Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 61 year old woman presented with profound hyponatremia and markedly low serum osmolality. Urine osmolality was greater than the serum osmolality, an abnormality that was corrected by water restriction, suggesting inappropriate ADH secretion. Although there were no physical signs of Cushing's syndrome, her serum potassium level was low and markedly elevated levels of plasma and urine corticosteroids were not altered by the administration of large amounts of dexamethasone, suggesting the ectopic ACTH-MSH syndrome. Plasma levels of immunoreactive ACTH and beta-MSH were elevated. At autopsy, a metastastic oat cell carcinoma of the lung, not detected antemortem by chest roentgenograms and bronchoscopy, was found. Immunoreactive ADH, ACTH and beta-MSH were detected in the primary tumor and in metastases to the liver. beta-MSH was also detected in the spleen, in which metastases were observed. This is the first documented case of the simultaneous production of ADH, ACTH and beta-MSH by neoplastic tissue associated with clinical manifestations of the syndrome of inappropriate ADH secretion and the ectopic ACTH-MSH syndrome.
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PMID:Ectopic production of antidiuretic hormone (adh), adrenocorticotrophic hormone (ACTH) and beta-melanocyte stimulating hormone (beta-MSH) by an oat cell carcinoma of the lung. 18 5

In some instances, tumors can produce signs and symptoms at a distance from the tumor or its metastases. These are defined as paraneoplastic syndrome or humoral syndrome associated with neoplasms. Paraneoplastic syndromes can arise from circulating substances secreted by tumors. The most well-recognized and frequent concomitant of neoplasms is the production of hormones by nonendocrine tumors. These are usually called ectopic hormone-producing tumors and bring about clinically endocrinologic manifestations secondary to hormone excess in patients with nonendocrine tumors. Paraneoplastic endocrine syndromes frequently observed are Cushing's syndrome due to ectopic production of ACTH, SIADH due to ectopic production of ADH, hyper-calcemia, hypoglycemia and so on. In order to establish a paraneoplastic etiology for alteration in hormone production, evidence that the hormone is produced by the tumor must be proved. Paraneoplastic endocrine syndromes should be distinguished from hormone production by benign cells, hormone production by a malignancy of an endocrine organ or alterations in hormone production being due to infiltration into the endocrine organ by a primary tumor. The treatment of ectopic endocrine syndromes should be directed primarily at the tumor. Because the course of this type of syndrome usually runs parallel to the course of the underlying tumor, the ectopically produced hormone can be a useful monitoring marker of the disease.
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PMID:[Paraneoplastic endocrine syndromes]. 301 95

Mouse fibrosarcoma (3T3 cells transfected with different oncogenes), human neuroblastoma, or human prostate carcinoma cells have been genetically-tagged with different histochemical marker genes (E. coli lacZ, placental alkaline phosphatase, or Drosophila alcohol dehydrogenase). Injection into athymic nude mice permits their tracking at all stages of primary tumor formation and micrometastasis to various organs at the single-cell level. Two different tumor classes, tagged with different marker genes, can be tracked together. Primary tumors display regional dominance of one tumor class with exclusion of other classes. During micrometastasis, tumor cells are detected binding to the endothelium of lung blood vessels, followed by establishment of multiple-cell micrometastases. Micrometastases in some organs are transient while in other organs there is differential expansion into overt metastases. Tagged tumors also reveal the timing of angiogenesis of developing primary tumors and overt metastases. In all three tumor systems, there are three classes of genetic stability of marker gene expression in clonal populations-high stability, intermediate stability, and high instability. Instability in marker gene expression in one tagged prostate carcinoma system does not depend on a hypermethylation mechanism, suggesting a genetic basis for loss of activity. Use of histochemical marker genes, combined with laser-capture microdissection and various PCR methods, can now be used to evaluate gene activities in single or multiple tumor cells in virtually any organ and primary tumor of the animal model system.
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PMID:Tumor progression, micrometastasis, and genetic instability tracked with histochemical marker genes. 1031 77

Neoplasms from almost every tissue have been reported to metastasize to the pituitary. Gastric carcinoma is a rare cause of metastases in pituitary gland. Gastric carcinoma will be the primary tumor in less than 2% of patients with pituitary gland metastases. We report the case of a 60-years old white man with liver metastasis from gastric cancer with fair presentation symptoms of pituitary gland metastasis. Basal endocrinological work-up showed corticotroph, gonadotroph, somatotroph and thyrotroph cell insufficiency; serum PRL was elevated and no deficit of the ADH level was observed. Despite the hormonal deficits the patient did not report any specific symptom. After diagnosis the patient began thyroid and adrenal-replacement therapy and was referred to Radiotherapy Unit for treatment on the sellar and pituitary gland region.
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PMID:Gastric cancer metastatic to the pituitary gland: a case report. 1755 75

According to a report by the National Cancer Institute, colorectal cancer (CRC) is one of the most common types of cancer worldwide. CRC is often recognized too late for successful therapy. Tumor markers have been sought for a number of years to detect the transformation of malignant cells at the earliest possible stage. They are usually proteins associated with a malignancy and might be clinically useful in patients with cancer. Several classical markers have been used to recognize colorectal cancer, including carcinoembryonic antigen (CEA), carbohydrate antigen (CA 19.9), tissue polypeptide specific antigen (TPS) and tumor-associated glycoprotein-72 (TAG-72). None of these tests, however, have excellent diagnostic accuracy. Recent studies have been conducted on the use of hematopoietic growth factors (HGFs) and various enzymes in the diagnosis and prognosis of colorectal cancer. These include macrophage-colony stimulating factor (M-CSF) and granulocyte-macrophage-colony stimulating factor (GM-CSF), interleukin-3, interleukin-6 and enzymes (alcohol dehydrogenase and lysosomal exoglycosidases). Significantly, most cancer deaths are not caused by the primary tumor itself but by its spread. Analysis of circulating cancer cells (CTCs), ie, factors responsible for metastasis, may be a source of information useful in the treatment of patients with colorectal cancer. Currently available markers have significant limitations.
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PMID:Biochemical Markers of Colorectal Cancer - Present and Future. 3260 68