Evidence map›Paper›PMID 38318525›Full record

ReviewCancer drug resistance (Alhambra, Calif.)2024

Glycogen synthase kinase 3β: the nexus of chemoresistance, invasive capacity, and cancer stemness in pancreatic cancer.

Masahiro Uehara, Takahiro Domoto, Satoshi Takenaka, Osamu Takeuchi, Takeo Shimasaki, Tomoharu Miyashita, Toshinari Minamoto

Abstract readReview
In one paragraph

Review in Cancer drug resistance (Alhambra, Calif.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Unveiling the resistance to therapies in pancreatic ductal adenocarcinoma.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 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

7 authors.

Masahiro UeharaDivision of Translational and Clinical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa 920-0934, Japan.
Takahiro DomotoDivision of Translational and Clinical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa 920-0934, Japan.
Satoshi TakenakaDivision of Translational and Clinical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa 920-0934, Japan.
Osamu TakeuchiBiomedical Laboratory, Department of Research, Kitasato University Kitasato Institute Hospital, Tokyo 108-8642, Japan.
Takeo ShimasakiDivision of Translational and Clinical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa 920-0934, Japan.
Tomoharu MiyashitaDivision of Translational and Clinical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa 920-0934, Japan.
Toshinari MinamotoDivision of Translational and Clinical Oncology, Cancer Research Institute, Kanazawa University, Kanazawa 920-0934, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The treatment of pancreatic cancer remains a significant clinical challenge due to the limited number of patients eligible for curative (R0) surgery, failures in the clinical development of targeted and immune therapies, and the pervasive acquisition of chemotherapeutic resistance. Refractory pancreatic cancer is typified by high invasiveness and resistance to therapy, with both attributes related to tumor cell stemness. These malignant characteristics mutually enhance each other, leading to rapid cancer progression. Over the past two decades, numerous studies have produced evidence of the pivotal role of glycogen synthase kinase (GSK)3β in the progression of over 25 different cancer types, including pancreatic cancer. In this review, we synthesize the current knowledge on the pathological roles of aberrant GSK3β in supporting tumor cell proliferation and invasion, as well as its contribution to gemcitabine resistance in pancreatic cancer. Importantly, we discuss the central role of GSK3β as a molecular hub that mechanistically connects chemoresistance, tumor cell invasion, and stemness in pancreatic cancer. We also discuss the involvement of GSK3β in the formation of desmoplastic tumor stroma and in promoting anti-cancer immune evasion, both of which constitute major obstacles to successful cancer treatment. Overall, GSK3β has characteristics of a promising therapeutic target to overcome chemoresistance in pancreatic cancer.

Indexed as

cancer stemnesschemoresistanceglycogen synthase kinase 3βPancreatic cancertumor invasion

Identifiers

PMID38318525
PMCPMC10838383

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.