Human papillomavirus genotypes in penile cancers from Japanese patients and HPV-induced NF-κB activation

Senba, Masachika; Mori, Nozomu; Wada, Akihiro; Fujita, Shuichi; Yasunami, Michio; Irie, Sumiko; Hayashi, Tomayoshi; Igawa, Tsukasa; Kanetake, Hiroshi; Takahara, Osamu; Toriyama, Kan

doi:10.3892/ol_00000047

Cited by 11 publications

(12 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The associations of HPV with cervical carcinoma [119], middle ear carcinoma [120], penile carcinomas [121,122], oropharyngeal cancer [123], tongue cancer [124], esophageal squamous cell carcinoma (ESCC) [125], colorectal cancer (CRC) [126,127], lung cancer [128][129][130], and breast cancer have since been demonstrated [131].…”

Section: Pathogenic Stimulus By Virusmentioning

confidence: 99%

Chronic inflammation evoked by pathogenic stimulus during carcinogenesis

Brücher

Jamall

2019

4open

View full text Add to dashboard Cite

A pathogenic (biological or chemical) stimulus is the earliest information received by a cell that can result in the disruption of homeostasis with consequent development of disease. Chronic inflammation involves many cell types with numerous cytokines and signaling pathways, the release of different components by the cells, and the crosstalk provoked by such stimuli involving subclinical chronic inflammation and is mechanistically manifold. Exosomes secrete chemicals that trigger the epithelium to produce exosome-like nanoparticles promoting chronic inflammation. Small molecules, together with various cytokines, selectively target signaling pathways inducing crosstalk that suppress apoptosis. 16S rRNA gene sequencing has become routine to provide information on the composition and abundance of bacteria found in human tissues and in reservoirs. The deregulation of autophagy with chronic stimulation of inflammation is an early phenomenon in carcinogenesis. The disruption of cell–cell integrity enables transcellular CagA migration and triggers deregulation of autophagy with the net result being chronic inflammation. The complex and insidious nature of chronic inflammation can be seen both inside and outside the cell and even with intracellular nuclear fragments such as chromatin, which itself can elicit a chronic inflammatory response within the cytoplasm and affect autophagy. The ultimate result of unresolved chronic inflammation is fibrosis, a step before tissue remodeling results in the formation of a precancerous niche (PCN). Various pathogenic stimuli associated with different neoplasms result in persistent inflammation. This ongoing disruption of homeostasis in the micromilieu of cells, tissues, and organs is an essential preamble to carcinogenesis and occurs early in that process.

show abstract

Section: Pathogenic Stimulus By Virusmentioning

confidence: 99%

Chronic inflammation evoked by pathogenic stimulus during carcinogenesis

Brücher

Jamall

2019

4open

View full text Add to dashboard Cite

show abstract

“…We demonstrated the correlation between HPV infection and nuclear and/or cytoplasmic NF-κB expression using the Fisher's exact probability test. HPV infection was considered to activate NF-κB resulting in cell transformation (11,12,24).…”

Section: Discussionmentioning

confidence: 99%

Human papillomavirus infection induces NF-κB activation in cervical cancer: A comparison with penile cancer

Senba

Buziba

Mori³

et al. 2010

Oncology Letters

Self Cite

View full text Add to dashboard Cite

Abstract. This study aimed to determine the relationship between human papillomavirus (HPV) and nuclear factor-κB (NF-κB) in cervical cancer using 62 tissues of cervical cancer, and to compare the findings to penile cancer. HPV-DNA integration is a crucial factor for malignant transformation in cervical cancer and can be identified using in situ hybridization. Of the 62 cases, HPV infection was detected in 28 (45.2%). This frequency was lower than in penile cancer (68.2%) as shown by our previous study. The earliest age of onset of cervical and penile cancer was 18 and 35, respectively, whereas the mean age of the initial diagnosis of cervical and penile cancer was 50.1 and 59.6, respectively. The discrepancies of HPV prevalence, earliest ages of onset and mean ages between cervical and penile cancer patients may result from the gender-based synergistic action of HPV associated with multiple epidemiological co-factors. Of the 28 HPV-infected cases, NF-κB expression was observed in the nucleus in 18 (64.3%), in the cytoplasm in 19 (67.9%) and in the nucleus and/or cytoplasm in 27 cases (96.4%). The overexpression of NF-κB in cervical cancer cases suggests that NF-κB activation is a key modulator in driving chronic inflammation to cancer.

show abstract

“…To the best of our knowledge, the immunohistochemical localization of NF-κB associated with HPV infection in penile cancer was previously reported using materials obtained from previous studies of Kenya, East Africa and Nagasaki, Japan (16,17). The purpose of this study was to determine the relationship among HPV infection, p16 INK4a , p53 and NF-κB in penile cancer in northern Thailand.…”

Section: Introductionmentioning

confidence: 96%

Relationship among human papillomavirus infection, p16INK4a, p53 and NF-κB activation in penile cancer from northern Thailand

Senba¹,

Mori²,

Fujita³

et al. 2010

Oncology Letters

Self Cite

View full text Add to dashboard Cite

Abstract. Human papillomavirus (HPV) E6 and E7 oncoproteins are essential factors for HPV oncogenesis. These E6 and E7 gene products play a central role in the induction of malignant transformation by interacting with several cellular regulatory proteins such as p16 INK4a , p53 and nuclear factor κB (NF-κB). In the present study, conducted in northern Thailand, HPV-DNA was detected in penile cancer cases using an in situ hybridization procedure and p16 INK4a , p53 and NF-κB were detected by immunohistochemistry. Using the cell cycle regulatory proteins p16 INK4a (61.5%) and p53 (71.8%), it was found that of the 51 cases, 39 (76.5%) were HPV-DNApositive in penile cancer. On the other hand, 25% p16 INK4a and 75% p53, respectively, were found in HPV-negative cases. Prevalence of HPV infection (76.5%) was shown in penile cancer cases in northern Thailand. No difference was found between HPV-positive and HPV-negative cases with respect to the presence of the cell cycle regulatory protein p53. On the other hand, p16 INK4a was found to be different between HPV-positive and HPV-negative cases. Inactivation of tumor suppressor genes, such as p16 INK4a and p53, to genetic instability, cell immortalization, accumulation of mutations and cancer formation, with or without HPV and irrespective of HPV infection, is therefore suggested. Of the 39 HPV-positive cases, 35 (89.7%) were NF-κB-positive in the nucleus, 29 (74.4%) in the cytoplasm and 37 (94.9%) in the nucleus and/or cytoplasm. NF-κB was detected in 4 (33.3%) of the 12 HPV-negative cases. Therefore, we propose that penile cancer cases with HPV infection are more likely to activate NF-κB than those without HPV infection.

show abstract

Human papillomavirus genotypes in penile cancers from Japanese patients and HPV-induced NF-κB activation

Cited by 11 publications

References 27 publications

Chronic inflammation evoked by pathogenic stimulus during carcinogenesis

Chronic inflammation evoked by pathogenic stimulus during carcinogenesis

Human papillomavirus infection induces NF-κB activation in cervical cancer: A comparison with penile cancer

Relationship among human papillomavirus infection, p16INK4a, p53 and NF-κB activation in penile cancer from northern Thailand

Contact Info

Product

Resources

About