Lectin-like transcript 1 (LLT1) expression is associated with nodal metastasis in patients with head and neck cutaneous squamous cell carcinoma.

The interaction of lectin-like transcript 1 (LLT1) with CD161 inhibits Natural Killer cell activation. Overexpression of LLT1 contributes to the immunosuppressive properties of tumor cells. However, there are little data about LLT1 expression in human solid tumors. The objective of this paper is to investigate the relationship between LLT1 expression with the clinicopathologic features and its impact on the prognosis of head and neck cutaneous squamous cell carcinoma (cSCC). LLT1 expression was analyzed on paraffin-embedded tissue samples obtained from 100 patients with cSCC by immunohistochemistry. The estimator of Fine and Gray was used to estimate the cumulative incidence curves for relapse. Proportional Hazard models and Hazard ratios (HRs) were used for studying the risk of tumor relapse and mortality. LLT1 strong expression was a significant risk factor for nodal metastasis with crude and adjusted ratios (HRs) of 3.40 (95% CI 1.39-9.28) and 3.25 (95% CI 1.15-9.16); and for cSCC specific death of 6.17 (95% CI 1.79-21.2) and 6.10 (95% CI 1.45-25.7). Strong LLT1 expression is an independent predictor of nodal metastasis and poor disease-specific survival and it might be helpful for risk stratification of patients with cSCC.

Distinctive clinicopathological associations of amplification of the cortactin gene at 11q13 in head and neck squamous cell carcinomas.

Amplification of the 11q13 region is a prevalent genetic alteration in head and neck squamous cell carcinoma (HNSCC). We investigated the clinical significance of cortactin (CTTN) and cyclin D1 (CCND1) amplification in both malignant transformation and tumour progression. CTTN and CCND1 amplification was analysed by differential and real-time PCR in a prospective series of laryngeal/pharyngeal carcinomas and archival premalignant tissues. CTTN mRNA and protein expression were respectively determined by real-time RT-PCR and immunohistochemistry, and correlated with gene status. Molecular alterations were associated with clinicopathological parameters and disease outcome. CTTN and CCND1 amplifications were respectively found in 75 (37%) and 90 (45%) tumours. Both correlated with advanced disease; however, only CTTN amplification was associated with recurrence and reduced disease-specific survival (p = 0.0022). Strikingly, CTTN amplification differentially influenced survival depending on tumour site (p = 0.0001 larynx versus p = 0.68 pharynx) and was an independent predictor of reduced survival in the larynx (p = 0.04). CCND1 amplification was detected in early tumourigenesis and increased with the severity of dysplasia. Importantly, CTTN amplification was only found in high-grade dysplasias that progressed to invasive carcinoma. CTTN gene status strongly correlated with mRNA and protein expression. Furthermore, CTTN overexpression correlated significantly with reduced disease-specific survival (p = 0.018). Taken together, these data indicate that CTTN may serve as a valuable biomarker to identify patients with laryngeal tumours at high risk of recurrence and poor outcome.

[Expression of annexins Al and A2 in the mucosa of the upper airdigestive tract]. / Expresión de las anexinas Al y A2 en la mucosa del tracto aerodigestivo superior.

INTRODUCTION: Annexins A1 and A2 have been related with the maintenance of tissue integrity. They have been identified in a wide variety of tissues, but little is known regarding their expression in upper the aerodigestive tract. The aim of this work is to describe the expression of these proteins in the mucosa of the upper aerodigestive tract. MATERIAL AND METHODS: Tissue samples from respiratory (nasal and laryngeal) and digestive (oral and pharyngeal) mucosa from non-oncological patients were studied. Annexin A1 and A2 expression was determined by immunohistochemistry. RESULTS: Both annexins were expressed in the ciliated and in the stratified non-keratinized epithelia, but with a different pattern; ANXA1 was expressed in the more differentiated cells whereas ANXA2 was expressed in the less differentiated ones (with the exception of the cilia of ciliated cells). CONCLUSION: Although annexins A1 and A2 are structurally and philogenetically related its expression pattern in the upper aerodigestive tract suggests that they have different functions.

[Detection of herpes simplex virus and Epstein-Barr virus in squamous cell carcinoma of the upper airways and digestive system]. / Detección del virus herpes simplex y del virus de Epstein-Barr en los carcinomas de células escamosas de vías aerodigestivas superiores.

OBJECTIVE: Previous studies have investigated the role of viruses in tumor origin of head and neck cancer. Despite this, mechanis of viral carcinogenesis remain unclear. The aim of this study is to determine the prevalence of herpes simplex virus (HSV) and Epstein-Barr virus (EBV) in malignant laryngeal and oropharyngeal lesions. MATERIAL AND METHODS: Fresh frozen specimens of 28 laryngeal and oropharyngeal squamous cell carcinomas were studied. The presence or absence of HSV and EBV was determined with polymerase chain reaction (PCR) assays. RESULTS: None of the samples showed evidence for EBV DNA. One tonsilar carcinoma case (3.5%) was positive for HSV DNA detection. CONCLUSIONS: These results do not support HSV and EBV as etiological factors in head and neck cancer.

[CCND1 oncogene amplification and cellular DNA content in squamous cell carcinomas of the head and neck]. / Amplificación del oncogén CCND1 y contenido celular de ADN en los carcinomas epidermoides de cabeza y cuello.

Cyclin D1 protein (encoded by the CCND1 gene) contributes to the progression of the cell cycle in the G1/S checkpoint. Cyclin D1 overexpression (for instance as a consequence of CCND1 amplification) might result in loss of control over genetic damage at this point and in an accumulation of chromosomal aberrations. In this work we analyze whether CCND1 amplification is associated with a higher incidence of alterations in cellular DNA content. 31 squamous cell carcinomas of the head and neck were studied. CCND1 amplification was determined by polymerase chain reaction. Cellular DNA content was determined by flow cytometry. CCND1 amplification was found in 6 (19%) cases. Thirteen (42%) cases were diploid and 18 (58%) were aneuploid. Two (33%) of the 6 cases with CCND1 amplification were aneuploid compared with 16 (64%) of the cases without CCND1 amplification (P = 0.36). We conclude that CCND1 amplification is not associated to a higher incidence of chromosomal aberrations in squamous cell carcinomas of the head and neck.