Metastasis to palatine tonsils are rare, accounting from only 0.8% of all tonsillar tumors, so far only 100 cases reported in the English literature. Only a few cases have been reported for small cell and non-small cell lung cancer as a primary site. With a diagnosis of small cell lung cancer, a 68-year-old male patient relapsed after six cycles of chemotherapy in tonsilla palatina and cervical lymph nodes. Patients died 26 months after being diagnosed with lung cancer and 2 months after detection of tonsil metastasis. We present the current case report because of the rarity of metastasis to tonsil in lung cancer.

The purpose of this study is to review the current literature concerning the indication of pelvic lymph node dissection (PLND), its extent and complications in prostate cancer (PCa) staging, the available tools, and the future perspectives to assess the risk of lymph node invasion (LNI).

Pleomorphic adenoma or mixed tumour is a benign salivary gland tumour, presenting usually in the parotid or submandibular glands. This tumour contains elements of both epithelial and mesenchymal origin. They are the most common tumours (50%), (60-65%) of the major and minor salivary glands. The palate is considered as the most common intraoral site (42.8-68.8%), followed by the upper lip (10.1%) and cheek (5.5%).

Glycosylation of proteins is an essential process in all eukaryotes. Mucin-type O-linked glycosylation is an evolutionarily conserved protein modification as a kind of glycosylation of proteins. The role of O-glycosylation was well documented in multiple cancers. While in breast cancer, the enzymes that catalyzed the initiation of O-glycosylation remained elusive. In this review, we briefly introduced the process of the initiation of O-glycosylation and summarized the roles of enzymes that catalyzed the initiation step of O-glycosylation in the breast cancer carcinogenesis, development, and progression. Finally, we summarized some attempts exploring the therapy against aberrant O-glycosylation.

Nodal mediastinal staging is a crucial part of the diagnostic workup of patients with non-small-cell lung cancer (NSCLC) for planning optimal treatment. Transesophageal endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) and real-time endobronchial ultrasounds transbronchial needle aspiration (EBUS-TBNA) are accurate, minimally invasive and safe diagnostic techniques for mediastinal staging. Because of the different accessibility to the mediastinum, they are considered complementary and their combination increases the diagnostic yield as compared with the either alone. Recent studies have shown that endosonography represents the best initial test for invasive mediastinal evaluation in NSCLC. Endoscopic ultrasound (with bronchoscope)-guided fine needle aspiration (EUS-B-FNA) is a recently introduced procedure consisting of a transesophageal needle aspiration using an ultrasound bronchoscope. It allows to perform both transbronchial and transesophageal needle sampling with the same instrument, in the same session and by one operator only, thus maximizing time and costs savings. In a recent study Oki et al. randomized 110 patients with hilar/mediastinal adenopathies or lung abnormalities adjoining both the esophagus and the bronchi, to undergo EBUS-TBNA or EUS-FNA performed by pulmonologists with an echobronchoscope. The Authors demonstrated that both procedures provide a high diagnostic yield, without any difference in the number of adverse events and a good comparable tolerance. Nevertheless, the transesophageal approach guaranteed a significantly lower dose of anesthetics and sedatives, a shorter procedural time, fewer oxygen desaturations, a significantly lower cough score and a higher operator satisfaction. In this review our aim was to discuss the findings by Oki et al. in the context of medical literature, highlighting the importance of the EUS-B needle aspiration technique in diagnosing mediastinal and lung lesions, when EBUS-TBNA is deemed less suitable. Finally, we pointed out the importance of interventional pulmonologists being trained to perform mediastinal sampling by the esophageal route, to choose the best solution in every technical and clinical occurence.

Non-homologous end joining (NHEJ) is one of the pathways used to repair the DNA double-strand breaks. A number of genes involved in NHEJ have been implicated as lung cancer susceptibility genes such as the LIG1. However, some studies have generated conflicting results. The aim of this review and meta-analysis was to investigate the association between the LIG1 gene polymorphism and lung cancer risk. Studies focusing on the relationship between the LIG1 gene polymorphisms and susceptibility to lung cancer were selected from several electronic databases, with the last search up to October 25, 2014. Data were extracted by two independent reviewers, and the meta-analysis was performed with STATA version 12.0 software, calculating odds ratios (ORs) with 95 % confidence intervals (95 % CIs). According to the inclusion criteria, we included ten studies with a total of 4012 lung cancer cases and 5629 healthy controls in the meta-analysis. The results showed that the rs156641 polymorphism was significantly associated with lung cancer risk (dominant model: OR 0.694, 95 % CI 0.549-0.878; homozygote model: OR 0.677, 95 % CI 0.526-0.871; heterozygote model: OR 0.712, 95 % CI 0.556-0.913; additive model: OR 0.859, 95 % CI 0.767-0.962), whereas no association was found between rs3730931/rs439132/rs20579 polymorphisms and lung cancer. Our meta-analysis suggested that the rs156641 polymorphism in the LIG1 gene might be associated with an increased risk of lung cancer.

Aggressive adult granulosa cell tumor (AGCT) of the ovary remains uncommon. We report a case of aggressive AGCT of the ovary who had rapid recurrence at two months after surgery. A patient was referred for further examination of a pelvic tumor. She underwent total abdominal hysterectomy, bilateral salpingo-oophorectomy, and pelvic lymphadenectomy. In the areas showing a sarcomatoid pattern, the mitotic count were 25/10 HPFs, and the mitoses were most prominent in foci composed of pleomorphic cells with enlarged and bizarre nuclei. In some areas, tumor cells with relatively uniform nuclei proliferated in a trabecular pattern. The mitotic count was 4/10 HPFs. Tumor cells were diffusely positive for α-inhibin. She was diagnosed as having aggressive AGCT. The Ki-67 labeling index in the sarcomatoid AGCT was higher (40%) than that in the areas of typical AGCT (3%). Immunostaining for p53 in the sarcomatoid AGCT was almost strongly positive, but that in typical AGCT was negative. Two months later after the initial surgery, a recurrent abdominal 12 cm-sized mass developed after performing adjuvant chemotherapy consisting of paclitaxel and carboplatin. She died of the disease at 3 months after initial surgery. A markedly higher mitotic count, a higher Ki-67 labeling index, and strong immunoreactivity of p53 in AGCT suggests highly malignant potential. In such a case, a careful follow-up is warranted due to the possibility of rapid recurrence.

The ovaries accessories, ectopic and supernumerary represent a rare gynecological disorder; incidence ranges from 129,000 to 1:700,000 cases.

While robotic surgery has seen much success in the treatment of gynecologic malignancies, the technical aspects of this approach raise concern for spreading tumor cells within the peritoneal cavity and to trocar sites. To date, robotic trocar site metastases have been identified following surgery for both endometrial and cervical cancer.

Primary leiomyoma of the liver is an extremely rare benign hepatic tumor in asymptomatic patients. While leiomyoma is frequently found in the genitourinary tract, to the best of our knowledge only 29 cases of primary hepatic leiomyoma have been reported in the English language medical literature. Primary hepatic leiomyoma in patients without an underlying systemic disease (immunosuppression) is even more uncommon. A leiomyoma is composed of bundles of smooth muscle fibers and rarely transforms into a malignant tumor. We present a previously healthy 44-year-old woman who was incidentally found to have a focal liver lesion while undergoing radiologic studies for evaluation of her low back pain. The primary leiomyoma of the liver has characteristic radiologic findings that distinguish it from other hepatic tumors. In this article we discuss the typical radiologic and pathologic findings of leiomyoma compared with other primary liver tumors.

Chromosome stability is ensured by precisely fine-tuned dynamics of mitotic spindles, which are controlled by a network of various microtubule-associated and interacting proteins including the kinesin-13 family. The best characterized member of this family is the mitotic centromere-associated kinesin (MCAK). By efficiently depolymerizing microtubules, MCAK influences various key events during mitosis. MCAK itself is regulated by its interaction partners, its intrinsic conformation switch and the phosphorylation of mitotic kinases like Aurora A/B, cyclin-dependent kinase 1 and Polo-like kinase 1. Perturbing its regulation alters MCAK's conformation, catalytic activity, subcellular localization and stability, leading further to mitotic defects in spindle formation and chromosome movement. Indeed, MCAK is aberrantly regulated in various cancer types, which is linked to increased invasiveness, metastasis and drug resistance. In the current review, we summarize recently published data concerning MCAK, correlate its conformation changes with its depolymerization activity and function, propose a model of its regulation by multiple mitotic kinases and highlight its potential involvement in oncogenesis and drug resistance.

The cytoprotective and anticancer action of dietary in-taken natural polyphenols has for long been attributed only to their direct radical scavenging activities. Currently it is well supported that those compounds display a broad spectrum of biological and pharmacological outcomes mediated by their complex metabolism, interaction with gut microbiota as well as direct interactions of their metabolites with key cellular signaling proteins. The beneficial effects of natural polyphenols and their synthetic derivatives are extensively studied in context of cancer prophylaxis and therapy. Herein we focus on cell signaling to explain the beneficial role of polyphenols at the three stages of cancer development: we review the recent proceedings about the impact of polyphenols on the cytoprotective antioxidant response and their proapoptotic action at the premalignant stage, and finally we present data showing how phenolic acids (e.g., caffeic, chlorogenic acids) and flavonols (e.g., quercetin) hamper the development of metastatic cancer.

Pioneer transcription factors constitute a heterogeneous group of regulatory proteins of animals, which, unlike other transcription factors, are able to recognize and bind target DNA sequences within closed chromatin. This binding can change the local chromatin structure and facilitate binding of other proteins, thus establishing competence for gene expression. The ability to bind silent genes in the closed environment makes the pioneer factors very useful in the processes leading to cardinal alteration of cell phenotype, such as differentiation in embryonic development or cell reprogramming. These proteins can remain bound to target sequences during mitotic division, and due to this probably take part in the maintenance of cellular memory. Apparently, pioneer transcription factors are active participants in carcinogenesis and maintenance of tumor cell phenotype, although their role in these processes needs additional research. It is reasonable to suppose that a further study will help to shed more light on the genetic processes in embryonic development, increase the efficiency of cell reprogramming and also develop new approaches to diagnostics and therapy of cancer diseases.

High mortality from breast cancer is associated with the high heterogeneity of tumor and the frequent recurrences of the pathological process, which are due to the presence of tumor stem cells. The review considers the biological properties of tumor stem cells, the molecular mechanisms of their regulation, interaction with the microenvironment, and their role in the heterogeneity of the morphological and clinical forms of breast cancer.

In most patients, lung cancer presents as advanced disease with metastases to lymph nodes and/or distant organs, and survival is poor. Lung cancer is also a highly immune-suppressing malignancy with numerous methods to evade antitumor immune responses, including deficiencies in antigen processing and presentation, release of immunomodulatory cytokines, and inhibition of T-cell activation. Advances in understanding the complex interactions of the immune system and cancer have led to novel therapies that promote T-cell activation at the tumor site, resulting in prolonged clinical benefit. Immune checkpoint inhibitors, specifically programmed death receptor 1 pathway antibodies, have demonstrated impressively durable responses and improved survival in patients with non-small cell lung cancer. This article will review the recent progress made in immunotherapy for lung cancer with data from trials evaluating programmed death receptor 1 and cytotoxic T-lymphocyte-associated protein 4 monoclonal antibodies in addition to cancer vaccines. The review will focus on studies that have been published and the latest randomized trials exploring immune therapy in lung cancer. These results form the framework for a new direction in the treatment of lung cancer toward immunotherapy.

Brain metastases are common in patients with small cell lung cancer (SCLC), and prophylactic cranial irradiation (PCI) has been shown to reduce the risk of brain metastases in these patients. But how great are the benefits, and do the benefits outweigh the toxicity? In this month's Counterpoints, Dr Ben J. Slotman makes the case for the use of PCI in nearly all patients with SCLC who have responded to treatment, whereas Jacob Yousef and Dr Henry Wagner argue that the role of PCI should be reassessed.

Substantial evidence supports the relationship between chronic inflammation and cancer development. Numerous studies suggest that chronic inflammatory disease, such as periodontitis, contributes to head and neck squamous cell carcinoma development. Oral squamous cell carcinoma (OSCC) is the most common malignant tumor in the oral and maxillofacial regions. Porphyromonas gingivalis, one of the most important pathogens in association with periodontal disease, might have a potential correlation with OSCC. Along with the development of molecular biological techniques, the association between Porphyromonas gingivalis and OSCC has been greatly emphasized in recent years. This review summarizes the association between these variables and the potential mechanisms involved in such relationship.