Chromosomal rearrangements of NTRK genes are oncogenic driver mutations in thyroid cancer (TC). This study aimed to identify NTRK fusion-positive thyroid tumors and to correlate them with clinical and pathological data and determine their prognostic significance. The cohort consisted of 989 different TC samples. Based on the detected mutation, samples were triaged, and those that were positive for a BRAF, HRAS, KRAS, NRAS, RET, RET/PTC or PAX8/PPARγ mutation were excluded from further analyses. NTRK fusion gene testing was performed in 259 cases, including 126 cases using next-generation sequencing. NTRK fusion genes were detected in 57 of 846 (6.7%) papillary thyroid carcinomas and in 2 of 10 (20.0%) poorly differentiated thyroid carcinomas. A total of eight types of NTRK fusions were found, including ETV6/NTRK3, EML4/NTRK3, RBPMS/NTRK3, SQSTM1/NTRK3, TPM3/NTRK1, IRF2BP2/NTRK1, SQSTM1/NTRK1 and TPR/NTRK1.NTRK fusion-positive carcinomas were associated with the follicular growth pattern, chronic lymphocytic thyroiditis and lymph node metastases. NTRK1-rearranged carcinomas showed a higher frequency of multifocality and aggressivity than NTRK3-rearranged carcinomas. Tumor size, presence of metastases, positivity for the NTRK3 or NTRK1 fusion gene and a late mutation event (TERT or TP53 mutation) were determined as factors affecting patient prognosis. NTRK fusion genes are valuable diagnostic and prognostic markers.

Tumor stroma is an active part influencing the biological properties of malignanciesviamolecular cross‐talk. Cancer‐associated fibroblasts play a significant role in this interaction. These cells frequently express smooth muscle actin and can be classified as myofibroblasts. The adhesion/growth‐regulatory lectin galectin‐1 is an effector for their generation. In our study, we set the presence of smooth muscle actin‐positive cancer‐associated fibroblasts in relation to this endogenous lectin and anin vivocompetitor (galectin‐3). In squamous cell carcinomas of head and neck, upregulation of galectin‐1 presence was highly significantly correlated to presence of smooth muscle actin‐positive cancer‐associated fibroblasts in the tumor (p= 4 × 10⁻⁸). To pinpoint further correlations on the molecular level, we applied microarray analyses to the transcription profiles of the corresponding tumors. Significant correlations of several transcripts were detected with the protein level of galectin‐1 in the cancer‐associated fibroblasts. These activated genes (MAP3K2,TRIM23,PTPLAD1,FUSIP1,SLC25A40andSPIN1) are related to known squamous‐cell‐carcinoma poor‐prognosis factors, NF‐κB upregulation and splicing downregulation. These results provide new insights into the significance of presence of myofibroblasts in squamous cell carcinoma.

Background. The aim of this study was to analyze complications of vestibular schwannoma (VS) microsurgery.Material and Methods. A retrospective study was performed in 333 patients with unilateral vestibular schwannoma indicated for surgical treatment between January 1997 and December 2012. Postoperative complications were assessed immediately after VS surgery as well as during outpatient followup.Results. In all 333 patients microsurgical vestibular schwannoma (Koos grade 1: 12, grade 2: 34, grade 3: 62, and grade 4: 225) removal was performed. The main neurological complication was facial nerve dysfunction. The intermediate and poor function (HB III–VI) was observed in 124 cases (45%) immediately after surgery and in 104 cases (33%) on the last followup. We encountered disordered vestibular compensation in 13%, permanent trigeminal nerve dysfunction in 1%, and transient lower cranial nerves (IX–XI) deficit in 6%. Nonneurological complications included CSF leakage in 63% (lateral/medial variant: 99/1%), headache in 9%, and intracerebral hemorrhage in 5%. We did not encounter any case of meningitis.Conclusions. Our study demonstrates that despite the benefits of advanced high-tech equipment, refined microsurgical instruments, and highly developed neuroimaging technologies, there are still various and significant complications associated with vestibular schwannomas microsurgery.

Epidermal stem cells (ESCs) are crucial for maintenance and self- renewal of skin epithelium and also for regular hair cycling. Their role in wound healing is also indispensable. ESCs reside in a defined outer root sheath portion of hair follicle—also known as the bulge region. ECS are also found between basal cells of the interfollicular epidermis or mucous membranes. The non-epithelial elements such as mesenchymal stem cell-like elements of dermis or surrounding adipose tissue can also contribute to this niche formation. Cancer stem cells (CSCs) participate in formation of common epithelial malignant diseases such as basal cell or squamous cell carcinoma. In this review article, we focus on the role of cancer microenvironment with emphasis on the effect of cancer-associated fibroblasts (CAFs). This model reflects various biological aspects of interaction between cancer cell and CAFs with multiple parallels to interaction of normal epidermal stem cells and their niche. The complexity of intercellular interactions within tumor stroma is depicted on example of malignant melanoma, where keratinocytes also contribute the microenvironmental landscape during early phase of tumor progression. Interactions seen in normal bulge region can therefore be an important source of information for proper understanding to melanoma. The therapeutic consequences of targeting of microenvironment in anticancer therapy and for improved wound healing are included to article.