BACKGROUND: Case-control studies from the early 2000s demonstrated that human papillomavirus-related oropharyngeal cancer (HPV-OPC) is a distinct entity associated with number of oral sex partners. Using contemporary data, we investigated novel risk factors (sexual debut behaviors, exposure intensity, and relationship dynamics) and serological markers on odds of HPV-OPC. METHODS: HPV-OPC patients and frequency-matched controls were enrolled in a multicenter study from 2013 to 2018. Participants completed a behavioral survey. Characteristics were compared using a chi-square test for categorical variables and a t test for continuous variables. Adjusted odds ratios (aOR) were calculated using logistic regression. RESULTS: A total of 163 HPV-OPC patients and 345 controls were included. Lifetime number of oral sex partners was associated with significantly increased odds of HPV-OPC (>10 partners: odds ratio [OR], 4.3 [95% CI, 2.8-6.7]). After adjustment for number of oral sex partners and smoking, younger age at first oral sex (<18 vs >20 years: aOR, 1.8 [95% CI, 1.1-3.2]) and oral sex intensity (>5 sex-years: aOR, 2.8 [95% CI, 1.1-7.5]) remained associated with significantly increased odds of HPV-OPC. Type of sexual partner such as older partners when a case was younger (OR, 1.7 [95% CI, 1.1-2.6]) or having a partner who had extramarital sex (OR, 1.6 [95% CI, 1.1-2.4]) was associated with HPV-OPC. Seropositivity for antibodies to HPV16 E6 (OR, 286 [95% CI, 122-670]) and any HPV16 E protein (E1, E2, E6, E7; OR, 163 [95% CI, 70-378]) was associated with increased odds of HPV-OPC. CONCLUSION: Number of oral sex partners remains a strong risk factor for HPV-OPC; however, timing and intensity of oral sex are novel independent risk factors. These behaviors suggest additional nuances of how and why some individuals develop HPV-OPC.
Histone acetyltransferases (HATs) and histone deacetylases (HDACs) counteract with each other to regulate gene expression by altering chromatin structure. Aberrant HDAC activity was reported in many human diseases including wide range of cancers, viral infections, cardiovascular complications, auto-immune diseases and kidney diseases. HDAC inhibitors are small molecules designed to block the malignant activity of HDACs. Chemokines and cytokines control inflammation, immunological and other key biological processes and are shown to be involved in various malignancies. Various HDACs and HDAC inhibitors were reported to regulate chemokines and cytokines. Even though HDAC inhibitors have remarkable anti-tumor activity in hematological cancers, they are not effective in treating many diseases and many patients relapse after treatment. However, the role of HDACs and cytokines in regulating these diseases still remain unclear. Therefore, understanding exact mechanisms and effector functions of HDACs are urgently needed to selectively inhibit them and to establish better a platform to combat various malignancies. In this review, we address regulation of chemokines and cytokines by HDACs and HDAC inhibitors and update on HDAC inhibitors in human diseases.
Introduction: Survivors of childhood cancer have an increased risk of developing a subsequent secondary malignant neoplasm (SMN). Among five-year survivors of primary cancer, SMNs account for nearly half of non-relapse deaths, which make them the most frequent cause of non-relapse mortality. Leukemia is the most common childhood cancer and the five-year survival rate of leukemia has drastically improved over the past two decades. Therefore, the chances of developing SMNs are higher in pediatric (0–19 years) leukemia survivors. Methods: The US based Surveillance, Epidemiology, and End Results (SEER-18) database (1973–2014) was probed for SMNs in the pediatric population (age ≤ 19). Variables Sequence-number central, primary site and ICCC3WHO were used to identify the first and second cancers among patients who developed SMN. Results: Our SEER database analysis found 99,380 cases of pediatric primary malignancies (0–19 years), of which 1803 (1.81%) patients developed SMN. The breakdown of SMNs in pediatric leukemia survivors (n = 251) showed thyroid carcinoma (18.33% of cases) as the most common second cancer, followed by sarcoma (15.14%), astrocytoma (10.36%), lymphoma (9.56%), salivary gland carcinoma (7.17%), melanoma (4.38%), and breast cancer (3.98%). Interestingly, we found that over 76% of SMNs that were developed by leukemia patients occurred within 20 years after initial leukemia diagnosis. However, some SMNs occur during later age, for example, the mean age for breast cancer occurrence in leukemia survivors is 26.20 ± 8.53 years after initial leukemia diagnosis. Conclusions: Our study presented comprehensive rates of SMNs among pediatric cancers survivors, and the potential SMNs for pediatric leukemia survivors. This information could we used by oncologists, patients, patient families, and cancer researchers to understand the long-term risks that are associated with the development of SMNs in pediatric leukemia survivors.
Background-Human papillomavirus (HPV)-positive oropharyngeal cancer (HPV-OPC) is distinct from HPV-unassociated head and neck cancer. However, whether risk factors for HPVpositive oropharyngeal and nonoropharyngeal cancer are the same is unclear.Methods-Incident cases of HPV-positive head and neck cancer and matched non-cancer controls were enrolled in a multi-institutional, prospective study examining risk factors, biomarkers, and survival.Results-HPV-nonOPC (n=20) were more likely to be ever smokers than controls (n=80, OR 3.49, 95%CI 1.11-10.9) and HPV-OPC (n=185, OR 3.28, 95%CI 1.10-10.2). Compared with HPV-OPC, HPV-nonOPC were less likely to have had over 3 oral sexual partners (OR 0.29, 95%CI 0.06-0.9), more likely to have multimorbidity (OR 3.30, 95%CI 1.04-10.5), and less likely to have antibodies to HPV16 E6 (90% vs. 28%, OR 0.05, 95%CI 0.02-0.2). HPV-nonOPC had worse 4-year OS (77% vs. 96%, p=0.001) and RFS (69% vs. 94%, p<0.001) than HPV-OPC.Conclusions-HPV-positive nonoropharyngeal cancers are distinct from HPV-OPC.
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