Evidence map›Paper›PMID 38607041›Full record

ReviewCells2024

Genetic Signature of Human Pancreatic Cancer and Personalized Targeting.

Stephan J Reshkin, Rosa Angela Cardone, Tomas Koltai

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Digestive cancers: mechanisms, therapeutics and management.Signal transduction and targeted therapy · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Molecular Targets for the Diagnosis and Treatment of Pancreatic Cancer.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Natural Compounds for Preventing Age-Related Diseases and Cancers.International journal of molecular sciences · 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

3 authors at 1 institution in 1 country.

Stephan J ReshkinDepartment of Biosciences, Biotechnologies and Environment, University of Bari "Aldo Moro", 70125 Bari, Italy.ORCID 0000-0001-9757-5908
Rosa Angela CardoneDepartment of Biosciences, Biotechnologies and Environment, University of Bari "Aldo Moro", 70125 Bari, Italy.ORCID 0000-0002-2011-9135
Tomas KoltaiOncomed, Via Pier Capponi 6, 50132 Florence, Italy.
University of Bari Aldo Moro · IT

Funding

European Marie Skłodowska-Curie Innovative Training Network 813834PRIN 2022 "AdaPtiviTy" 20227YTZE3PRIN 2022 PNRR "PhOXyOmicGEM" P2022L5HAZ
6 · The paper itself

Abstract

Pancreatic cancer is a highly lethal disease with a 5-year survival rate of around 11-12%. Surgery, being the treatment of choice, is only possible in 20% of symptomatic patients. The main reason is that when it becomes symptomatic, IT IS the tumor is usually locally advanced and/or has metastasized to distant organs; thus, early diagnosis is infrequent. The lack of specific early symptoms is an important cause of late diagnosis. Unfortunately, diagnostic tumor markers become positive at a late stage, and there is a lack of early-stage markers. Surgical and non-surgical cases are treated with neoadjuvant and/or adjuvant chemotherapy, and the results are usually poor. However, personalized targeted therapy directed against tumor drivers may improve this situation. Until recently, many pancreatic tumor driver genes/proteins were considered untargetable. Chemical and physical characteristics of mutated KRAS are a formidable challenge to overcome. This situation is slowly changing. For the first time, there are candidate drugs that can target the main driver gene of pancreatic cancer: KRAS. Indeed, KRAS inhibition has been clinically achieved in lung cancer and, at the pre-clinical level, in pancreatic cancer as well. This will probably change the very poor outlook for this disease. This paper reviews the genetic characteristics of sporadic and hereditary predisposition to pancreatic cancer and the possibilities of a personalized treatment according to the genetic signature.

Indexed as

Lung NeoplasmsPancreatic NeoplasmsBiomarkers, TumorHumansNeoadjuvant TherapyProto-Oncogene Proteins p21(ras)Biomarkers, TumorProto-Oncogene Proteins p21(ras)driver mutationsKRASPDAC (pancreatic ductal adenocarcinoma)personalized treatment

Identifiers

PMID38607041
PMCPMC11011857
OpenAlexW4393353310

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.