Immunosuppression-associated soft-tissue tumours

Immunodeficiency and therapeutic immunosuppression inform the pathogenesis of certain soft tissue tumours, namely Kaposi sarcoma (KS) and Epstein–Barr virus (EBV)-associated smooth muscle tumours. KS comprises a group of clinical categories associated with local or systemic immunodysregulation: sporadic/classic KS, endemic (African) KS, epidemic (AIDS-related) KS, and iatrogenic (transplantation-associated) KS. Histologically, KS lesions progress from early (patch) stages, comprising networks of bland vascular proliferations, to later (plaque) stages, wherein spindle cells proliferate between vascular structures, and finally to the nodular (tumour) stage, which may show fascicles of intersecting spindle cells and PASD-positive hyaline globules. By immunohistochemistry, KS shows lymphovascular differentiation. EBV-associated smooth muscle tumours comprise a rare subset of smooth muscle tumours that typically occur in children with HIV/AIDS and adults following solid organ transplantation. They can occur in peripheral soft tissues, intracranially, or in visceral sites. Multiplicity is common and presumably a result of multiple infection events rather than metastasis from a primary site. Histologically, the differential diagnosis is limited to other smooth muscle tumours. These indolent tumours often persist despite therapy but rarely metastasize. Mortality usually results from the underlying disease process

Essential laboratory tests for medical education.

Medical practice requires physicians to have a broad understanding of the basic sciences, have competent clinical skills, and have an ability to practice in evolving health systems in a cost-effective and evidence-based manner. Essential to the practice of medicine is an understanding of the common laboratory tests and the ability to use them effectively. The Essential Laboratory Tests for Medical Education (ELTME) is a concise document explaining the pathophysiology of common laboratory tests and clinical context for each test and was developed in response to an expressed need from medical students, residents and fellows, and medical educators. The ELTME is linked to the Pathology Competencies in Medical Education and its third competency of diagnostic medicine and therapeutic pathology. The ELTME table is a document of common laboratory tests in alphabetical listing. Laboratory tests may be easily queried by name or organ system, and with simple editing tools, new tables may be constructed to fit the needs of individual curricula or learners. Furthermore, the table may be easily expanded by educators who wish to add specific tests to complement their curricula

Cytoplasmic and/or nuclear accumulation of the beta-catenin protein is a frequent event in human osteosarcoma.

The molecular events that precede the development of osteosarcoma, the most common primary malignancy of bone, are unclear, and concurrent molecular and genetic alterations associated with its pathogenesis have yet to be identified. Recent studies suggest that activation of beta-catenin signaling may play an important role in human tumorigenesis. To investigate the potential role of beta-catenin deregulation in human osteosarcoma, we analyzed a panel of 47 osteosarcoma samples for beta-catenin accumulation using immunohistochemistry. Potential activating mutations were investigated by sequencing exon 3 of the beta-catenin gene in genomic DNA isolated from tumor samples. Our findings revealed cytoplasmic and/or nuclear accumulation of beta-catenin in 33 of 47 samples (70.2%); however, mutation analysis failed to detect any genetic alterations within exon 3, suggesting that other regulatory mechanisms may play an important role in activating beta-catenin signaling in osteosarcoma. In our survival analysis, beta-catenin deregulation conferred a hazard ratio of 1.05, indicating that beta-catenin accumulation does not appear to be of prognostic value for osteosarcoma patients. When analyzed against other clinicopathologic parameters, beta-catenin accumulation correlated only with younger age at presentation (26.4 vs. 39.8 years). Nevertheless, our results demonstrate that the deregulation of beta-catenin signaling is a common occurrence in osteosarcoma that is implicated in the pathogenesis of osteosarcoma

Cytoplasmic and/or nuclear accumulation of the beta-catenin protein is a frequent event in human osteosarcoma.

The molecular events that precede the development of osteosarcoma, the most common primary malignancy of bone, are unclear, and concurrent molecular and genetic alterations associated with its pathogenesis have yet to be identified. Recent studies suggest that activation of beta-catenin signaling may play an important role in human tumorigenesis. To investigate the potential role of beta-catenin deregulation in human osteosarcoma, we analyzed a panel of 47 osteosarcoma samples for beta-catenin accumulation using immunohistochemistry. Potential activating mutations were investigated by sequencing exon 3 of the beta-catenin gene in genomic DNA isolated from tumor samples. Our findings revealed cytoplasmic and/or nuclear accumulation of beta-catenin in 33 of 47 samples (70.2%); however, mutation analysis failed to detect any genetic alterations within exon 3, suggesting that other regulatory mechanisms may play an important role in activating beta-catenin signaling in osteosarcoma. In our survival analysis, beta-catenin deregulation conferred a hazard ratio of 1.05, indicating that beta-catenin accumulation does not appear to be of prognostic value for osteosarcoma patients. When analyzed against other clinicopathologic parameters, beta-catenin accumulation correlated only with younger age at presentation (26.4 vs. 39.8 years). Nevertheless, our results demonstrate that the deregulation of beta-catenin signaling is a common occurrence in osteosarcoma that is implicated in the pathogenesis of osteosarcoma