Evidence map›Paper›PMID 32781676›Full record

ReviewCancers2020

High-Risk Human Papillomavirus and Tobacco Smoke Interactions in Epithelial Carcinogenesis.

Francisco Aguayo, Juan P Muñoz, Francisco Perez-Dominguez, Diego Carrillo-Beltrán, Carolina Oliva, Gloria M Calaf, Rances Blanco, Daniela Nuñez-Acurio

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.5field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

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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

8 authors at 2 institutions in 2 countries.

Francisco AguayoUniversidad de Tarapacá, Arica 1000000, Chile.ORCID 0000-0002-9619-7535
Juan P MuñozInstituto de Alta Investigación, Universidad de Tarapacá, Arica 1000000, Chile.
Francisco Perez-DominguezLaboratorio Oncovirología, Programa de Virología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, Chile.
Diego Carrillo-BeltránLaboratorio Oncovirología, Programa de Virología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, Chile.
Carolina OlivaLaboratorio Oncovirología, Programa de Virología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, Chile.
Gloria M CalafInstituto de Alta Investigación, Universidad de Tarapacá, Arica 1000000, Chile.
Rances BlancoLaboratorio Oncovirología, Programa de Virología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, Chile.
Daniela Nuñez-AcurioLaboratorio Oncovirología, Programa de Virología, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, Chile.ORCID 0000-0003-4865-2131
University of Chile · CLUniversity of Tarapacá · CL

Funding

Fondo Nacional de Desarrollo Científico y Tecnológico 1161219
6 · The paper itself

Abstract

Cervical, anogenital, and some head and neck cancers (HNC) are etiologically associated with high-risk human papillomavirus (HR-HPV) infection, even though additional cofactors are necessary. Epidemiological studies have established that tobacco smoke (TS) is a cofactor for cervical carcinogenesis because women who smoke are more susceptible to cervical cancer when compared to non-smokers. Even though such a relationship has not been established in HPV-related HNC, a group of HPV positive patients with this malignancy are smokers. TS is a complex mixture of more than 4500 chemical compounds and approximately 60 of them show oncogenic properties such as benzo[α]pyrene (BaP) and nitrosamines, among others. Some of these compounds have been evaluated for carcinogenesis through experimental settings in collaboration with HR-HPV. Here, we conducted a comprehensive review of the suggested molecular mechanisms involved in cooperation with both HR-HPV and TS for epithelial carcinogenesis. Furthermore, we propose interaction models in which TS collaborates with HR-HPV to promote epithelial cancer initiation, promotion, and progression. More studies are warranted to clarify interactions between oncogenic viruses and chemical or physical environmental factors for epithelial carcinogenesis.

Indexed as

cancercervixpapillomavirussmokingtobacco

Identifiers

PMID32781676
PMCPMC7465661
OpenAlexW3047492692

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.