Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-phosphorylative transglucosylation, GGT and LAP activity, the level of some "acute phase" proteins i.e. sialic acids, ceruloplasmin, papain and trypsin inhibitors were examined in the serum, normal myometrium around tumours and in the uterine myoma of women. It was observed that the contents of proteins in the "acute phase" as well as GGT and LAP activity increased in the serum, whereas a decreased activity of these enzymes accompanied by increased transferase activity was observed in uterine myoma.
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PMID:Non-phosphorylative transglucosylation and other biochemical indices in serum and uterine myoma in women. 172 93

To evaluate the effects of drugs on uterine leiomyoma and to clarify the histogenesis of uterine leiomyoma, we studied the establishment of primary culture of cells derived from uterine leiomyoma. Myoma tissues were cut into small pieces and suspended in trypsin. The primary cell culture, as a monolayer, was able to be passaged four times. To confirm that the cultured cells were derived from the myoma, the cells were stained with desmin by the enzyme-labelled antibody method. The cultured cells derived from uterine muscle cells were similarly treated with desmin staining. The results confirmed the morphological similarity between the two groups of cells. To confirm that the cultured cells were myoblast, fibroblasts derived from the myoma were cultured selectively. The cells that resembled myoblasts, morphologically appeared spindle-shaped. The cells that resembled fibroblast, appeared polygonal and extended over the bottom of the culture flask. The growth curve of cultured myoma cells (8.0 X 10(4) cells in 0.2 ml) in Petri dishes (60 X 15 mm) revealed logarithmic proliferation after about 5 days. The colony formation of cultured myoma cells (2 X 10(5) cells in 0.2 ml) in culture flasks (25 cm2 in the area of the base) morphologically appeared to have an irregular border and had many independent scattered cells around the colony when the medium was renewed twice a week. The myoma cells (8.8 X 10(4) in 0.2 ml) in the logarithmic phase were cultured, fixed after 12 days when the medium was not renewed, and stained with crystal-violet. Morphologically, the colony had a comparatively regular border, was round, and each cell in the colony was epithelioid. The plating efficiency was 0.07%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Establishment of primary culture of cells derived from uterine leiomyoma]. 243 84

Surgically removed solid human benign and malignant neoplasms and nonneoplastic tissues were examined for the presence of transforming growth factors (TGFs). TGFs are polypeptide growth factor-like substances which cause the appearance of a reversible neoplastic phenotype in nontransformed, anchorage-dependent cells in culture, including the induction of the ability to grow while suspended in semisolid medium. Acid-ethanol extracts from adenocarcinomas of the breast, colon, kidney, and ovary; fibrosarcoma and leiomyosarcoma; Hodgkin's lymphoma; fibroadenoma of the breast; uterine leiomyoma; and nonneoplastic kidney and lung were found to cause growth in soft agar of both nontransformed mouse AKR-2B and rat NRK cells. This colony-stimulating activity, where tested, was heat and acid stable but was destroyed by trypsin and dithiothreitol treatment, indicating that the activity is due to a polypeptide with disulfide bonds. Extracts from several of the tumors provided sufficient material for purification by molecular sieve chromatography. Peaks of colony-stimulating activity from a Bio-Gel P-60 column eluted with 1 M acetic acid were detected in the M, 3,000 to 25,000 range with the apparent molecular weight varying depending on the type of tumor being studied and the indicator cells used. The data suggest that at least three TGFs are present in human tumors. Evidence is presented differentiating these TGFs into TGFa, which has selective activity for stimulating AKR-2B cells, and TGFn, which has selective activity for stimulating NRK cells. The NGFn activity was further subdivided into a TGFns fraction and TGFnl fraction, denoting small (less than 6,000) and large (12,000 to 20,00) apparent molecular weights, respectively. The TGFa and TGFnl activities were present in malignant and nonneoplastic (kidney and lung) tissue, whereas the TGFns activity predominated in benign neoplasms. These TGFs exhibited no competition with epidermal growth factor for binding to the epidermal growth factor receptor, and the TGFnl activity was potentiated by epidermal growth factor.
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PMID:Transforming growth factors in solid human malignant neoplasms. 629 35

Benign mesenchymal neoplasms associated with rearrangements of the DNA architectural factor gene HMGIC on chromosome 12 include lipomas, uterine leiomyomata, pulmonary chondroid hamartomas, endometrial polyps, salivary gland pleomorphic adenomas, and breast fibroadenomas. Although HMGIC also has been implicated in the pathobiology of aggressive angiomyxoma of the vulva, the molecular mechanisms pertaining to this neoplasm are unclear. Tissue from a recurrent aggressive angiomyxoma was investigated by cytogenetic and expression analysis for HMGIC and HMGIY. The trypsin-Giemsa-banded karyotype showed a clonal translocation between chromosomes 8 and 12 [46,XX,t(8;12)(p12;q15)]. Fluorescence in situ hybridization (FISH) analysis with whole chromosome paint probes for chromosomes 8 and 12 excluded cryptic involvement of other chromosomes. The chromosome 12 breakpoint was mapped with two-color FISH analysis using cosmid probes at the 5' and 3' termini of HMGIC. Both cosmid probes showed hybridization to the normal chromosome 12 and the der(12) chromosome, indicating that the breakpoint was 3' (telomeric) to the gene. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed HMGIC expression in the tumor, and immunohistochemistry localized HMGIC expression to the tumor's spindle cells. Like numerous benign mesenchymal tumors, this locally aggressive tumor is associated with rearrangements near or within HMGIC, but chimeric gene formation was not required for tumorigenesis. Inappropriate expression of this DNA binding protein, however, may be important in the pathobiology of this tumor. Understanding the pathogenetic mechanism may also be helpful in developing new diagnostic tools for identifying residual disease.
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PMID:Chromosomal translocation t(8;12) induces aberrant HMGIC expression in aggressive angiomyxoma of the vulva. 1155 Feb 85