Human Papillomavirus 16/18 Infections in Lung Cancer Patients in Mexico

Badillo-almaráz, IsaÍAs; Zapata‐Benavides, Pablo; Saavedra-Alonso, Santiago; Zamora-Ávila, Diana Elisa; Reséndez‐Pérez, Diana; Taméz-Guerra, Reyes; Herrera‐Esparza, Rafael; Rodríguez‐Padilla, Cristina

doi:10.1159/000351075

Cited by 8 publications

(4 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…HPV infection, particularly high-risk HPV16/18 infection, has been identified as a risk factor for the development of cervical cancer, lung cancer and other malignant tumors (1,2,17,18). Previous studies have reported that the involvement of HPV16/18 infection in lung tumorigenesis may be mediated through FHIT and p53 (7,13,14,19,20).…”

Section: Discussionmentioning

confidence: 99%

Effect of FHIT loss and p53 mutation on HPV-infected lung carcinoma development

Liu

Yang

et al. 2015

Oncology Letters

View full text Add to dashboard Cite

Abstract. High-risk human papillomavirus (HPV)16/18 infection in the development of lung cancer has previously been identified, and fragile histidine triad (FHIT) loss and p53 mutation are frequently observed in the disease. However, the association between these factors has not been well studied. The present study aimed to further investigate the significance of HPV infection, FHIT loss and p53 mutations in the development of lung cancer and their possible associations. DNA was extracted from paraffin-embedded specimens from 88 cases of squamous cell carcinoma (SCC), 56 of adenocarcinoma (AC), 36 of small cell lung carcinoma (SCLC) and 110 non-cancer control cases of lung neoplasms. The prevalence of HPV infection was determined by polymerase chain reaction analysis, and FHIT loss and p53 mutations were detected by immunohistochemistry. The χ 2 , Fisher's exact and Pearson correlation tests were applied for statistical analysis. The results of the present study demonstrated that HPVL1 (the major capsid protein of HPV), HPV16 and HPV18 infection were more prevalent in the lung cancer samples compared with the non-cancer controls (all P<0.001). FHIT loss occurred more frequently in the lung cancer samples (44.44%) compared with the non-cancer controls (7.25%) (P<0.001). FHIT loss in the HPVL1-positive group was significantly increased compared with the HPVL1-negative group in the lung cancer cases and the non-cancer controls (P<0.05). In the lung cancer cases, the p53 mutation rates in the HPVL1-and HPV16/18-positive groups were significantly increased compared with the HPVL1-and HPV16/18-negative groups (P<0.05). In the 180 lung cancer cases, the coexistence rate of FHIT loss and a history of smoking was 38.33% (69/180; Pearson contingency coefficient of r=0.318; P<0.001). FHIT loss and p53 mutation exhibited a synergistic effect on HPV-associated lung cancer (Pearson contingency coefficient r= 0.357, P<0.001). The present study demonstrated that FHIT loss may be important in the occurrence of lung cancer, particularly in lung SCCs. FHIT loss may therefore be used as an early indicator for lung cancer, particularly for patients with a history of smoking. HPV infection in lung tumorigenesis may, at least in part, be mediated through FHIT loss. FHIT loss and p53 mutation may coordinate together in the development of HPV-associated lung cancer, and accelerate the occurrence and development of lung cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of FHIT loss and p53 mutation on HPV-infected lung carcinoma development

Liu

Yang

et al. 2015

Oncology Letters

View full text Add to dashboard Cite

show abstract

“…Some estimations show that the presence of HPV represents 12 more opportunities to develop cervical cancer than general population [30] and the HPV infection the most important between the factor risk for cervical cancer [21]. Recently, HPV was associated, lung cancer [31][32][33][34] to larynx and pharynx carcinoma that their incidence are increasing in the last years [35,36]. The global incidence of head and neck squamous cells and cervical cancer is similar; infection at both sites is strongly associated with sexual behavior: similarities in chromosomal aberrations, gene expression, and methylation and micro RNA profiles between Positive HPV head and neck squamous cells and cervical cancer.…”

Section: Biomedical Importancementioning

confidence: 99%

Infection by Human Papillomavirus (HPV), Chlamydia trachomatis and Ureaplasma urealyticum, in Relation with Reproductive Failure

Ancer‐Arellano¹,

Áncer‐Rodríguez²,

Hardisson³

et al. 2017

Fundamentals of Sexually Transmitted Infections

View full text Add to dashboard Cite

Recent studies suggest that besides oncogenic capacity, HPV could have etiological role on infertility, but more evidence is necessary to confirm these results. We present in this chapter the microbiological and clinical outcome of 104 infertile women aleatory selected, from northeast of Mexico: 84.6%, with genital infection (GI) by multiple germs: Chlamydia trachomatis (Ct) [86.5%], HPV [49%], Ureaplasma urealyticum (Uu) [47.11%] and Mycoplasma hominis [35.57%]. Significant association (P ≤ 0, 05) was observed between the HPV presence and Uu diagnosis, assisted-reproduction unsuccessful like previous treatment, cervical cytology with inflammatory process, multiple sexual partners, white-dense-mucous, secretion into the vagina, and HPV diagnosed in early years. The more frequent genotypes of HPV present in the infertile women studied were 6/18/16/58/11 and 68. In 60% of them, more than two genotypes were founded. The most frequent associations of high-risk HPV (HPVhr) were 16/18, 16/58, 16/33, 16/52 and 18/58. Considering the isolate or combined presentation of HPVhr, 79.5% of these women would have a potential to develop cervix carcinoma. GI by HPV/Uu/Ct affects the fertility. Infertile women with GI that include these microorganisms with probed (HPV/Ct) or suspicious carcinogenic effect (Uu) would be considered a group of high risk for cervical cancer.

show abstract

“…After 2010, new studies were reported in America. In Mexico, Badillo-Almaraz et al (2013) reported an HPV presence in 16 out of 39 (41%) lung cancer tissues by using PCR [ 127 ]. In USA, Joh et al, (2010) reported an HPV presence in five out of thirty (16.7%) lung carcinomas by using PCR and DNA sequencing.…”

Section: Epidemiology Of Hpv In Lung Cancermentioning

confidence: 99%

High-Risk Human Papillomavirus Infection in Lung Cancer: Mechanisms and Perspectives

Osorio

Candia-Escobar

Corvalán

et al. 2022

Biology

View full text Add to dashboard Cite

Lung cancer is a very prevalent and heterogeneous group of malignancies, and most of them are etiologically associated with tobacco smoking. However, viral infections have been detected in lung carcinomas, with high-risk human papillomaviruses (HR-HPVs) being among them. The role of HR-HPVs in lung cancer has been considered to be controversial. This issue is due to the highly variable presence of this virus in lung carcinomas worldwide, and the low viral load frequently that is detected. In this review, we address the epidemiological and mechanistic findings regarding the role of HR-HPVs in lung cancer. Some mechanisms of HR-HPV-mediated lung carcinogenesis have been proposed, including (i) HPV works as an independent carcinogen in non-smoker subjects; (ii) HPV cooperates with carcinogenic compounds present in tobacco smoke; (iii) HPV promotes initial alterations being after cleared by the immune system through a “hit and run” mechanism. Additional research is warranted to clarify the role of HPV in lung cancer.

show abstract

Human Papillomavirus 16/18 Infections in Lung Cancer Patients in Mexico

Cited by 8 publications

References 20 publications

Effect of FHIT loss and p53 mutation on HPV-infected lung carcinoma development

Effect of FHIT loss and p53 mutation on HPV-infected lung carcinoma development

Infection by Human Papillomavirus (HPV), Chlamydia trachomatis and Ureaplasma urealyticum, in Relation with Reproductive Failure

High-Risk Human Papillomavirus Infection in Lung Cancer: Mechanisms and Perspectives

Contact Info

Product

Resources

About