Squamous Cell Carcinoma In Population Research Articles

Prevalence and clinical implications of the HPV16 infection in oral cancer in Montenegro - Evidence to support the immunization program.

Oral squamous cell carcinoma (OSCC) makes 85-95% of all malignances in the oral cavity. Increasing evidence shows that the Human Papillomaviruses (HPVs) are preferentially associated with some oropharyngeal and OSCCs, namely the genotype 16. The aim of the present study was to determine the prevalence and clinical implications of HPV16 infection in oral squamous cell carcinoma in population of Montenegro. This study included 60 patients with OSCC (localized on the lower lip, tongue or/and floor of the mouth), surgically treated at the Clinical Centre of Montenegro from 2012 to 2018. Surgically obtained formalin-fixed and paraffin-embedded specimens were used for histopathological analysis and HPV16 genome detection using standard Polymerase Chain Reaction (primers for detection of E6 gene). Each individual was further followed up for the period of three years and for different clinico-pathological characteristics, including disease free interval (DFI). The prevalence of HPV16 infection in OSCCs was 23.3% and the infection was significantly more common in female patients (P = 0.038). No significant correlation was detectable between HPV16 infection and the patients' age (P = 0.302), tumor site (P = 0.125), tumor grade (P = 0.363) and disease stage (P = 0.995). Observing the total sample the DFI was not significantly different for HPV16-positive versus HPV16-negative patients (P = 0.427), but a gender-based difference in DFI was observed, with the significantly shorter DFI (Log Rank test, P = 0.003) in HPV16 positive female patients compared to male patients (P = 0.003). The results obtained in this study provide scientific evidence for the development of national HPV vaccination program in Montenegro.

Association of DFNA5, SYK, and NELL1 variants along with HPV infection in oral cancer among the prolonged tobacco-chewers.

Southeast Asia, especially India, is well known for the highest use of smokeless tobacco. These products are known to induce oral squamous cell carcinoma. However, not all long-term tobacco-chewers develop oral squamous cell carcinoma. In addition, germline variants play a crucial role in susceptibility, prognosis, development, and progression of the disease. These prompted us to study the genetic susceptibility to oral squamous cell carcinoma among the long-term tobacco-chewers. Here, we presented a retrospective study on prolonged tobacco-chewers of Northeast India to identify the potential protective or risk-associated germline variants in tobacco-related oral squamous cell carcinoma along with HPV infection. Targeted re-sequencing (n = 60) of 170 genetic regions from 75 genes was carried out in Ion-PGM™ and validation (n = 116) of the observed variants was done using Sequenom iPLEX MassARRAY™ platform followed by polymerase chain reaction-based HPV genotyping and p16-immunohistochemistry study. Subsequently, estimation of population structure, different statistical and in silico approaches were undertaken. We identified one nonsense-mediated mRNA decay transcript variant in the DFNA5 region (rs2237306), associated with Benzo(a)pyrene, as a protective factor (odds ratio = 0.33; p = 0.009) and four harmful (odds ratio > 2.5; p < 0.05) intronic variants, rs182361, rs290974, and rs169724 in SYK and rs1670661 in NELL1 region, involved in genetic susceptibility to tobacco- and HPV-mediated oral oncogenesis. Among the oral squamous cell carcinoma patients, 12.6% (11/87) were HPV positive, out of which 45.5% (5/11) were HPV16-infected, 27.3% (3/11) were HPV18-infected, and 27.3% (3/11) had an infection of both subtypes. Multifactor dimensionality reduction analysis showed that the interactions among HPV and NELL1 variant rs1670661 with age and gender augmented the risk of both non-tobacco- and tobacco-related oral squamous cell carcinoma, respectively. These suggest that HPV infection may be one of the important risk factors for oral squamous cell carcinoma in this population. Finally, we newly report a DFNA5 variant probably conferring protection via nonsense-mediated mRNA decay pathway against tobacco-related oral squamous cell carcinoma. Thus, the analytical approach used here can be useful in predicting the population-specific significant variants associated with oral squamous cell carcinoma in any heterogeneous population.

Serum Pepsinogens and Helicobacter Pylori are not Associated with Esophageal Squamous Cell Carcinoma in a High-Risk Area in China

The role of serum pepsinogen level and Helicobacter pylori infection in esophageal carcinoma remains controversial. It may be a risk or protective factor, or without association with esophageal carcinoma. We prospectively examined associations between serum pepsinogen status, H pylori infection and the risk of esophageal squamous cell carcinoma in the Chinese population. In the present study, 1501 subjects from a community-based general population of Northern China were included. The incidence of esophageal carcinoma among the subjects was registered during a 15-year follow-up period by annual home visit, and the risks of low serum pepsinogen level and H pylori infection in the development of ESCC were evaluated using logistic regression. The total accumulated incidence of ESCC in the cohort was 666/100,000 during the 15-year follow-up. Notably, all the cases were verified to be ESCC. Logistic regression analysis showed that age ≥60 (OR = 9.67; 95% CI, 2.797-33.423) was the only risk factor for esophageal squamous cell carcinoma in the population. There was no significant association between sex, H pylori infection, pepsinogen level (PG I ≤70 ng/ml alone, PG I/II ratio ≤3 alone, or PG I ≤70 ng/ml and PG I/II ratio ≤3) and esophageal squamous cell carcinoma. In this prospective study, neither H pylori infection nor abnormal pepsinogen status had a predictive role for the development of esophageal squamous cell carcinoma in the rural population of China.

Serum pepsinogens and Helicobacter pylori are not associated with esophageal squamous cell carcinoma in a high-risk area in China.

The role of serum pepsinogen level and Helicobacter pylori infection in esophageal carcinoma remains controversial. It may be a risk or protective factor, or without association with esophageal carcinoma. We prospectively examined associations between serum pepsinogen status, H pylori infection and the risk of esophageal squamous cell carcinoma in the Chinese population. In the present study, 1501 subjects from a community-based general population of Northern China were included. The incidence of esophageal carcinoma among the subjects was registered during a 15-year follow-up period by annual home visit, and the risks of low serum pepsinogen level and H pylori infection in the development of ESCC were evaluated using logistic regression. The total accumulated incidence of ESCC in the cohort was 666/100,000 during the 15-year follow-up. Notably, all the cases were verified to be ESCC. Logistic regression analysis showed that age ≥60 (OR = 9.67; 95% CI, 2.797-33.423) was the only risk factor for esophageal squamous cell carcinoma in the population. There was no significant association between sex, H pylori infection, pepsinogen level (PG I ≤70 ng/ml alone, PG I/II ratio ≤3 alone, or PG I ≤70 ng/ml and PG I/II ratio ≤3) and esophageal squamous cell carcinoma. In this prospective study, neither H pylori infection nor abnormal pepsinogen status had a predictive role for the development of esophageal squamous cell carcinoma in the rural population of China.

Epoxide hydrolase Tyr113His polymorphism is not associated with susceptibility to esophageal squamous cell carcinoma in population of North China.

To investigate the possible association of microsomal epoxide hydrolase (mEH) Tyr113His polymorphism with susceptibility to esophageal squamous cell carcinoma (ESCC) in a population of North China. The mEH Tyr113His genotypes were determined by polymerase-chain reaction (PCR)-restriction fragment length polymorphism (RFLP) analysis in 257 patients with esophageal squamous cell carcinoma (ESCC) and 252 healthy subjects as a control group. The frequencies for Tyr and His alleles were 44.2%, 55.8% in ESCC patients, and 44.0% and 56.0% in healthy subjects, respectively. No statistic difference in allele distribution was observed between ESCC patients and controls (chi2=0.008, P=0.929). The overall genotype distribution difference was not observed between cancer cases and controls (chi2=2.116, P=0.347). Compared with Tyr/Tyr genotype, neither His/His genotype nor in combination with Tyr/His genotype significantly modified the risk of the development of ESCC, the adjusted odds ratio was 1.076 (95% CI=0.850-1.361) and 0.756 (95% CI=0.493-1.157), respectively. When stratified for sex, age, smoking status and family history of upper gastrointestinal cancer, His/His genotype alone or in combination with Tyr/His genotype also did not show any significant influence on the risk of developing ESCC. MEH Tyr113His polymorphism may not be used as a stratification marker in screening individuals at a high risk of ESCC.