Human papillomavirus infections as a marker to predict overall survival in lung adenocarcinoma

Wang, Jinn-Li; Fang, Chia Lang; Wang, Mey; Yu, Ming Chih; Bai, Kuan Jen; Lu, Pei Chih; Liu, H. Eugene

doi:10.1002/ijc.28349

Cited by 26 publications

(30 citation statements)

References 30 publications

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“…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

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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.

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Section: Discussionmentioning

confidence: 99%

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

Liu

Yang

et al. 2015

Oncology Letters

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“…A recent Taiwanese study, however, associated HPV DNA presence with improved lung cancer survival. This study, based on nearly 200 cases, focused on lung adenocarcinoma and oversampled women (8).…”

Section: Introductionmentioning

confidence: 99%

No Causal Association Identified for Human Papillomavirus Infections in Lung Cancer

Anantharaman¹,

Gheit²,

Waterboer

et al. 2014

Cancer Research

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Human papillomavirus (HPV) infections have been implicated in lung carcinogenesis, but causal associations remain uncertain. We evaluated a potential causal role for HPV infections in lung cancer through an analysis involving serology, tumor DNA, RNA, and p16 protein expression. Association between type-specific HPV antibodies and risk of lung cancer was examined among 3,083 cases and 4,328 controls in two case-control studies (retrospective) and one nested case-control study (prospective design). Three hundred and thirty-four available tumors were subjected to pathologic evaluation and subsequent HPV genotyping following stringent conditions to detect all high-risk and two low-risk HPV types. All HPV DNA-positive tumors were further tested for the expression of p16 protein and type-specific HPV mRNA. On the basis of the consistency of the results, although HPV11 and HPV31 E6 antibodies were associated with lung cancer risk in the retrospective study, no association was observed in the prospective design. Presence of type-specific antibodies correlated poorly with the presence of the corresponding HPV DNA in the tumor. Although nearly 10% of the lung tumors were positive for any HPV DNA (7% for HPV16 DNA), none expressed the viral oncogenes. No association was observed between HPV antibodies or DNA and lung cancer survival. In conclusion, we found no supportive evidence for the hypothesized causal association between HPV infections and lung cancer. Cancer Res; 74(13); 3525-34. Ó2014 AACR.

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“…Among these articles, five studies were conducted in China [16–18, 21, 22], two in Japan [19, 20] and one in Russia [15]. Of all the selected articles, three evaluated HR s [15, 16, 21], while in the other five articles [17–20, 22], HR s were absent, and needed to be calculated from the survival curves. Three articles did not give accurate data for follow-up [16, 19, 20].…”

Section: Resultsmentioning

confidence: 99%

“…Among the nine studies included, five [17–21] showed negative association comparing HPV-positive to HPV-negative cancers, one [20] showed statistical significance and the other four [15, 16, 20, 22] showed positive associations without statistical significance. The heterogeneity test indicated moderate degree of heterogeneity among included studies (Q-test P heterogeneity =0.038, I 2 =51.0%) and therefore, random effects model was used to obtain the pooled HR .…”

Section: Resultsmentioning

confidence: 99%

“…Among the included studies, only Wang et al . [21] demonstrated that patients with HPV-positive lung adenocarcinoma had a superior prognosis than patients with HPV-negative ones, with a 32% reduction in overall mortality. However, it is unclear about the biologic basis for the improved survival among the HPV positive patients and further study is needed.…”

Section: Discussionmentioning

confidence: 99%

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Human papillomavirus infection as a prognostic marker for lung adenocarcinoma: a systematic review and meta-analysis

et al. 2017

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Although a number of studies have investigated the association between human papillomavirus (HPV) and lung cancer prognosis, the results remain inconsistent. We therefore conducted a meta-analysis of epidemiologic studies to address this issue. Searches of the MEDLINE and EMBASE electronic databases from their inception until June 30, 2016 yielded nine studies involving a total of 1,205 lung cancer cases that were used to conduct the meta-analysis. Study-specific risk estimates were pooled using a random-effects model. The pooled hazard ratio (HR) comparing HPV-positive to HPV-negative cancers 1.00 (95% confidence interval (CI): 0.78-1.28) was not significantly correlated with overall survival. However, lung adenocarcinoma patients with HPV infections exhibited a survival benefit compared to those without HPV infection (HR=0.69, 95% CI: 0.50-0.96). This meta-analysis suggests HPV infection is a prognostic marker in lung adenocarcinoma. To further elucidate the epidemiology and pathogenesis of HPV infections in lung cancer, future large prospective studies are encouraged to stratify survival analysis based on the pathological type and clinical stage of the cancer.

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Human papillomavirus infections as a marker to predict overall survival in lung adenocarcinoma

Cited by 26 publications

References 30 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

No Causal Association Identified for Human Papillomavirus Infections in Lung Cancer

Human papillomavirus infection as a prognostic marker for lung adenocarcinoma: a systematic review and meta-analysis

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