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Objectives: Laryngeal squamous cell carcinomas (LSCC) is one of the most common aggressive neoplasms of the head and neck region. There is a significant need for identification of successful and accurate prognostic markers to better estimate the clinical outcomes for LSCC patients. In this study, we aimed at analyzing the differential expressions of inhibitor growth (ING) family members and to evaluate the prognostic values of deregulated ING genes in LSCC. Methods: We investigated the relative expressions of ING genes in laryngeal tumor-normal tissue pairs at mRNA level using quantitative real-time polymerase chain reaction and relative expression of ING3 in the protein level using Western Blot analysis. Results: The rate of genetic alterations of ING3 was relatively higher in head and neck cancers including LSCC. ING3 expression was significantly upregulated in LSCC tissue samples at both mRNA and protein level. Higher expression of ING3 was also correlated with poor disease-free survival of patients with head and neck cancer. Conclusions: Our findings assigned an oncogenic feature for ING3 in laryngeal cancer with a significant upregulation detected in advanced cases and suggested a vital prognostic potential for ING3. [ABSTRACT FROM AUTHOR]

Objectives: Diets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods of animal origin facilitates carcinogenesis. In this study, we aimed at investigating the possible involvement of vitamin D deficiency (VDD) and high cholesterol (HC) together in oral squamous cell carcinoma (OSCC) through modulating glycolysis. Subjects and Methods: We compared total cholesterol, LDL, HDL, triglycerides, LDH, and vitamin D levels of OSCC patients and control individuals. We used GEO datasets for gene set enrichment and 4‐nitroquinoline‐1‐oxide induced in vivo oral carcinogenesis models to investigate contribution of VDD and HC during carcinogenesis via possible modulation of glycolysis. Results: We found that VDD and HC co‐exist in OSCC patients, and deregulation of cholesterol and vitamin D levels results in enrichment of genes related to glycolysis. We, then, demonstrated that VDD and HC on their own and together facilitated the formation of larger tumors in 4NQO‐induced in vivo cancer models, which are suppressed by glycolysis inhibition. Conclusion: We reported collaborative contribution of HC and VDD during oral carcinogenesis, which is mainly carried out via altering energy metabolism in tumor cells. [ABSTRACT FROM AUTHOR]

Background. Cyclophosphamide is a drug used in various types of cancer. It can cause oxidative and inflammatory ovarian damage and infertility. Thiamine pyrophosphate (TPP) to be investigated for its effect on cyclophosphamide-induced ovarian damage and reproductive dysfunction in the present study is the active metabolite of thiamine. It has been shown that TPP protects organs and tissues from oxidative stress and proinflammatory cytokine damage. Objectives. To investigate the effect of TPP against the ovarian damage and reproductive dysfunction caused by cyclophosphamide in rats. Materials and methods. Albino Wistar type female rats were divided into healthy control (HG), cyclophosphamide (CYC) and TPP + cyclophosphamide (TPPC) groups (for each group, n = 12). Thiamine pyrophosphate at a dose of 25 mg/kg was injected intraperitoneally (ip.) in the TPPC group, and 0.9% NaCI solution was injected ip. in the CYC and HG groups. One hour after the injection, 75 mg/kg of cyclophosphamide was administered ip. in the TPPC and CYC groups. This procedure was repeated once a day for 30 days. At the end of this period, 6 rats from each group were euthanized with a high dose of anesthetic (50 mg/kg of sodium thiopental). Biochemical and histopathological examinations were performed on the extracted ovarian tissue. The remaining animals were kept in the laboratory with mature male rats for 2 months for reproduction. Results. Thiamine pyrophosphate significantly decreased the cyclophosphamide-induced increase in the levels of the oxidant parameter malondialdehyde (MDA), proinflammatory nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), and interleukin 1 beta (IL-1β). In addition, TPP decreased the severe histopathological damage associated with cyclophosphamide in the ovarian tissue and prevented infertility. Conclusions. Our experimental results have suggested that TPP could be beneficial in the treatment of cyclophosphamide-induced ovarian injury and infertility. [ABSTRACT FROM AUTHOR]

Objective: In this study, we aimed to compare the results of patients who underwent surgery by thoracotomy and Video-assisted thoracoscopic surgery (VATS) in mediastinal neurogenic tumors. Materials and Methods: Twenty-six consecutive cases (12 males and 14 females; mean age 39.4 ± 22.3 years; range 1--72 years) who were histopathologically diagnosed as having mediastinal neurogenic tumors between January 2000 and August 2020 were included in a single-center, retrospective study. Results: There were 5 (19.2%) children and 21 (80.8%) adults. Lesions in all cases were located in the posterior mediastinum. Schwannoma was detected histopathologically in 18 cases (69.2%), and all of these cases were adult patients. Resection was performed by thoracotomy in 14 cases (7 right and 7 left) and 12 cases by thoracoscopy (7 right and 5 left). The mean tumor size was 7.4 ± 1.9 cm (range 5--12 cm) in the thoracotomy group and 4.3 ± 1.9 cm (range 2--7 cm) in the VATS group (P = .001). Mean operative time was 101.7 ± 27.8 min (range 70--150 min) in the thoracotomy group and 77.9 ± 24.3 min (range 60--150 min) in the VATS group (P = .014). Mean postoperative hospital stay was 7.4 ± 4.0 days (range 3--20 days) in the thoracotomy group and 4.7 ± 1.7 days (range 2--7 days) in the VATS group (P = .040). Conclusion: Most of the mediastinal neurogenic tumors are benign and surgical resection is required in their treatment. With increasing experience, resection can be performed thoracoscopically in most cases. [ABSTRACT FROM AUTHOR]

Aziz Sancar, Nobel Prize winning Turkish scientist, made several discoveries which had a major impact on molecular sciences, particularly disciplines that focus on carcinogenesis and cancer treatment, including molecular pathology. Cloning the photolyase gene, which was the initial step of his work on DNA repair mechanisms, discovery of the "Maxicell" method, explanation of the mechanism of nucleotide excision repair and transcription-coupled repair, discovery of "molecular matchmakers", and mapping human excision repair genes at single nucleotide resolution constitute his major research topics. Moreover, Sancar discovered the cryptochromes, the clock genes in humans, in 1998, and this discovery led to substantial progress in the understanding of the circadian clock and the introduction of the concept of "chrono-chemoterapy" for more effective therapy in cancer patients. This review focuses on Aziz Sancar's scientific studies and their reflections on molecular pathology of neoplastic diseases. While providing a new perspective for researchers working in the field of pathology and molecular pathology, this review is also an evidence of how basic sciences and clinical sciences complete each other. [ABSTRACT FROM AUTHOR]