Evidence map›Paper›PMID 23900891›Full record

ReviewPathology oncology research : POR2013

HSP90: chaperone-me-not.

J M Patki, S S Pawar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pathology oncology research : POR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Necroptosis inhibitors: mechanisms of action and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2024
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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

2 authors at 2 institutions in 1 country.

J M PatkiDepartment of Biotechnology and Bioinformatics, Padmashree Dr D.Y. Patil University, Sector-15, Plot-50, CBD Belapur, Navi Mumbai, India, jyotitope8@gmail.com.
S S Pawar
D.Y. Patil University · INUniversity of Mumbai · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With increasing understanding of the molecular basis of carcinogenesis, its progression and metastasis, the cancer therapy has shifted from empirical approaches to targeting specific molecules that regulate the complex network of signalling pathways for cell survival and proliferation. These include key players in malignant transformation like protein kinases, transcription factors, steroid hormone receptors, cell cycle regulators, signal transduction proteins and regulators of apoptosis. Almost all these proteins depend upon the molecular chaperone Hsp90 for their proper folding, stability and function and thus are a part of the Hsp90 clientele. Dependence of these proteins on Hsp90 makes this chaperone an appealing target for cancer therapeutics. Inhibition of Hsp90 can affect multiple oncogenic pathways simultaneously. Moreover Hsp90 inhibitors selectively kill cancer cells compared to normal cells and cancer cells have greater dependence on Hsp90 for the maintenance of intracellular protein homeostasis. All this has led to a rapid pace discovery of Hsp90 clients as well as chemical inhibitors of Hsp90. The role of hsp90 in cancer, tumor selectivity of Hsp90 inhibitors and the current status of Hsp90 inhibitors are discussed in the present review.

Indexed as

Biomarkers, TumorHSP90 Heat-Shock ProteinsHumansNeoplasmsBiomarkers, TumorHSP90 Heat-Shock Proteins

Identifiers

PMID23900891
OpenAlexW2099460892

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.