Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By counterimmunoelectrophoresis in agarose gel the presence of alpha 2-PGA in the sera of 28 untreated patients with different localization of cancer was demonstrated. In 17 (60.7%) a precipitation line between the well with patient serum and that with monospecific anti-alpha 2-PGA serum, diluted 1 : 7 was obtained. At 1 : 7 dilution, with the sera from 28 healthy persons precipitation lines were not obtained. The determination of alpha 2-PAG can be made quickly and contributes to cancer diagnosis in men.
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PMID:Demonstration of alpha 2-pregnancy associated-glycoprotein (alpha 2-PGA) in serum of men with different localization of cancer. 9 8

The concentration of different prostaglandins (PG's) was determined in both cells and culture medium of growing BALB/3T3 and BALB/3T3 (3T3) cultures transformed by simian virus 40 (SV3T3). Most PG's were found in the culture medium rather than in the cells. Further, the larger PG measurements were PGE and a composite measurement of PGA and PGB. PGF was detected at lower levels. The sum of PGE and the composite measurement (PGA+PGB) was the best indication of PG production in culture. When 2-day medium collections from 3T3 and SV3T3 cells were measured by radioimmunoassay for PGs, higher concentrations of PG were detected in the media of SV3T3 cultures. This difference in PG production was not due merely to differences in cell density, since SV3T3 cells produced higher PG concentrations, even at equal cell densities. PG production for a 2-day interval was more a function of cell type than cell density.
J Natl Cancer Inst 1976 Mar
PMID:Prostaglandin production in cultures of BALB/3T3 and SV3T3 mouse fibroblasts. 17 97

Antiserum raised in rabbits against the FBP obtained from CML cells, and the purified binder labeled with 125I, have been used for an RIA which can measure an immunologically similar protein in human serum. The concentration of the binding protein in normal serums ranged from 1.2 to 9.3 ng/ml, with a mean +/- S.E.M. of 3.8 +/- 0.4 ng/ml. Elevated values of the binder protein were measured in the serums from patients with folate deficiency, vitamin B12 deficiency, liver disease, uremia, myeloproliferative disease, chronic lymphocytic leukemia, and various types of cancer and in the serum from pregnant women. The concentration of the binder protein and the capacity of the serum to specifically bind isotopically labeled PGA correlated poorly, indicating that the binding protein concentration and degree of saturation by endogenous serum folate vary independently in many instances.
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PMID:The identification and measurement of a folate-binding protein in human serum by radioimmunoassay. 27 99

Parathyroid tumors may occur in a sporadic fashion or, more rarely, as part of a familial syndrome (such as familial multiple endocrine neoplasia type I). The MENI gene has been mapped by linkage analysis to chromosome 11 at band q11-q13, and presumably acts as a tumor suppressor gene. In the present study, which is an extension of our previous studies, we examined 41 parathyroid tumors from patients with familial multiple endocrine neoplasia type I and 61 sporadic parathyroid tumors with markers on chromosome 11, to assess the extent of allelic loss in those tumors. Twenty-four of the MENI-associated tumors (58%) and 16 of the sporadic parathyroid tumors (26%) displayed allelic loss from chromosome 11. The region of overlap of the allelic losses in the MENI-associated tumors enables us to place the MENI gene between PGA centromerically and INT2 telomerically, a region spanning about 7.5 cM. Taken together with locus ordering by linkage analysis, this clearly localizes the MENI gene telomeric to the PGA locus. Our inability to detect allelic loss on chromosome 11 in some parathyroid tumors suggests the existence of other genes involved in the development and/or progression of this subgroup of presumably monoclonal tumors; or that localized events involving the 11q tumor suppressor gene have occurred in some parathyroid tumors whose detection is beyond the sensitivity of our analysis; or that at least some of the specimens analyzed were in fact primarily hyperplastic parathyroid tissue.
Cancer Res 1992 Dec 15
PMID:Allelic loss from chromosome 11 in parathyroid tumors. 136 Aug 70

Expression of the cysteine proteinase cathepsin B and its physiological inhibitor cystatin C was analyzed in vitro in 1 human fibrosarcoma and 4 human colon carcinoma cell lines. Cystatin C antigen as well as cathepsin B activity were detected in the conditioned media of the 5 cell lines. The corresponding cell extracts expressed high levels of cathepsin B activity, whereas only trace amounts of cystatin C antigen could be found. Northern-blot analysis revealed the presence in the 5 cell lines of a 0.8-kb cystatin C mRNA transcript and 2 cathepsin B transcripts of 2.3 and 4.3 kb. Pepsin treatment of tumor-cell-released cathepsin B induced an average 7.3-fold increase in activity, indicating that the enzyme was mainly present as a latent form in conditioned medium. The pepsin-activated cathepsin B from one colon carcinoma cell line was further characterized using the cysteine proteinase inhibitors E-64, recombinant cystatin C, a cystatin-C-derived peptidyl inhibitor (Z-LVG-CHN2), and cathepsin-B-specific diazomethyl ketone inhibitors (Z-FT(OBzl)-CHN2, Z-FS(OBzl)-CHN2). This activity was totally neutralized by recombinant cystatin C, suggesting a potential for interaction between released extracellular cathepsin B and cystatin C. In vitro assays of degradation of extracellular matrix showed that cysteine proteinase inhibitors could decrease matrix degradation induced by pepsin-activated conditioned media. With colon cells, this inhibition was not observed, indicating a requirement for an extracellular activation of latent cathepsin B. Our data provide evidence that cystatin C and latent cathepsin B are both released extracellularly by colon carcinoma cells in vitro. They suggest that cystatin C and cathepsin B interactions may participate, in an as yet unelucidated way, in the modulation of the invasive phenotype of human colonic tumors.
Int J Cancer 1992 Oct 21
PMID:Cystatin C and cathepsin B in human colon carcinoma: expression by cell lines and matrix degradation. 139 47

The effect of reduced and oxidized folates on the development of methotrexate (MTX) resistance has been examined in human leukemia cell line K562 (K562/S). K562/S cells were made resistant to MTX by soft-agar cloning either in RPMI-1640 medium (K562/MTX-PGA) or in folic-acid-free RPMI-1640 medium containing 10 nM leucovorin (K562/MTX-LV). The optimal concentrations of leucovorin for the growth of K562/S, K562/MTX-PGA and K562/MTX-LV cells were 1 nM, 5 nM and 10 nM respectively. K562/MTX-PGA cells were 24-fold resistant to MTX as noted by impaired MTX transport. In contrast, K562/MTX-LV cells were 26-fold resistant to MTX as noted by gene amplification of dihydrofolate reductase. Furthermore cross-resistance to cytosine arabinoside was only demonstrated in K562/MTX-PGA, while the K562/MTX-LV cells showed no significant cross-resistance to cytosine arabinoside. These results suggest that the type and level of folates used during the development of MTX resistance may play a role in the mechanism for MTX resistance. Leukemia cells that are grown in leucovorin might serve as a model for acquired MTX resistance in vivo.
J Cancer Res Clin Oncol 1992
PMID:The role of folates in the development of methotrexate resistance in human leukemia cell line K562. 142 25

Multiple endocrine neoplasia type 1 is an autosomal dominant condition characterized by the development of parathyroid hyperplasia, pituitary adenomas, and pancreatic islet cell tumors. Recently the gene for multiple endocrine neoplasia type 1 was mapped to the long arm of chromosome 11 between the loci PGA and INT2. We tested the hypothesis that tumor development is the result of a somatic deletion that unmasks a constitutional mutation. By investigating DNA isolated from tumors and somatic tissues in 12 patients from 4 different families with multiple endocrine neoplasia type 1, we found loss of heterozygous markers mapped to 11q13 in 9 (82%) of 11 informative tumors. In contrast, we were unable to identify allelic loss from other chromosomes using a variety of informative probes. This high incidence of chromosomal deletion of 11q13 suggests that this region is important in the oncogenesis of this disorder.
Cancer Res 1990 Oct 15
PMID:Loss of heterozygosity of markers on chromosome 11 in tumors from patients with multiple endocrine neoplasia syndrome type 1. 197 36

In this paper the role of pepsinogen has been reviewed in its physiological and clinical aspects. Although acid secretion has traditionally received far more attention clinically and has therefore been studied in great detail, the development of cellular systems has recently seen a revival in interest of pepsinogen secretion. These systems have made it possible to study pepsinogen secretion in more detail. Although many questions remain unanswered, a picture of a stimulus-secretion coupling mechanism of the chief cell has emerged that resembles in many aspects the pancreatic acinar cell, but also possesses some unique features of its own. The chief cell monolayer culture has also made it possible to study pepsinogen synthesis, and these studies seem to have solved the old controversy of whether or not modulation of pepsinogen synthesis occurs as a result of increased secretion. It now seems that pepsinogen synthesis does indeed increase in response to stimulated secretion. In addition to physiological studies, this review has discussed clinical aspects of the human pepsinogens in various gastric disorders. The clinical implications of genetic heterogeneity of the human pepsinogens are especially intriguing. Relationships between certain PGA phenotypes and certain gastric disorders have been described and some studies have tried to evaluate the relevance of these findings for diagnostic purposes. So far, it seems that PGA phenotyping alone has only limited diagnostic value, but, in combination with serum PGA determinations, could be of additional help in the diagnosis of gastric malignancy. In addition, various studies suggest that the ratio of serum PGA and PGC levels may be helpful in determining the histological status of the gastric mucosa. A very promising possibility in solving the many problems involved in exact genotype determinations through phenotyping is the recent availability of cDNA probes. With this technique, the question of whether the association between PGA phenotypes and gastric malignancy is primary or secondary may be solved in the near future. In view of the very poor prognosis for gastric cancer, further studies concerning the relationships between gastric cancer, serum pepsinogen levels, and PGA phenotypes or genotypes will hopefully lead to the possibility of an earlier diagnosis for gastric malignancy.
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PMID:Pepsinogens: an update of biochemical, physiological, and clinical aspects. 332 41

Cyclopentenone prostaglandins (PGs) such as prostaglandin A1 (PGA1) and prostaglandin J2 (PGJ2) significantly increased the life span of Ehrlich ascites tumor-bearing mice. In order to obtain PG derivatives which have more potent antitumor activity than PGA1 and PGJ2, we synthesized a number of alkylidenecyclopentenone PGs and studied the antitumor activity of these compounds in vitro and in vivo. delta 7-PGA1, 12-epi-delta 7-PGA1, and delta 12,14-PGJ2 showed 50% inhibitory concentrations of 0.3 microgram/ml against the growth of L1210 culture cells. These compounds are several times more cytotoxic than parent compounds. From a structure-activity relationship analysis, we concluded that, as for PGA derivatives: (a) a double bond in C7-8 potentiates the cytotoxicity; (b) a 15-hydroxy group is not essential for cytotoxicity; (c) the stereochemistry of R2 chain is not essential, while 12-epi derivatives also have full activity; (d) a double bond in C12-13 seems to be essential for full activity, and for PGJ derivatives a double bond in C12-13 and C14-15 potentiates the cytotoxicity. These compounds showed marked antitumor activity against Ehrlich ascites tumor in vivo. At doses of 20-30 mg/kg/day three or five consecutive i.p. treatments with these compounds resulted in a 66 to 111% increase in life span with long-term survivors. A single i.p. injection with 12-epi-delta 7-PGA1 (100 mg/kg) resulted in 73% increase in life span with 33% of long-term survivors, indicating an activity comparable to that of cyclophosphamide (200 mg/kg). However, delta 7-PGA1 and 12-epi-delta 7-PGA1 were marginally effective against P388 leukemia. Treatment with delta 7-PGA1 (10 mg/kg/day i.p.) and 12-epi-delta 7-PGA1 (20 mg/kg/day i.p.) on Days 1-9 resulted in 25.8 and 29.6% increases in life span, respectively. delta 7-PGA1 and delta 12-PGJ2 derivatives may be a potential new class of antitumor agents.
Cancer Res 1986 Jul
PMID:Antitumor activity of delta 7-prostaglandin A1 and delta 12-prostaglandin J2 in vitro and in vivo. 370 85

From July 1985 through January 1986, 43 patients underwent urinary diversion that included creation of a continent reservoir from an ileal segment, according to the method described originally by Kock. An important modification included removal of a narrow strip of mesentery for 8 cm along the afferent and efferent limbs of the pouch to allow adequate ileal intussusception and fixation of the nipple valves to prevent reflux and to ensure continence. A strip of PGA mesh serves as a collar to fix the afferent-efferent limb to the pouch once the intussusception technique has been accomplished. The use of a narrow Marlex strip allows fixation to the abdominal wall both lateral and medial to the stoma site (insert). This strip is important in preventing a parastomal hernia and helps fix the continence valve mechanism to the posterior abdominal wall. Previous urinary diversion was by ureterosigmoidostomy in 2 patients, standard ileal conduit in 8 and chronic dialysis after nephrectomy of solitary kidney and cystectomy in 1. A total of 32 patients underwent simultaneous anterior exenteration or radical cystectomy for pelvic malignancy. There were 4 postoperative deaths and early complications occurred in one patient. Late complications occurred in only 3 patients: they required reoperation and revision of the continence valve mechanism. The end result in 39 of 43 patients has been an overwhelming success. Patients perform self-catheterization every 4 to 6 hours during the day and once at night for volumes ranging up to 1,400 cc. Serum electolytes have remained normal in all patients. X-ray of the Kock pouch have shown no evidence of reflux, and all excretory urograms have demonstrated either normal upper tracts without obstruction or improvement in patients with preoperative hydronephrosis. Although preliminary, this clinical trial suggests that the quality of life for patients considered previously to be candidates for cutaneous diversion can be improved markedly by a modified Kock continent ileal reservoir. During the same time, 21 patients out of 278 patients who underwent creation of a Kock continent ileal urinary reservoir since August 1982, underwent revision of Kock pouch. Two of those required subsequent reoperation and revision of the continence valve mechanism. The end result in all patients has been an overwhelming success.
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PMID:[The Kock continent ileal urinary reservoir: surgical technic and clinical results]. 377 74


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