Evidence map›Paper›PMID 35626089›Full record

ReviewCancers2022

Resistance to Gemcitabine in Pancreatic Ductal Adenocarcinoma: A Physiopathologic and Pharmacologic Review.

Tomas Koltai, Stephan Joel Reshkin, Tiago M A Carvalho, Daria Di Molfetta, Maria Raffaella Greco, Khalid Omer Alfarouk, Rosa Angela Cardone

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 1% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Necroptosis in pancreatic cancer: Molecular mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026
    Pooled it
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7 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Tomas KoltaiVia Pier Capponi 6, 50132 Florence, Italy.
Stephan Joel ReshkinDepartment of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70126 Bari, Italy.ORCID 0000-0001-9757-5908
Tiago M A CarvalhoDepartment of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70126 Bari, Italy.
Daria Di MolfettaDepartment of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70126 Bari, Italy.ORCID 0000-0003-4696-9944
Maria Raffaella GrecoDepartment of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70126 Bari, Italy.
Khalid Omer AlfaroukZamzam Research Center, Zamzam University College, Khartoum 11123, Sudan.ORCID 0000-0001-8656-6117
Rosa Angela CardoneDepartment of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70126 Bari, Italy.ORCID 0000-0002-2011-9135
University of Bari Aldo Moro · IT

Funding

the European Marie Skłodowska-Curie Innovative Training Network (ITN) pH and Ion Transport in Pancreatic Cancer-pHioniC 813834; H2020-MSCA-ITN-2018
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a very aggressive tumor with a poor prognosis and inadequate response to treatment. Many factors contribute to this therapeutic failure: lack of symptoms until the tumor reaches an advanced stage, leading to late diagnosis; early lymphatic and hematic spread; advanced age of patients; important development of a pro-tumoral and hyperfibrotic stroma; high genetic and metabolic heterogeneity; poor vascular supply; a highly acidic matrix; extreme hypoxia; and early development of resistance to the available therapeutic options. In most cases, the disease is silent for a long time, andwhen it does become symptomatic, it is too late for ablative surgery; this is one of the major reasons explaining the short survival associated with the disease. Even when surgery is possible, relapsesare frequent, andthe causes of this devastating picture are the low efficacy ofand early resistance to all known chemotherapeutic treatments. Thus, it is imperative to analyze the roots of this resistance in order to improve the benefits of therapy. PDAC chemoresistance is the final product of different, but to some extent, interconnected factors. Surgery, being the most adequate treatment for pancreatic cancer and the only one that in a few selected cases can achieve longer survival, is only possible in less than 20% of patients. Thus, the treatment burden relies on chemotherapy in mostcases. While the FOLFIRINOX scheme has a slightly longer overall survival, it also produces many more adverse eventsso that gemcitabine is still considered the first choice for treatment, especially in combination with other compounds/agents. This review discusses the multiple causes of gemcitabine resistance in PDAC.

Indexed as

desmoplastic reactiongemcitabinehydroxyureapancreatic ductal adenocarcinomaproteasome inhibitorsresistance to treatment

Identifiers

PMID35626089
PMCPMC9139729
OpenAlexW4280509181

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.