Evidence map›Paper›PMID 19073969›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2008

Inhibition of Mammalian target of rapamycin by rapamycin causes the regression of carcinogen-induced skin tumor lesions.

Panomwat Amornphimoltham, Kantima Leelahavanichkul, Alfredo Molinolo, Vyomesh Patel, J Silvio Gutkind

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

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  13. mTOR, metabolism, and the immune response in HPV-positive head and neck squamous cell cancer.World journal of otorhinolaryngology - head and neck surgery · 2016
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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

5 authors at 1 institution in 1 country.

Panomwat AmornphimolthamOral and Pharyngeal Cancer Branch, National Institute of Craniofacial and Dental Research, NIH, Bethesda, Maryland 20892-4330, USA.
Kantima Leelahavanichkul
Alfredo Molinolo
Vyomesh Patel
J Silvio Gutkind
National Institute of Dental and Craniofacial Research · US

Funding

Oral CarcinogenesisZIADE000558 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, JORGE SILVIO · 2009 to 2015
$11.4M
Intramural NIH HHS ZIA DE000558
6 · The paper itself

Abstract

purposeThe activation of Akt/mammalian target of rapamycin (mTOR) pathway represents a frequent event in squamous cell carcinoma (SCC) progression, thus raising the possibility of using specific mTOR inhibitors for the treatment of SCC patients. In this regard, blockade of mTOR with rapamycin prevents the growth of human head and neck SCC cells when xenotransplanted into immunodeficient mice. However, therapeutic responses in xenograft tumors are not always predictive of clinical anticancer activity. EXPERIMENTAL

designAs genetically defined and chemically induced animal cancer models often reflect better the complexity of the clinical setting, we used here a two-step chemical carcinogenesis model to explore the effectiveness of rapamycin for the treatment of skin SCC.

resultsRapamycin exerted a remarkable anticancer activity in this chemically induced cancer model, decreasing the tumor burden of mice harboring early and advanced tumor lesions, and even recurrent skin SCCs. Immunohistochemical studies on tumor biopsies and clustering analysis revealed that rapamycin causes the rapid decrease in the phosphorylation status of mTOR targets followed by the apoptotic death of cancer cells and the reduction in the growth and metabolic activity of the surviving ones, concomitant with a decrease in the population of cancer cells expressing mutant p53. This approach enabled investigating the relationship among molecular changes caused by mTOR inhibition, thus helping identify relevant biomarkers for monitoring the effectiveness of mTOR inhibition in the clinical setting.

conclusionsTogether, these findings provide a strong rationale for the early evaluation of mTOR inhibitors as a molecular targeted approach to treat SCC.

Indexed as

9,10-Dimethyl-1,2-benzanthraceneAnimalsAntineoplastic AgentsCarrier ProteinsFemaleMicePhosphotransferases (Alcohol Group Acceptor)SirolimusSkin NeoplasmsTOR Serine-Threonine Kinases9,10-Dimethyl-1,2-benzanthraceneAntineoplastic AgentsCarrier ProteinsMTOR protein, humanmTOR protein, mousePhosphotransferases (Alcohol Group Acceptor)SirolimusTOR Serine-Threonine Kinases

Identifiers

PMID19073969
PMCPMC3407681
OpenAlexW2104065210

What OpenQuestion holds

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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.