Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Piroxantrone, a synthetic intercalating agent, was studied in patients with advanced, measurable gastric adenocarcinoma who had not received prior chemotherapy. The starting piroxantrone dose was 150 mg/m2 given intravenously over 1 hour on day 1 and repeated every 21 days. Response and toxicity could be evaluated in 15 patients. No complete, partial, or minor responses were observed. Toxic effects included granulocytopenia, anemia, vomiting, nausea, anorexia, fatigue, stomatitis, alopecia, hyperbilirubinemia, and increased alkaline phosphatase levels. At the stated dose and schedule, piroxantrone does not possess significant activity against advanced gastric cancer.
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PMID:Phase II trial of piroxantrone in metastatic gastric adenocarcinoma. 789 47

Seventy-seven cases of prostate cancer were treated for 5 years at our department and all cases were followed by bone scintigraphy and tumor markers. Of these cases on case of flare response on bone scintigraphy was recognized. A 51-year-old man was hospitalized with chief complaint of lumbago. Serum PAP and gamma-Sm levels were 320 ng/ml and 15 ng/ml, respectively. Prostate biopsy revealed moderately differentiated adenocarcinoma. Bone scintigraphy and CT scan demonstrated multiple bone metastases and lymph nodes involvements. Treatment was started with diethylstilbestrol diphosphate (DES). At one month after the initiation of treatment tumor markers fell down to the normal level and lumbago was diminished, but only serum alkaline phosphatase was elevated and bone scintigraphy showed apparent progression of individual lesions (flare response). The treatment was not altered. At the times after 2, 8, 12 and 36 months successful treatment the bone imaging improved with reduced tracer uptake and no new lesions. The flare response is a healing reaction and is followed apparent improvement. In general, serial bone scintigrams accurately depict the activity of bone metastases in the patients of prostate cancer, but between 1 and 3 months after starting treatment the paradoxical "flare phenomenon" should be taken care.
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PMID:[Flare response on bone scintigraphy in metastatic prostate cancer]. 802 46

Very late activation (VLA) receptors mediate cell adhesion to extracellular matrix, mainly by acting as adhesion receptors to fibronectin, collagen, and laminin as well as to other cells. These interactions not only regulate normal cell-extracellular matrix contact, but also are thought to be involved in metastasis and invasive tumor growth. Using immunohistochemistry [the alkaline phosphatase-anti-alkaline phosphatase (APAAP) technique] we compared the expression and distribution of VLA receptors in normal pancreatic tissue, chronic pancreatitis, and ductal pancreatic adenocarcinoma. Immunohistochemically, VLA alpha 2 and VLA alpha 6 were moderately to strongly expressed on the basal surface of ductal and acinar cells in normal pancreatic tissue, whereas centroacinar cells predominantly expressed VLA alpha 3 and VLA alpha 5. Similarly, pancreatic carcinoma showed an intensive staining for VLA alpha 2 and VLA alpha 6 with a diffuse distribution on the cell surface. Expression of VLA alpha 3 and VLA alpha 5 in pancreatic carcinoma was heterogeneous, ranging from moderate to weak and lost in about 50% of the cells. As our results suggest, cell-basement membrane interaction in ductal and acinar pancreatic cells is primarily mediated through VLA alpha 2 and VLA alpha 6, whereas VLA alpha 3 and VLA alpha 5 are the major VLA receptors on centroacinar cells. In pancreatic carcinoma a loss (VLA alpha 5) or redistribution (VLA alpha 2, VLA alpha 6) of VLAs was observed. This redistribution of VLA alpha 2 and VLA alpha 6 may reflect a loss of spatial arrangement of tumor cells and their ability to randomly interact with extracellular matrix structures during invasion and metastasis.
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PMID:Expression and distribution of VLA receptors in the pancreas: an immunohistochemical study. 825 85

We report two young men with clinical and laboratory evidence of macroscopic ulcerative colitis, sclerosing cholangitis, and insulin-dependent diabetes mellitus. The first patient presented at age 15 with vomiting, abdominal pain, weight loss, and abnormal liver function test results. Liver biopsy and endoscopic retrograde cholangiopancreatography (ERCP) demonstrated sclerosing cholangitis. Colonoscopy with biopsy revealed ulcerative colitis which responded to sulfasalazine. Diabetes occurred at age 18 and insulin therapy was begun. The second patient was 19 at presentation with diarrhea, hematochezia, and weight loss. Proctosigmoidoscopy revealed ulcerative colitis, and sulfasalazine led to clinical remission. Three months later he developed diabetes requiring insulin therapy. At age 28, he developed elevated alkaline phosphatase, and ERCP revealed sclerosing cholangitis. At age 37 he expired from adenocarcinoma that metastasized to the liver. Literature review revealed only one possible case report of this association with microscopic asymptomatic ulcerative colitis in that patient. Statistical analysis suggests that this association is real rather than a chance occurrence. An autoimmune process may be involved and a specific histocompatibility locus antigen (HLA) type may exert a regulatory influence.
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PMID:Associated ulcerative colitis, sclerosing cholangitis, and insulin-dependent diabetes mellitus. 828 9

To determine whether the poorly differentiated AMOC-2 human ovarian adenocarcinoma cell line was capable of undergoing differentiation, AMOC-2 cells were exposed to 2 mM sodium butyrate, 2.5% dimethylsulfoxide, or 4 mM dibutyryl cyclic adenosine monophosphate (dibutyryl cAMP) for 6 days. These treatments resulted in growth inhibition, a reduction in clonogenicity and an increase in cellular glycogen content. Significant increases in heat stable alkaline phosphatase activity also occurred after exposure to sodium butyrate. In addition, a thorn-like microfilament structure observed in untreated cells was diminished concomitantly with morphological changes that included flattening, enlargement and extended cytoplasmic processes after exposure to sodium butyrate or dibutyryl cAMP. Furthermore, treatment with sodium butyrate increased the intracellular concentrations of beta-tubulin, vimentin, neurofilaments (M(r) 210,000) and cytokeratin (M(r) 56,000-58,000). These changes were completely reversed after removal of the inducing agent. The findings suggest that treatment of AMOC-2 cells with sodium butyrate induced a more differentiated phenotype, although terminal differentiation was not achieved.
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PMID:Effects of sodium butyrate, dimethylsulfoxide and dibutyryl cAMP on the poorly differentiated ovarian adenocarcinoma cell line AMOC-2. 830 43

This study reviews the clinicopathologic features of 25 adult patients without a known history of malignancy presenting with metastatic carcinoma in the bone marrow. The disease mainly affected middle-aged to elderly males (mean age, 61.6 years). Bone pain, generalized or confined to the back, was a common presenting complaint. Organomegaly was often absent. Laboratory abnormalities included anaemia, leukocytosis, thrombocytopenia and a leukoerythroblastic blood picture. Serum alkaline phosphatase level was raised in the majority of cases. In about one-third of the cases, malignancy was not suspected clinically, and bone marrow aspiration was carried out because of incidental finding of abnormal blood counts. The marrow aspirate findings were characterized by numerous to sparse cohesive tumour clusters with nuclear moulding. Over two-thirds of the patients had metastatic adenocarcinoma, and the lung was found to be the commonest site of primary disease. We conclude that since the marrow infiltration can be subtle, marrow smears should be carefully scrutinized for tumour cells in patients with leukoerythroblastic blood picture, in particular those with an elevated serum alkaline phosphatase level.
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PMID:Solid tumour with initial presentation in the bone marrow--a clinicopathologic study of 25 adult cases. 832 25

The distribution of type-VII collagen, the main molecular component of the anchoring fibrils (AF) attaching the basal lamina (BL, lamina densa of the basement membrane) to the surrounding connective tissue, was investigated in four xenografted human carcinomas of the hypopharynx (H-Stg 1), the lung (L 261), the sigmoid colon (CA 1), and the rectum (R 85). The studies were performed with a recently prepared, affinity-purified and highly specific antibody to type-VII collagen by using the indirect immunofluorescence and the APAAP (alkaline phosphatase anti-alkaline phosphatase) techniques. For comparison, the localization of the intrinsic BL components laminin and type-IV collagen were additionally analyzed in all four carcinomas. It was shown that type-VII collagen usually colocalized to laminin and type-IV collagen and was deposited at the borderline between carcinoma cell clusters and the surrounding strands of connective tissue in a similar, but more diffuse and less continuous distribution than both intrinsic BL components. In the squamous cell carcinoma H-Stg 1 and the adenocarcinoma L261, type-VII collagen was additionally accumulated in enlarged extracellular spaces between carcinoma cells, away from the contact zone to the connective tissue and again colocalized to laminin and type-IV collagen. Numerous carcinoma cells of both xenografts showed remarkable intracytoplasmic immunoreactivity for the antibody to type-VII collagen. Even in the case of the gastrointestinal carcinomas CA 1 and R 85, faint immunoreactivity for type-VII collagen was found at the contact zone between the mucosal epithelium and the surrounding connective tissue. These results confirm that epithelial carcinoma cells are obviously involved with the synthesis of the main molecular component of AF usually attaching the BL to the adjacent connective tissue and hint at a possible correlation between the localization of type-VII collagen and the observed pattern of the BL. However, it cannot be decided whether there is a direct causal relation between both phenomena or whether they are both the consequence of an independent but common cause, such as abnormal cellular differentiation of carcinoma cells. In no case, can the discontinuities in the distribution of type-VII collagen be explained by active tumor cell invasion since xenografted human carcinomas neither invade nor metastasize.
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PMID:Distribution of type-VII collagen in xenografted human carcinomas. 833 16

Selected G1 events associated with butyrate-induced differentiation were examined in HT-29 colon adenocarcinoma cells. [3H]Thymidine incorporation by HT-29 cells was decreased to 40% of control levels by treatment with 5 mM butyrate for 24 h, and cell numbers decreased to 21% of control levels after 48 h of treatment. Cells released from butyrate arrest entered S phase approximately 24 h after release, and serum-deprived HT-29 cells escaped growth inhibition if butyrate was added 8 h or more after serum restimulation. Northern analysis of RNA isolated from rapidly growing HT-29 cells showed a marked induction of alkaline phosphatase mRNA expression within 12 h of treatment with 5 mM butyrate. The appearance of alkaline phosphatase mRNA was temporally associated with a 5-fold increase in expression of transforming growth factor beta 1 (TGF-beta 1) mRNA. Expression of the nuclear protooncogene c-myc began to decrease 30 min after treatment with butyrate and was decreased 4.5-fold 4 h after treatment; however, expression of other immediate-early genes (nup/475 and zif/268) was not significantly affected. Histochemical staining of HT-29 monolayers showed that no cells were positive for alkaline phosphatase protein prior to treatment, and 90% were positive 48 h after treatment. TGF-beta 1 and TGF-beta 2 had no effect on HT-29 cell growth. TGF-beta 1 did not induce alkaline phosphatase mRNA or histochemical positivity. These data indicate that butyrate arrests HT-29 cell growth early in G1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Butyrate rapidly induces growth inhibition and differentiation in HT-29 cells. 837 33

Sulofenur is a member of a new class of antineoplastic agents with a novel chemical structure and unique pharmacological and biological properties. Preclinical studies have demonstrated a wide spectrum of anti-tumor activity against murine solid tumors and human tumor xenografts. In phase I trials, only mild toxicities were observed. Twenty-six patients (pts), two of whom were inevaluable, with advanced non small cell lung cancer without prior chemotherapy were entered on this phase II trial. Pts received 800 mg/m2 sulofenur po Monday-Friday x 21 days, q 28 days. Seventeen male and 9 female pts with median performance status 1 received a median of 2 courses. Twenty pts had stage IV disease and 19 pts had adenocarcinoma, 6 squamous cell and 1 undifferentiated carcinoma. The main toxicity was grade 1 to 3 anemia in 16 (62%) pts, with hemolysis noted in 9 pts. Although methemoglobinemia was observed in 19 pts, it was severe in only 3 pts. Transient elevation of alkaline phosphatase was seen in 11 pts and one pt had a minor abnormality in glucose metabolism. Other common chemotherapy related side effects such as granulocytopenia or alopecia were not encountered with this agent. Of 24 evaluable pts, two pts had stable disease or minor response and 22 pts had progressive disease. In conclusion although sulofenur had only minor side effects, in the dosage and schedule used, it did not produce any significant response in advanced non-small cell lung cancer.
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PMID:Phase II study of sulofenur (LY 186641). A novel antineoplastic agent in advanced non-small cell lung cancer. 839 98

The effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and of two synthetic analogs, 1,25S,26-tri-hydroxy-delta 22-vitamin D3 (1,25,26(OH)3-22ene-D3, Ro 23-4319) and 1,25-dihydroxy-delta 16-23yne-vitamin D3 (1,25(OH)2-16ene-23yne-D3, Ro 23-7553) on cell growth was evaluated by determination of [3H]thymidine incorporation into DNA of human colon adenocarcinoma-derived Caco-2 cells. The extent of growth inhibition by the vitamin D compounds varied between 20-40% (at 10(-8) M), depending on particular growth conditions of Caco-2 cells as well as on the molecular structure of the vitamin D sterols. In confluent, i.e., rather quiescent cells, all three vitamin D compounds were equipotent in suppressing growth. In rapidly dividing log phase cells, 1,25(OH)2-16ene-23yne-D3 or 1,25,26(OH)3-22ene-D3 were ten or five times, respectively, more efficient than 1,25(OH)2D3. A substantial effect on induction of the colonocyte differentiation marker alkaline phosphatase was only elicited by 1,25(OH)2-16ene-23yne-D3. The ability of the vitamin D compounds to raise intestinal calcium absorption was evaluated by determination of 45Ca2+ accumulation in embryonic chick duodenal explants. In this assay, both synthetic analogs were less effective than 1,25(OH)2D3 by a factor of 20. The intrinsic bone resorbing activities of the vitamin D analogs were compared in organ-cultured neonatal mouse calvariae. The most effective antiproliferative compound, 1,25(OH)2-16ene-23yene-D3, stimulated calcium release from cultured bones at concentrations less than 10(-11) M, and was thus ten times more potent than 1,25(OH)2D3 and hundred times more than 1,25,26(OH)3-22ene-D3.
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PMID:Growth inhibition of human colon adenocarcinoma-derived Caco-2 cells by 1,25-dihydroxyvitamin D3 and two synthetic analogs: relation to in vitro hypercalcemic potential. 844 78


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