Lipids, and Metabolism

Pancreatic cancer

Open access
Kleeff, Jorg, Korc, Murray, Apte, Minoti, La Vecchia, Carlo, Johnson, Colin D., Biankin, Andrew V., Neale, Rachel E., Tempero, Margaret +3 more·2016·Nature Reviews Disease Primers

Abstract

Pancreatic cancer is a major cause of cancer-associated mortality, with a dismal overall prognosis that has remained virtually unchanged for many decades. Currently, prevention or early diagnosis at a curable stage is exceedingly difficult; patients rarely exhibit symptoms and tumours do not display sensitive and specific markers to aid detection. Pancreatic cancers also have few prevalent genetic mutations; the most commonly mutated genes are KRAS, CDKN2A (encoding p16), TP53 and SMAD4 - none of which are currently druggable. Indeed, therapeutic options are limited and progress in drug development is impeded because most pancreatic cancers are complex at the genomic, epigenetic and metabolic levels, with multiple activated pathways and crosstalk evident. Furthermore, the multilayered interplay between neoplastic and stromal cells in the tumour microenvironment challenges medical treatment. Fewer than 20% of patients have surgically resectable disease; however, neoadjuvant therapies might shift tumours towards resectability. Although newer drug combinations and multimodal regimens in this setting, as well as the adjuvant setting, appreciably extend survival, ∼80% of patients will relapse after surgery and ultimately die of their disease. Thus, consideration of quality of life and overall survival is important. In this Primer, we summarize the current understanding of the salient pathophysiological, molecular, translational and clinical aspects of this disease. In addition, we present an outline of potential future directions for pancreatic cancer research and patient management.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/nrdp.2016.22

Cites

275 of 275 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The focus of treatment in the majority of pancreatic cancer patients has been about achieving a balance between palliative chemotherapy and maintaining quality-of-life.

    “Hence, the focus of treatment in the majority of the patients has been about achieving a balance between palliative chemotherapy and maintaining quality-of-life [4].”
  • Pancreatic ductal adenocarcinoma (PDAC) lines were chosen because cancers of the pancreas are characterized by rapid progression, invasiveness, and elevated fermentative metabolism.

    “Pancreatic ductal adenocarcinoma (PDAC) lines were chosen for our study because cancers of the pancreas are characterized by rapid progression,9,10 invasiveness,11,12 and elevated fermentative metabolism.13,14,15,16”
  • A central reason PDAC is lethal is that it is usually detected late, often after distant metastasis has occurred.

    “The factors driving the lethality of PDAC are numerous, centered on an inability to detect the disease until late in progression, often after distant metastasis3.”

    From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [3]

  • Only 15-20% of PDAC patients are eligible for surgery at diagnosis.

    “only 15–20% of patients are eligible for surgery at diagnosis3.”

    From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [3]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Kleeff, J., Korc, M., Apte, M., La Vecchia, C., Johnson, C. D., Biankin, A. V., Neale, R. E., Tempero, M., Tuveson, D. A., Hruban, R. H., & Neoptolemos, J. P.
Affiliations
  • University of Liverpool (GB)
  • Indiana University Melvin and Bren Simon Comprehensive Cancer Center (US)
  • UNSW Sydney (AU)
  • University Hospital Southampton NHS Foundation Trust (GB)
  • University of Glasgow (GB)
  • University of California, San Francisco (US)
  • Cold Spring Harbor Laboratory (US)
  • Johns Hopkins University (US)
Corresponding author
Kleeff, Jorg
Venue
Nature Reviews Disease Primers
Published
2016-04-21
Volume
2
Issue
1
Pages
16022-16022
ISSN
2056-676X (ISSN-L)
OpenAlex
W4211181525
Cited by
1,982
References
275
Citations by year
2026: 155 · 2025: 243 · 2024: 234 · 2023: 232 · 2022: 257 · 2021: 301 · 2020: 231 · 2019: 154 · 2018: 95 · 2017: 58 · 2016: 16 · 2014: 1 · 2013: 1 · 2012: 1
FWCI
10.83
Type
journal article
Language
en
Open access
Locations
  • Nature Reviews Disease Primers (publishedVersion)
  • PubMed (publishedVersion)
  • Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
  • UNSWorks (University of New South Wales, Sydney, Australia) (submittedVersion, cc-by-nc-nd)
  • ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
  • IUScholarWorks (Indiana University) (submittedVersion)
Funders
  • U.S. Department of Defense (W81XWH‐13‐PRCRP‐IA, W81XWH, W81XWH-13)
  • Pancreatic Cancer UK (FLF2015_04_GLASGOW)
  • Cancer Research UK (17263, 15957, 22533)
  • National Institute for Health and Care Research (PB-PG-0407-13363, NF-SI-0510-10126)
  • National Institutes of Health (W81XWH, 5P30CA45508-26, 5P30CA45508, CA62924, 5U01CA168409-3)
  • Medical Research Council (MR/N005813/1)
  • National Health and Medical Research Council
  • National Cancer Institute (P50CA101955, U10CA180944, CA075059, CA 62924, R01CA190092)
  • DOD Peer Reviewed Cancer Research Program
Topics
  • Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
  • Health Sciences › Medicine › Surgery › Pancreatitis Pathology and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
Keywords
pancreatic cancer, KRAS mutation, CDKN2A, TP53, SMAD4, tumor microenvironment, stromal cells, neoadjuvant therapy, adjuvant therapy, drug resistance, epigenetics, cancer metabolism, prognosis, quality of life
MeSH terms
Animals, Diabetes Mellitus, Humans, Jaundice, Magnetic Resonance Imaging, Neoplasm Proteins, Pancreatic Neoplasms, Prognosis, Risk Factors, Tomography, X-Ray Computed, Biomarkers, Tumor, Weight Loss, Proto-Oncogene Proteins p21(ras), Models, Animal, Animals, Genetically Modified, Mice, Early Detection of Cancer

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review