Evidence map›Paper›PMID 22130737›Full record

ReviewAmino acids2013

Tissue transglutaminase: a new target to reverse cancer drug resistance.

Alfredo Budillon, Carmine Carbone, Elena Di Gennaro

Open access · hybridAbstract readReview
In one paragraph

Review in Amino acids, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.2field-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

34 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The Role of Transglutaminase 2 in Cancer: An Update.International journal of molecular sciences · 2024
    Review
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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

3 authors at 1 institution in 1 country.

Alfredo BudillonExperimental Pharmacology Unit, Department of Research, Istituto Nazionale Tumori, National Cancer Institute G. Pascale, Via M. Semmola, 80131 Naples, Italy. a.budillon@istitutotumori.na.it
Carmine Carbone
Elena Di Gennaro
Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer resistance mechanisms, which result from intrinsic genetic alterations of tumor cells or acquired genetic and epigenetic changes, limit the long-lasting benefits of anti-cancer treatments. Tissue transglutaminase (TG2) has emerged as a putative gene involved in tumor cell drug resistance and evasion of apoptosis. Although some reports have indicated that TG2 can suppress tumor growth and enhance the growth inhibitory effects of anti-tumor agents, several studies have presented both pro-survival and anti-apoptotic roles for TG2 in malignant cells. Increased TG2 expression has been found in several tumors, where it was considered a potential negative prognostic marker, and it is often associated with advanced stages of disease, metastatic spread and drug resistance. TG2 mediates drug resistance through the activation of survival pathways and the inhibition of apoptosis, but also by regulating extracellular matrix (ECM) formation, the epithelial-to-mesenchymal transition (EMT) or autophagy. Because TG2 knockdown or inhibition of TG2 enzymatic activity may reverse drug resistance and sensitize cancer cells to drug-induced apoptosis, many small molecules capable of blocking TG2 have recently been developed. Additional insight into the multifunctional nature of TG2 as well as translational studies concerning the correlation between TG2 expression, function or location and cancer behavior will aid in translating these findings into new therapeutic approaches for cancer patients.

Indexed as

AnimalsAntineoplastic AgentsDrug Resistance, NeoplasmEnzyme InhibitorsGTP-Binding ProteinsHumansMolecular Targeted TherapyNeoplasmsProtein Glutamine gamma Glutamyltransferase 2TransglutaminasesAntineoplastic AgentsEnzyme InhibitorsGTP-Binding ProteinsProtein Glutamine gamma Glutamyltransferase 2Transglutaminases

Identifiers

PMID22130737
PMCPMC3535412
OpenAlexW1963811337

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.