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Oral squamous cell carcinoma (OSCC) is a category of aggressive malignancies that represent clinically, molecularly, and etiologically heterogeneous tumors. The majority of OSCCs are associated with tobacco and alcohol use, acting both independently and synergistically, which suggests that the environment plays an important role in carcinogenesis; however, the mechanisms associated with the development of OSCC are not well understood. It has been proposed that the epigenetic components could be implicated in the initiation and progression of OSCC. Primarily, aberrant DNA methylation patterns have been widely addressed in the study of OSCC. Diverse studies have proposed that other epigenetic processes such as post-translational histone modification, the deposition of histone variants, histone chaperones, and recently non-coding RNA, can be also involved in the development of oral cancer. In this review we focus on describing the new insights of the epigenetics processes that are related with OSCC as histones variants and long non-coding RNAs.

Air pollution has been recognized as a global health problem, causing around 7 million deaths worldwide and representing one of the highest environmental crises that we are now facing. Close to 30% of new lung cancer cases are associated with air pollution, and the impact is more evident in major cities. In this review, we summarize and discuss the evidence regarding the effect of particulate matter (PM) and its impact in carcinogenesis, considering the “hallmarks of cancer” described by Hanahan and Weinberg in 2000 and 2011 as a guide to describing the findings that support the impact of particulate matter during the cancer continuum.

Summary Promoter methylation is believed to inactivate the expression of hMLH1. This process has been implicated in the tumorigenesis of oral squamous cell carcinoma (OSCC). Thus, the aim of this study was to determine the profile of hMLH1 methylation and protein expression in OSCC. The matched case-control study included 50 OSCC cases and 200 controls, with a median of age 64 (Q1–Q3 54–71) years. Protein expression was determined by immunohistochemical staining, and hMLH1 gene promoter methylation was analyzed by methylation-specific polymerase chain reaction (MSP). A conditional logistic regression model for risk factors was built for OSCC cases and matched controls. Promoter methylation of hMLH1 was detected in 38 (76%) OSCC cases, but in none of the control samples. Of the 38 OSCC samples with promoter methylation, 12 (32%) were negative for hMLH1 protein, and corresponded to early clinical stages (10 in stage II and 2 in stage I). All 12 unmethylated samples showed positive stain for hMLH1. Multiple logistic regression analysis showed an OR of 16.54 (IC 95%: 1.69–161.68, p = 0.016) for methylation of the hMLH1 gene and early stages of OSCC, adjusting by gender and tobacco use. This study showed a high frequency of hMLH1 promoter methylation that occurred in most of the early stage cases and in about half of the late stage cases. It is proposed that hMLH1 promoter methylation is an early event that is maintained during tumor progression.

The exposure to particulate matter with a mean aerodynamic diameter ≤10 μm (PM10) from urban zones is considered to be a risk factor in the development of cancer. The aim of this work was to determine if PM10 exposure induces factors related to the acquisition of a neoplastic phenotype, such as cytoskeletal remodeling, changes in the subcellular localization of p21(CIP1/WAF1), an increase in β-galactosidase activity and changes in cell cycle. To test our hypothesis, PM10 from an industrial zone (IZ) and a commercial zone (CZ) were collected, and human adenocarcinoma lung cell cultures (A549) were exposed to a sublethal PM10 concentration (10 μg/cm(2)) for 24 h and 48 h. The results showed that PM10 exposure induced an increase in F-actin stress fibers and caused the cytoplasmic stabilization of p21(CIP1/WAF1) via phosphorylation at Thr(145) and Ser(146) and the phosphorylation of ERK1/2 on Thr(202). Changes in the cell cycle or apoptosis were not observed, but an increase in β-galactosidase activity was detected. The PM10 from CZ caused more dramatic effects in lung cells. We conclude that PM10 exposure induced cytoplasmic p21(CIP1/WAF1) retention, ERK1/2 activation, cytoskeleton remodeling and the acquisition of a senescence-like phenotype in lung cells. These alterations could have mechanistic implications regarding the carcinogenic potential of PM10.

Objective Studies reporting low prevalence of HPV in OSCC with declining age at presentation are increasing. The aim of this study was to determine the prevalence of HPV in a group of OSCC cases and controls in a Mexican population. Methods The matched case-control study included 80 OSCC cases and 320 controls. HPV/DNA presence was evaluated through PCR amplification using three sets of consensus primers for the L1 gene. A conditional logistic regression analysis was carried out for the matched OSCC cases and controls. Interactions between risk factors and OCSS were tested in the construction process of the models. Results HPV prevalence was 5% in OSCC cases and 2.5% in controls. HPV-detected types were 16, 18 and 56. According to conditional logistics regression model, an association was detected between HR-HPV and OSCC. All HR-HPV-positive OSCC cases corresponded to young patients (

Summary Background Many studies have shown gemcitabine and cisplatin are radiosensitizers. Concurrent chemoradiation seems to be an efficient approach for treatment of advanced head and neck cancer (HNC), but toxicity is significant. Objective To evaluate safety and explore efficacy of alternating chemotherapy with gemcitabine and cisplatin concurrent with radiotherapy in patients with advanced non-metastatic HNC. Patients and Methods Twenty-eight patients diagnosed with advanced Squamous Cell Carcinomas of the Head and Neck (SCCHN) in stages III (28%), IVa (36%), and IVb (36%) were treated with gemcitabine: 100 mg/m 2 alternating with cisplatin: 50 mg/m 2 concurrent with radiotherapy at doses of 2 Gy/day until completing 70 Gy. While awaiting for concurrent treatment, eleven patients received induction chemotherapy with cisplatin: 100 mg/m 2 and 5-FU: 1000 mg/m 2 . Toxicity, especially in relation to mucositis, xerostomy, dysphagia, leucopenia and radiodermitis was evaluated. Results 5-year progression-free survival was 27.8 ± 17.2% (CI-95: 0–61.5) and overall survival was 55.9 ± 11% (CI: 34.4–77.5). Overall response rate was 93%; complete response was 64.3% and partial response was 28.6%. Extensive surgery for primary site was avoided in 19 patients (70.4%). Grade 3–4 adverse events were mucositis (46.4%), leucopenia (14.2%), dysphagia (25%), xerostomy (10.7%) and radiodermitis (3.6%). Response rates and toxicity were not significantly different among those patients with and without induction chemotherapy, but survival was higher in patients receiving induction. Conclusions Gemcitabine alternating with cisplatin concurrent with radiotherapy is an active and safe treatment that deserves further study.

We report the case of an immunocompromised female patient with external otitis, who developed a picture of external otitis with poor response to conventional treatment and subsequent isolation of Pseudomona Aeruginosa in the ear secretion culture. The final diagnosis was malignant external otitis. Our objective is to describe the scintigraphic findings as well as to analyze their correlation with the clinical pattern and to evaluate the possible causes of the discordance found.

DNA methylation is an important regulator of gene transcription, and its role in carcinogenesis has been a topic of considerable interest in the last few years. Of the all epigenetic modifications, methylation, which represses transcription of the promoter region of tumor suppressor genes leading to gene silencing, has been most extensively studied. Oral squamous cell carcinoma (OSCC) has long been known to be the endpoint of many genetic changes, not only genomic mutations but also abnormal epigenetic modifications, as such, promoter methylation, contribute to development of this tumors. Recent studies have shown that promoter methylation of tumor suppressor genes is an important factor in carcinogenesis of OSCC. Some of the main genes that frequently showed promoter methylation in OSCC are those that participate in diverse processes such as regulation of the cell cycle, DNA repair, proliferation, and apoptosis. The aim of this review is to assess the current state of knowledge regarding promoter methylation of diverse genes in OSCC.

The origin of spindle cells (SC) in oral Kaposi's sarcoma (OKS) is still an intriguing aspect. Thus the aim of the present study was to compare the clinical, histological and immunohistochemical characteristics of OKS and oral pyogenic granuloma (OPG), in order to contribute to the knowledge of the cells involved in Kaposi's sarcoma pathogenesis.In this retrospective, observational and comparative study, 39 OKS and 30 OPG cases were included. Immunohistochemical studies were performed for vimentin, alpha SMA, desmin, C-kit, CD34, D2-40 and LANA-1 [human herpesvirus-8(HHV-8)]. Statistical comparisons were done using the chi-square and Wilcoxon-Mann-Whitney rank sum tests.Fourteen (35.9%) OKS cases also affected the skin, and 83.8% involved the palate. All OKS and OPG were positive for vimentin and CD34. OKS samples were positive for alpha SMA, and 25.6% expressed C-kit. All OKS cases were positive for HHV-8, and the number of positive cells increased significantly from early / intermediate to late histological stage. D2-40 was expressed in the cellular component and vascular walls of all OKS cases, but it was negative in OPG. HHV-8 expression was increased in late histological stages of OKS lesions.The expression of D2-40 marker in the vascular walls and SC supports the view of a lymphatic differentiation in neoplastic cells of OKS. Desmin, alpha SMA, D2-40, C-kit and HHV-8 were the main markers differently expressed in OKS and OPG.