Evidence map›Paper›PMID 30094104›Full record

ReviewAmerican journal of cancer research2018

Chemoresistance and targeting of growth factors/cytokines signalling pathways: towards the development of effective therapeutic strategy for endometrial cancer.

Fengjun Guo, Haina Zhang, Zanhui Jia, Manhua Cui, Jingyan Tian

Open access · greenAbstract readReview
PubMed Full text at PMC
In one paragraph

Review in American journal of cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  16. Could Vaspin Be a Potential Diagnostic Marker in Endometrial Cancer?International journal of environmental research and public health · 2023
    Article
  17. Article
  18. Article
  19. Review
  20. miR-338-3p blocks TGFβ-induced myofibroblast differentiation through the induction of PTEN.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
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

5 authors at 2 institutions in 1 country.

Fengjun GuoDepartment of Gynaecology and Obstetrics, The Second Hospital of Jilin University 218 Ziqiang Rd, Changchun 130041, Jilin, People's Republic of China.
Haina ZhangDepartment of Rehabilitation, The Second Hospital of Jilin University 218 Ziqiang Rd, Changchun 130041, Jilin, People's Republic of China.
Zanhui JiaDepartment of Gynaecology and Obstetrics, The Second Hospital of Jilin University 218 Ziqiang Rd, Changchun 130041, Jilin, People's Republic of China.
Manhua CuiDepartment of Gynaecology and Obstetrics, The Second Hospital of Jilin University 218 Ziqiang Rd, Changchun 130041, Jilin, People's Republic of China.
Jingyan TianDepartment of Urology, Second Division of The First Hospital of Jilin University 3302 Jilin Rd, Changchun 130031, Jilin, People's Republic of China.
Second Affiliated Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometrial cancer tends to be an aggressive malignancy. Although the disease prognosis can be good at the early stages of disease, the advanced condition is not curable. Chemotherapy regimens and hormone-based therapy in combination with surgery are major approaches for the management of endometrial cancers. However, intrinsic chemoresistance reduces the success rate and increases the possibility of disease relapse. Investigation of underlying mechanisms revealed altered activation of PI3K/AKT, MAPK, fibroblast growth factor (FGF), mTOR and WNT pathways and reduced gene expression of tumor suppressor p53 in recurrent endometrial cancer. A PTEN mutation, deletion or degradation induces positive p-AKT expression, while PI3K knock-down increases the level of pro-apoptotic proteins and decreases the level of anti-apoptotic ones in cancerous cells. Additionally, RAS proteins trigger both the RAF-MEK-ERK and PI3K-PTEN-AKT signalling mechanisms, thus conferring resistance to anti-tumor agents. FGF up-regulates angiogenesis via receptor-mediated tyrosine kinase activation. Single nucleotide polymorphism, gene amplification or missense mutations of FGFR2 are associated with endometrial cancer. The mTOR complex integrates the nutrient and mitogen signals via AMPKs, S6 kinase 1 (S6K1) and eukaryotic initiation factors, causing unrestricted endometrial cellular proliferation. WNT signalling molecules, such as frizzled receptors, β-catenin, PORCN, RSPO3 and DKK1 undergo dysregulation, and drugs targeting these pathways are under clinical trials in patients with endometrial cancer. Common therapies for endometrial tumor include platinum-based anti-neoplastics, taxanes, nucleoside analogues, immune modulators, FGFR and tyrosine kinase inhibitors, small-molecule mTOR inhibitors and drugs that trigger cell cycle arrest in the G1 phase. Taken together, the current review elucidates the mechanism underlying endometrial cancer, existing therapies and chemoresistance, and points towards the need for novel therapeutics that may promote disease-free survival.

Indexed as

chemotherapyfibroblast growth factorsMAP kinasesmTOR pathwayWnt pathway

Identifiers

PMID30094104
PMCPMC6079151
OpenAlexW2983109199

What OpenQuestion holds

Textmetadata
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.