Rogelio González-González

Papillary Thyroid Carcinoma: Differential Diagnosis and Prognostic Values of Its Different Variants: Review of the Literature

Papillary thyroid carcinoma is the most common thyroid malignancy, and has an excellent prognosis, even with cervical lymph node metastasis; however, histological variants are considered relevant, which may be associated with familial adenomatous polyposis and tumor aggressiveness. Histological features, such as vascular and/or lymphatic invasion, angiogenesis, multifocality, high cellular proliferation rate, neoplastic cell dissemination, and the histological varieties, are indicative of poor prognosis, together with associated clinical factors: age, sex, and tumor size.

Molecular markers of cell adhesion in ameloblastomas. An update.

Ameloblastoma is the most common odontogenic tumor of epithelial origin, and though it is of a benign nature, it frequently infiltrates the bone, has a high rate of recurrence and could potentially become malignant. Cellular adhesion potentially plays an important role in the manifestation of these characteristics and in the tumor biology of ameloblastomas. Losses of cell-cell and extracellular matrix adhesion and cohesion are among the first events that occur in the invasion and growth of tumors of epithelial origin. The present review includes a description of the molecules that are involved in cell adhesion as reported for various types of ameloblastomas and discusses the possible roles of these molecules in the biological behaviors of this odontogenic tumor. Knowledge of the complex mechanisms in which these molecules play a role is critical for the research and discovery of future therapeutic targets. Key words:Ameloblastoma, cellular adhesion, molecular markers, cell-cell adhesion, extracellular matrix-cell adhesion.

Expression of Syndecan-1 in Papillary Carcinoma of the Thyroid with Extracapsular Invasion

BACKGROUND AND AIMS Syndecan-1 (SDC-1) is a member of the family of transmembrane heparan sulfate proteoglycans, which are involved in cell-cell adhesion and the interaction of cells with the extracellular matrix. Evidence suggests that loss of SDC-1 expression in several benign and malignant epithelial neoplasms is an unfavorable prognostic indicator, but its expression profile in thyroid gland neoplasms remains to be elucidated. The aim of this study was to evaluate SDC-1 expression in papillary carcinomas of the thyroid (PCT) that were both larger and smaller (papillary microcarcinoma) than 10mm, with or without extracapsular extension (PCT-E and PCT-NE). METHODS The expression of SDC-1 was studied in 62 cases of PCT-E and PCT-NE using a tissue microarrays technique (TMA). SDC-1 positivity was predominantly observed in the cytoplasm of neoplastic epithelial cells and in the stroma of PCT. RESULTS SDC-1 is expressed in both neoplastic epithelial cells and the stroma. It is more frequently expressed in PCT-E than PCT-NE (p=0.002) and the stromal expression of SDC-1 is more intense in PCT-E that are >10 mm (p=0.026). CONCLUSIONS The epithelial and stromal expression of SDC-1 observed in this series of PCT suggests that the expression of this protein may be related to extracapsular invasion.

Immunoexpression of Ki-67, MCM2, and MCM3 in Ameloblastoma and Ameloblastic Carcinoma and Their Correlations with Clinical and Histopathological Patterns

Cell proliferation assays are performed using antibodies against nuclear proteins associated with DNA replication. These nuclear proteins have gained special interest to predict the biological and clinical behaviors of various tumors. The aim of this study was to analyze the presence of Ki-67 protein and the minichromosome maintenance-2 (MCM2) and maintenance-3 (MCM3) proteins in ameloblastoma. Materials and Methods. Cell proliferation marker expression levels were assessed via immunohistochemistry in 111 ameloblastoma cases (72 unicystic ameloblastoma samples, 38 solid/multicystic ameloblastoma samples, and 1 ameloblastic carcinoma). The label index was performed as described previously. Results. MCM2 and MCM3 showed higher proliferation indexes in all variants of ameloblastoma compared to the classic marker Ki-67. No correlation between the proliferation index and the clinical and protein expression data was observed. Conclusion. The results suggest that clinical features do not directly affect tumor cell proliferation. Moreover, the high levels of cellular proliferation of MCM2 and MCM3 compared with Ki-67 may indicate that MCM2 and MCM3 are more sensitive markers for predicting the growth rate and eventually might be helpful as a tool for predicting aggressive and recurrent behaviors in these tumors.

Immunohistochemical Expression of Survivin and Its Relationship with Cell Apoptosis and Proliferation in Ameloblastomas

Ameloblastoma behavior is related to the potential of tumor cells to inhibit apoptosis and to initiate a proliferative phase. This study was performed to compare the immunoexpression of Survivin with Bcl-2, Bax, and Ki-67 and to associate them with the histopathological type of each variant of ameloblastoma. Material and Methods. Using the World Health Organization (WHO) criteria for ameloblastoma, 110 cases were selected. The cases were classified as solid/multicystic and unicystic ameloblastomas. Cellular counts of cytoplasmic immunoexpression were assessed for cytoplasmic Survivin, Bcl-2, and Bax, while the nuclear immunoexpression of Survivin and Ki-67 was assessed using label index. Results. Cytoplasmic Survivin and Bcl-2 showed higher percentages of immunoexpression in solid multicystic ameloblastomas compared to unicystic ameloblastomas (P < 0.05). Bax, Ki-67, and nuclear Survivin were expressed in higher percentages in unicystic ameloblastomas. Conclusions. Cytoplasmic Survivin and Bcl-2 immunoexpression levels were elevated in relation to Bax immunoexpression, suggesting aggressive ameloblastoma behavior, while Ki-67 and nuclear Survivin immunoexpression may be associated with the type of tumor morphology that influences cellular counts or with the greater capacity for cellular proliferation and tumor growth.

Diagnóstico Tardío de Carcinoma Escamo Celular en Boca: Reporte de Caso

Es de gran importancia que el odontologo este entrenado en la deteccion temprana de cualquier lesion de la cavidad bucal, mas aun cuando se trata de una lesion pre-maligna o maligna. El odontologo es el primer profesional de la salud que entra en contacto con la cavidad bucal del paciente y por lo tanto el encargado de preservar la salud de la misma, no solo de los organos dentarios si no de todos los tejidos que componen el aparato estomatognatico. En el presente caso se muestra un paciente masculino de 72 anos de edad que acude al Instituto Dermatologico de Jalisco “Dr. Jose Barba Rubio” con una lesion exofitica ulcerada de aproximadamente cinco anos de evolucion localizada en piel de mejilla, se realiza excision quirurgica, el estudio histopatologico diagnostica carcinoma de celulas escamosas bien diferenciado originado en cavidad bucal que posteriormente invade tejido blando y piel. Se remite al Instituto Jalisciense de Cancerologia para continuar el tratamiento.

Expression of hMLH1 and hMSH2 proteins in ameloblastomas and tooth germs

Background Mismatch repair proteins (MMRPs) are a group of nuclear enzymes that participate in the repair of base mismatches that occur during DNA replication in all proliferating cells. The most studied MMRPs are hMSH2 and hMLH1, which are known to be highly expressed in normal tissues. A loss of MMRPs leads to the accumulation of DNA replication errors in proliferating cells. Ki-67 is a biomarker regarded to be the gold-standard tool for determining cell proliferation by immunohistochemical methods. The aim of this study was to investigate the immunohistochemical expression of hMLH1, hMSH2 and Ki-67 proteins in ameloblastomas and tooth germs, to contribute to the understanding of the development of this odontogenic neoplasm. Material and Methods Immunohistochemical assays to determine the presence of proteins hMSH2, hMLH1 and Ki-67 were performed in 80 ameloblastomas (40 solid and 40 unicystic) and five tooth germs. Results Unicystic ameloblastomas showed higher MMRP expression (hMLH1: 62.5 ± 43.4; hMSH2: 83.3 ± 47.8) than did solid ameloblastomas (hMLH1: 59.4 ± 13.5; hMSH2: 75.8 ± 40.2). Additionally, the cell proliferation index assessed by Ki-67 was inversely proportional to the expression of MMRP. Comparison between tooth germs and ameloblastoma revealed significantly higher expression of hMLH1, hMSH2 and Ki-67 in tooth germs (p=0.02). Conclusions The differences of MMRP and Ki-67 immunoexpression between ameloblastomas and tooth germ suggest that alterations in the MMRP mechanisms could participate in the biological behavior of ameloblastomas. Key words:hMLH1, hMSH2, Ki-67, Ameloblastomas, Tooth germs.

Comparative Study of the Minichromosome Maintenance Proteins Complex (MCM 4/5/6) in Ameloblastoma and Unicystic Ameloblastoma

Introduction. Solid/conventional ameloblastoma (AM) and unicystic ameloblastoma (UAM) are the most frequent benign epithelial odontogenic tumors located in the maxillary region, and their treatment usually consists of extensive surgical resection. Therefore, it is relevant to study molecular markers to better understand the biological behavior of these tumors. The aim of this study was to describe and compare the expression of proteins related to cellular proliferation: Ki-67 and MCM4-6 complex. Materials and Methods. An immunohistochemistry technique was performed, with antibodies against Ki-67, MCM4, MCM5, and MCM6, in 10 AM and 10 UAM tumors. The results were quantified using label index and analyzed statistically. Results. AM and UAM had greater expression of MCM6, followed by MCM5, MCM4, and Ki-67 (P < .05). Immunoexpression of Ki-67 and MCM5 was exclusively nuclear, whereas the expression of MCM4 and MCM6 was nuclear and cytoplasmic. Conclusion. The results suggest that MCM5 is a trustable cell proliferation marker with higher sensitivity compared with Ki-67 and may be useful to predict the biological behavior of AM and UAM. Despite this, further studies are necessary, including a correlation with clinical parameters to confirm these findings.

Molecular Markers of Anticancer Drug Resistance in Head and Neck Squamous Cell Carcinoma: A Literature Review

This manuscript provides an update to the literature on molecules with roles in tumor resistance therapy in head and neck squamous cell carcinoma (HNSCC). Although significant improvements have been made in the treatment for head and neck squamous cell carcinoma, physicians face yet another challenge—that of preserving oral functions, which involves the use of multidisciplinary therapies, such as multiple chemotherapies (CT) and radiotherapy (RT). Designing personalized therapeutic options requires the study of genes involved in drug resistance. This review provides an overview of the molecules that have been linked to resistance to chemotherapy in HNSCC, including the family of ATP-binding cassette transporters (ABCs), nucleotide excision repair/base excision repair (NER/BER) enzymatic complexes (which act on nonspecific DNA lesions generated by gamma and ultraviolet radiation by cross-linking and forming intra/interchain chemical adducts), cisplatin (a chemotherapeutic agent that causes DNA damage and induces apoptosis, which is a paradox because its effectiveness is based on the integrity of the genes involved in apoptotic signaling pathways), and cetuximab, including a discussion of the genes involved in the cell cycle and the proliferation of possible markers that confer resistance to cetuximab.

Epigenetic mechanisms in odontogenic tumors: A literature review

OBJECTIVE Epigenetic mechanisms, such as DNA methylation, regulate important biological processes as gene expression and it was suggested that these phenomena play important roles in the carcinogenesis and tumor biology. The aim of this review is to provide the current state of knowledge about epigenetic alterations, focusing mainly on DNA methylation, reported in odontogenic tumors. DESIGN Literatures were searched based in the combination of the following keywords: odontogenic tumors, epigenetics, DNA methylation, histone modifications, non-coding RNA, microRNA, DNA methyltransferases. Electronic databases (Medline/PubMed, Scopus and Web of Science) were screened. RESULTS The analysis of epigenetic alterations in different tumors has rapidly increased; however, limited information is available about epigenetic mechanisms involved in the formation of odontogenic tumors. DNA methylation is the most studied epigenetic modification in these tumors and the participation of non-coding RNAs in odontogenic tumors has been recently addressed. Differential expression of DNA methyltransferases, altered DNA methylation patterns and aberrant expression of non-coding RNAs were reported in odontogenic tumors. CONCLUSIONS Current studies suggest epigenetics as an emerging mechanism, possibly implicated in etiopathogenesis of odontogenic tumors. Deeper understanding of the epigenetic abnormalities in these tumors could show potential applications as biomarkers or therapeutic possibilities in the future.