To evaluate the prognostic significance of CTTN/cortactin alterations in head and neck squamous cell carcinoma (HNSCC).
We searched PubMed, Embase, Web of Science, and Scopus for studies published before May 2018. We conducted a meta-analysis to quantify the impact of CTTN/cortactin alterations on clinicopathological and survival variables.
Eighteen studies (1633 patients) met inclusion criteria. Quantitative evaluation revealed a strong association of CTTN/cortactin alterations with N+ status (P < .001), higher T status (P < .001), advanced clinical stage (P < .001), high histological grade (P = .001), and lower overall survival (OS) (P < .001). We found heterogeneity in T status, histological grade, and OS and observed small-study effects on N status and OS. In subgroup analyses, a significant association of CTTN amplification and cortactin overexpression with the above variables was preserved. The strongest association between CTTN/cortactin alterations and a worse outcome was observed in the subgroups of Asian patients and pharyngolaryngeal squamous cell carcinomas.
CTTN/cortactin alterations should be evaluated to predict the HNSCC prognosis.

This is a mini-review summarizing recent findings on the effect of flutamide (FLUT), an anti-androgenic toxicant, on the mouse testis, particularly on the ectoplasmic specialization (ES) in the testis. FLUT induces a reduction in the weight of male reproductive tissues, such as the prostate, because it inhibits the formation of the androgen receptors and testosterone retention. The present review summarizes the abnormal histological changes produced in the mouse testis by FLUT. In addition, we outline the effect of FLUT on the expression of cortactin, an actin-binding protein, in the mouse testis. FLUT is often used as a positive control for the identification of endocrine disrupting chemicals having anti-androgenic activities; therefore, a detailed understanding of the adverse effects of FLUT is important for the analysis of the risks to spermatogenesis by anti-androgen-like endocrine disruptors.

Amplification of oncogenes has been observed frequently in various human malignancies and might be of clinical relevance. In the last decade, the exploration of oncogene activation due to DNA amplification in cancer research has mainly focussed on three aspects: (i) the assessment of oncogene amplification as a prognostic marker for survival of cancer patients, (ii) the development of reliable methods for detection of tumors which harbor DNA amplification of oncogenes and (iii) the identification of the gene or genes responsible for the biological (prognostic) significance in tumors with DNA amplification and the characterization of these candidate proto-oncogenes that might help to elucidate their normal function and the role in tumor development. In this review, these three aspects will be highlighted with regard to DNA amplification of the chromosome 11q13 region. Chromosome 11q13 amplification has been found frequently in certain human malignancies; in cancer of the breast and of the head and neck region, amplification of this region is observed in 13 and 29% of tumors, respectively. The 11q13 amplification has been reported to be of clinical relevance in these cancers, since patients with this amplification show a poor clinical course of disease. The amplified 11q13 region is estimated to be 3-5 Mb in size and to harbor many (putative) genes. Recently, two candidate genes, CCND1 and EMS1, were identified which were both over-expressed in all carcinomas with an 11q13 amplification. Therefore, the activation of these genes might confer the selective advantage to these tumors. In addition, the characterization of these two novel genes sustained their potential role in carcinomas with 11q13 amplification.