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Tumor cell plasticity poses a significant clinical challenge in that the fate and function of tumor cells can be elusive until a tumor mass is evident. An overview of key molecular events in prostate cancer, initiated by an epithelial-to-mesenchymal transition, highlights the cooperative interactions of diverse prostatic subpopulations within heterogeneous tumors. A remarkable example of plasticity is demonstrated by subpopulations of E-cadherin-positive and E-cadherin-negative tumor cells working in concert to form de novo vasculogenic-like networks while expressing vascular-associated genes, called vasculogenic mimicry, resulting in acquisition of the metastatic phenotype. A better understanding of the molecular mechanisms underlying prostate tumor cell plasticity may provide new prognostic markers for clinical diagnosis and novel therapeutic intervention strategies for disease management. [ABSTRACT FROM AUTHOR]

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Prostate cancer is one of the most prevalent cancers in the United States. The current standard treatments for early stage confined disease include surgery and radiation therapy. However, advanced diseases or tumors that relapse are treated with hormone deprivation therapy. Unfortunately, most men relapse with advanced metastatic and aggressive hormone refractory disease for which there is no cure. Although prostate-specific antigen (PSA) screening and digital rectal examinations have improved detection of early stage disease, prognosis for advanced metastatic disease is still poor. Therefore, there is a need to understand the biology and genetics of the normal prostate gland and the molecular and biochemical pathways that are deregulated in prostate malignancy. Animal models of prostate cancer have been developed to delineate the key factors that contribute to the initiation, progression, and metastasis of prostate cancer. Such models are also used for preclinical screening of therapeutic regimens for the prevention and treatment of prostate cancer. Animal models of prostate cancer such as rat, canine and mouse models will be discussed. Emphasis will be placed on autochthonous genetically engineered mouse (GEM) models of prostate cancer. [ABSTRACT FROM AUTHOR]

Genitourinary (GU) disorders are pervasive in the adult population and broadly include the diagnoses of 15-20% of patients who are discharged from hospitals in the United States. The percentage is higher for ambulatory visits. Along with susceptibility to the common disorders of the general population, the GU system of astronauts is additionally vulnerable to spaceflight- related stresses, both in flight as well as immediately preflight and postflight. These stresses may include rigorous exercise, microgravity, dietary changes, limited availability of drinking water, thermal stress, effects of other spaceflightrelated disorders such as space motion sickness, and influence of medications used to treat other spaceflight-related disorders. Some of these conditions may increase the risk of occurrence of genitourinary disorders or complicate their presentation. Exposure to microgravity causes a number of metabolic and physiological changes. Fluid volume, electrolyte levels, and bone and muscle undergo changes as the human body adapts to weightlessness. Changes in urinary chemical composition occurring as a part of this adaptation process may lead to the potentially serious consequences of renal stone formation. With the length of human exposure to microgravity extending as we maintain a permanent presence on the International Space Station (ISS), the probability of GU-related illnesses such as renal stones or infections will undoubtedly increase. Exploration-class lunar missions for long-duration settlement and missions to Mars will pose even greater challenges for GU diagnosis and management as immediate return to Earth will not be possible. This chapter reviews spaceflight influences on GU function and disorders that might arise involving this system and describes treatment methods and countermeasures. [ABSTRACT FROM AUTHOR]

Copyright of Kompendium Internistische Onkologie is the property of Springer Nature / Books and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

An encyclopedia entry of the term "metastasis" is presented. It refers to the process by which tumor cells disseminate to distant sites to establish discontinuous secondary colonies. The series of sequential steps by which tumor cells migrate from a tumor mass to proliferate at the secondary site is called metastatic cascade.