TL;DR: This work focuses on the role of Tumor-Host Components as Elements of Malignancy in Invasion and Metastasis, and the roles of Hydrolases and Cell-Cell Adhesion Molecules in Malignancies.
Abstract: INTRODUCTION. CLINICAL ASPECTS OF INVASION AND METASTASIS. MALIGNANCY-RELATED PHENOTYPES. A Model for Analysis. Criteria for Phenotyping. Combinations of Phenotypes. TRANSITIONS BETWEEN PHENOTYPES: FIELD AND PROGRESSION THEORIES OF TUMOR DEVELOPMENT. PATTERNS OF METASTASIS. Anatomical Considerations. Late Metastases. Metastasis or Second Primary. FACTORS INFLUENCING INVASION AND METASTASIS. Factors Related to the Tumor-Host Ecosystem. Environmental Factors. Therapeutics. INVASION AND METASTASIS: DETERMINANTS OF TUMOR MALIGNANCY. SUMMARY. BIOASSAYS FOR INVASION AND METASTASIS. GENERAL CONSIDERATIONS. IN VITRO BIOASSAYS FOR INVASION AND METASTASIS. Organ Culture. Tissue Explants. Reconstituted Tissues. Cell Cultures. Matrices. Tissue Extracts. IN VIVO ASSAYS FOR INVASION. Subcutaneous Inoculation. Intraperitoneal Injections. Inoculations at Particular Sites. Injections into the Vasculature. IN VIVO ASSAYS FOR METASTASIS. Discrimination Between M Phenotypes. Current Models for Mspo and Mexp Assays. Scores for the M Phenotype. Relevance of the Assays. SUMMARY AND CONCLUSIONS. CELLULAR ACTIVITIES IMPLICATED IN INVASION AND METASTASIS. CELL-CELL ATTACHMENT AS AN ELEMENT OF MALIGNANCY. Structure and Occurrence of Cell-Cell Adhesion Molecules. Normal Role of Cell-Cell Adhesion Molecules. Role of Cell-Cell Adhesion Molecules in Malignancy. Role of Intercellular Junctional Communication in Malignancy. CELL-SUBSTRATE INTERACTIONS AS ELEMENTS OF MALIGNANCY. Extracellular Matrix (ECM): A Multifunctional Network Implicated in Malignancy. Integrins: Major Receptors for ECM Components. Collagens and Elastin: ECM Skeletons and Scaffolds. Fibronectin, Some Other Integrin Ligands, and Their Receptors. Tenascin/Cytotactin. Laminin. Glycosaminoglycans and Proteoglycans. HYDROLASE ACTIVITIES AS ELEMENTS OF MALIGNANCY. Are Hydrolases Implicated in Invasion and Metastasis? Overview of Tumor-Associated Hydrolases. Serine Proteases and Malignancy. Cathepsins and Malignancy. Met alloproteases and Malignancy. Glycosidases and Malignancy. Synergism Between Hydrolases and Hydrolases Cascades. Additional Activities of Hydrolases Implicated in Malignancy. MOTILITY AND MIGRATION AS ELEMENTS OF MALIGNANCY. Notions of Motility and Migration. Is Motility Implicated in Invasion and Metastasis? Motility-Modulating Factors Possibly Implicated in Malignancy. EVALUATION AND SUMMARY. CONTRIBUTIONS OF THE HOST TO INVASION AND METASTASIS. HOST-TUMOR INTERACTIONS AT THE PRIMARY SITE. Tumor-Associated Leukocytes: Origin and Regulation of Accumulation. Tumor-Associated Leukocytes: Accumulation and Activation During Neoplastic Development. Tumor-Host Components as Elements of Malignancy. HOST-TUMOR INTERACTIONS IN THE CIRCULATION. Role of Host Components in Tumor Cell Arrest and Lodgement. Role of Host Components in Tumor Cell Extravasation. HOST-TUMOR INTERACTIONS AT SECONDARY SITES. Host-Mediated Control of the Im Phenotype. Host-Mediated Control of the Gm Phenotype. TUM OR CELL ACQUISITION
TL;DR: Esophageal cancer appears to be more amenable to immune modulation than EAC, and it is becoming clearer that segregating these two histological subtypes in trials should be the goal of future trial designs.
Abstract: ABSTRACT Introduction Esophageal cancer (EC) is a worldwide healthcare concern and represents an aggressive malignancy. Squamous cell carcinoma (ESCC) and adenocarcinoma (EAC) are the two primary histological subtypes but have yet to vastly differ in management. Outcomes remain poor with current treatment approaches; however, recent progress is focused on distinguishing separate targets based on thistology. Areas covered Here we provide an overview of EC management via a historical review and recent discoveries. As noted in this review, targeted therapy has lagged behind other solid tumors. Over the previous decade, for EACs there were only two targeted therapies used in the advanced setting with limited benefits. ESCC progress was rather non-existent. We present current ongoing advancements that have occurred in the realm of immunotherapy and emerging new agents. Expert opinion It is becoming clearer that segregating these two histological subtypes in trials should be the goal of future trial designs. ESCC appears to be more amenable to immune modulation than EAC; however, we are navigating in exciting times as molecular interrogations of EC has expanded with the hope of making more rapid progress. There is still hard work ahead of us to painfully define subsets representing heterogeneity and then finding appropriate agents.
TL;DR: On reviewing 75 patients from the literature, non-haematological malignancy was found to be the commonest cause of death, and long-term follow-up did reveal a very slow progression in the group as a whole.
Abstract: Eighteen patients are described, all of whom had chronic demyelinating peripheral neuropathy and benign IgM para-proteinaemia. All patients had serum antibodies against peripheral nerve myelin or myelin-associated glycoprotein. Seventeen were followed up clinically and electrophysiologically for between 1 and 14 years (mean 7.4 years). The presenting symptoms and signs were almost always those of a distal sensory disturbance in the limbs followed by distal weakness. All patients developed tremor or ataxia in the arms, and gait ataxia. The severity of the neuropathy varied greatly between patients at similar stages. Some had a predominantly sensory deficit and others a predominantly motor deficit. All patients eventually developed both motor and sensory signs. The neuropathy became slowly worse over the first 2–5 years and then appeared to stabilize, although long-term follow-up did reveal a very slow progression in the group as a whole. No patient developed evidence of haematological malignancy but two patients died of malignancy involving other systems. On reviewing 75 patients from the literature, non-haematological malignancy was found to be the commonest cause of death.
TL;DR: Comparison-enhanced, three-dimensional power Doppler sonography provides better visualization of tumor vascularity in complex adnexal masses and might precisely discriminate benign from malignantAdnexal lesions.
TL;DR: An approach to thyroid nodules is presented, from the clinical or incidental finding of a nodule to the suggested treatment baselines, which are considered to be the "gold standard" in the selection of patients for surgery.
Abstract: Thyroid nodules are common in clinical practice. They may be solitary within a "normal" thyroid gland or dominant within a multinodular goiter. The incidence of thyroid nodules has been on the rise in recent decades, mainly due to the wider use of neck imaging. Therefore, the incidental finding of a thyroid nodule in an asymptomatic patient is not rare. The differential diagnosis of a thyroid nodule is crucial, as malignancy necessitates surgery, while strict patient follow-up is necessary in the case of benignity. Fine-Needle Aspiration biopsy is considered to be the "gold standard" in the selection of patients for surgery. Ultrasonography (US) can be used to determine changes in the size of nodules during follow-up or to detect recurrent lesions in patients suspected for thyroid malignancy, although there are no specific US findings that suggest malignancy. Surgery is mandatory in cytologically malignant nodules or in cases suspicious for malignancy. The definite diagnosis and consequent therapy is based on the histological findings after surgery. In this review we present an approach to thyroid nodules in five distinct steps, from the clinical or incidental finding of a nodule to the suggested treatment baselines.