Gene/Protein Disease Symptom Drug Enzyme Compound
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 21,692 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tenascin is a novel extracellular matrix glycoprotein which appears to have a major role in tissue development. Previous studies have stated that tenascin is absent from the normal human, rat and mouse breast, its distribution being restricted to embryonic and malignant mammary tissues. No previous studies have investigated tenascin distribution as a function of the normal menstrual cycle. Therefore this study addresses the cyclical appearance of tenascin in the normal breast and associated changes in distribution in preinvasive cancer (carcinoma-in-situ) and invasive infiltrating ductal carcinoma. Tenascin is present in the normal human adult mammary gland, principally in the basement membrane, sub-basement-membrane zone and delimiting layer of fibroblasts around the ductules. Both the distribution and quantity of tenascin change during the menstrual cycle. In carcinoma-in-situ (preinvasive cancer) tenascin is present in the attenuated basement membrane/sub-basement-membrane zone around the expanded ductules and in small amounts in the stroma. In infiltrating ductal carcinoma, tenascin is absent from the remnants of the basement membrane and sub-basement-membrane zone but greatly increased in the adjacent intralobular and interlobular stroma. Therefore, if tenascin is used as a basement membrane/sub-basement-membrane marker for distinguishing carcinoma-in-situ from invasive ductal carcinoma, the time of the menstrual cycle is of importance in interpreting the biopsy appearance. This study suggests that the optimal time for biopsy is between weeks 3 and 4 of the cycle, to avoid confusion between the normal low levels of tenascin (due to hormonal status) and those due to microinvasive disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tenascin distribution in the normal human breast is altered during the menstrual cycle and in carcinoma. 169 95

A French population was investigated for genetic polymorphism of alpha 2HS-glycoprotein (A2HS; nomenclature according to Human Gene Mapping 7, Los Angeles, 1983) using isoelectric focusing and immunoblotting. Three variants were observed together with two common alleles A2HS 1 and A2HS 2, whose frequencies were significantly different from the data in Canadians and Egyptians. An anodal variant to A2HS 1 was identical to a variant with two different nomenclatures reported by three different groups, indicating that there is a confusion in the A2HS nomenclature. The others were new variants with cathodal isoelectric points to A2HS 2 in the native state.
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PMID:Genetic polymorphism of alpha 2HS-glycoprotein in a French population. Description of two new rare variants. 339 69

The immunoconjugate XMMCO-791/RTA consists of ricin A chain bound to a murine monoclonal antibody MoAb 791T. This monoclonal antibody (MoAb) binds to a glycoprotein of 72 kD, which is expressed on human colorectal carcinoma, ovarian carcinoma, and osteogenic sarcoma. XMMCO-791/RTA was tested in a Phase I trial with proposed dose escalation steps of 0.02, 0.04, 0.15, and 0.2 mg/kg per day. Twelve patients with metastatic colorectal carcinoma were treated at 0.02, 0.03, and 0.04 mg/kg per day dose levels administered over 1 hour on days 1-5. Study-related toxicities were hypotension (6 patients); greater than 10% weight gain (6 patients); peripheral edema (9 patients); fever (4 patients); confusion (3 patients); diarrhea (3 patients); proteinuria, as identified by dipstick (3 patients), greater than 0.6 mg/dl decrease in serum albumin (11 patients); greater than 25% decrease in oncotic pressure (10 patients), and a decrease in ionized calcium (8 patients). Six patients received a second course of treatment. HAMA levels developed in 9 patients and titers increased with number of courses administered. Decreased overall toxicity, in comparison to the first course, was noted, but one patient had an allergic-type response (hypotension, crushing chest pain, diaphoresis) after the test dose of the second course (HAMA level > 10,000 IgG). Life-threatening toxicity in the form of fluid shift, resulting in noncardiac pulmonary edema and third-spacing occurred after course 1 in 1 of 3 patients at the 0.04 mg/kg per day level. No further dose escalation was attempted and no antitumor activity was seen.
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PMID:Phase I study of monoclonal antibody-ricin A chain immunoconjugate Xomazyme-791 in patients with metastatic colon cancer. 762 72

Interactions between cancer cells and laminin, a major component of basement membranes, play a critical role at several steps of the complex process of tumor invasion and metastasis. These interactions are mediated through a large variety of cell surface proteins designated as laminin receptors and/or laminin-binding proteins. The growing number of identified laminin binding proteins and domains of this glycoprotein that are biologically active illustrate the complexity of cellular interactions with laminin. The 67-kD laminin receptor (67 LR) was the first protein identified in 1983 as a high-affinity laminin receptor, and its expression is dramatically increased in a large variety of cancer cells. The 67 LR is the subject of several controversies and confusion generated mainly by two events. First, the identification of several new laminin-binding proteins has raised the difficult task of attributing specific functions to specific receptors in contrast to initial beliefs that all cellular laminin-driven biological activities were mediated through the 67 LR. The second source of controversy is the large molecular-weight discrepancy between the 37-kD polypeptide encoded by the 67 LR cDNA clone and the mature 67 LR. In this manuscript, a critical and extensive review of the data accumulated on the 67 LR is presented regarding both its molecular structure and its role during tumor invasion and metastasis. A hypothetical model of the 67 LR is also proposed. Since the first identification of the 67 LR, at least 14 other cell surface molecules have been reported to be potential laminin receptors or laminin-binding proteins. These include members of the beta-galactoside-binding lectin family, seven members of the integrin family, the galactosyltransferase and some not yet fully characterized cell surface molecules. These laminin receptors and laminin-binding proteins are also described and their functions are also discussed with a particular emphasis on their participation in the constitution of the invasive phenotype.
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PMID:Laminin receptors and laminin-binding proteins during tumor invasion and metastasis. 840 8

Villin (V) is a glycoprotein of microvilli associated with rootlet formation. Most colonic adenocarcinomas have a V positive (+), cytokeratin (CK) 20 (+), CK7-negative (-) immunophenotype; most lung adenocarcinomas have a CK20(-), CK7(+) immunophenotype. The reports of villin immunoreactivity in lung adenocarcinoma range from 6% to 68% in studies using various fixations and varied anti-villin antibodies. Some lung adenocarcinomas have microvilli with rootlets leading to possible diagnostic confusion with metastatic colonic adenocarcinoma to lung. Nine primary lung adenocarcinomas with rootlets on ultrastructure (including four bronchioloalveolar carcinomas [BAC]), four metastatic lung adenocarcinomas with rootlets, nine metastatic colon adenocarcinomas to lung, and 10 randomly selected lung adenocarcinomas without rootlets (including five BAC), were immunostained with monoclonal antibodies to villin (1D2C3), CK7 (OV-TL12/30), and CK20 (Ks20.8) using a streptavidin peroxidase technique with heat-induced epitope retrieval. All primary lung adenocarcinomas with rootlets were CK7(+) CK20(-), and six of nine (67%) were V(+). Cytoplasmic villin positivity occurred in a diffuse--five of nine (56%), focal--two of nine (22%), or brush border pattern--two of nine (22%). Two of four metastatic lung adenocarcinomas with rootlets were V(+). One metastatic lung adenocarcinoma had a CK7(+), CK20(+), V(-) phenotype. All metastatic colonic adenocarcinomas were V(+), CK20(+), CK7(-), and 1 of 10 (10%) lung adenocarcinomas without rootlets was V(+), and all 10 were CK20(-), and CK7(+). In summary, villin positivity is more common in lung adenocarcinoma with rootlets (67%) than those without rootlets (10%). AU primary lung adenocarcinomas were CK7(+), CK20(-). The combination of villin, CK 7, and CK 20 is helpful in differentiating metastatic colon adenocarcinoma from lung adenocarcinoma with rootlets.
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PMID:Villin, cytokeratin 7, and cytokeratin 20 expression in pulmonary adenocarcinoma with ultrastructural evidence of microvilli with rootlets. 956 90

Antiphospholipid antibodies were first linked to pregnancy loss more than 20 years ago, and the condition known as antiphospholipid syndrome is perhaps the most convincing 'immunologic' disturbance other than anti-erythrocyte and anti-platelet alloimmunization disorders. Specific criteria for the antiphospholipid syndrome have been delineated, the anticardiolipin assay has been standardized, and authorities agree on laboratory criteria defining lupus anticoagulant. Nonetheless, considerable confusion exists regarding antiphospholipid syndrome and related reproductive problems. The state of affairs primarily derives from two problems: the first is the premature introduction of non-standardized antiphospholipid assays into clinical use without rigorous standardization and prior to convincing proof of clinical utility. As a result, well-intending, but less well-versed clinicians sometimes make the diagnosis of antiphospholipid syndrome in women who are negative for lupus anticoagulant and anticardiolipin antibodies. This is especially confusing in the face of of growing evidence that the relevant in vivo antiphospholipid antigen is formed by a complex between beta 2-glycoprotein 1 and phospholipids. A second major problem is that of unwarranted discrepancies in the clinical and laboratory features of patients considered to have a diagnosis of antiphospholipid syndrome. This problem is most apparent in the case selection for pregnancy-loss treatment series and trials. Many series have included women with predominantly pre-embryonic and embryonic pregnancy losses, while others included a large majority of patients with one or more second or third trimester pregnancy losses. Some treatment trials purposefully excluded patients with a history of thrombosis or systemic lupus erythematosus, features found in nearly 50% of patients in other series. Though most authorities require the presence of either lupus anticoagulant or medium-to-high titer IgG anticardiolipin antibodies to make a diagnosis of antiphospholipid syndrome, in some series no more than half of the study patients had lupus anticoagulant and as many as 20% had only IgM anticardiolipin antibodies. It is very unlikely that patients with such disparate clinical and laboratory findings have the same autoimmune syndrome, and a stated or implicit diagnosis of antiphospholipid syndrome in such a wide variety of women is scientifically unsound and clinically dangerous. The relationship between antiphospholipid antibodies and poor reproductive outcomes must be approached through rigorous scientific study and appropriate treatments established by well-designed clinical trials.
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PMID:Antiphospholipid antibodies and reproductive outcome: the current state of affairs. 961 79

The transmission of bovine spongiform encephalopathy to humans as variant Creutzfeldt-Jakob disease (vCJD) has focused public attention on how prion diseases are transmitted and how prions reach the brain after exposure. Prion diseases are characterised by transmissibility and neuropathological features of gliosis, neuronal loss and microscopic vacuoles, termed spongiosis. The principal component of prions is the glycoprotein PrP(Sc), which is a conformational modified isoform of the normal membrane protein PrP(C). How are prions transmitted and how do prions find their way once they have been ingested? Prion models in mouse and hamster point to lymphoreticular cells which support an early replication phase of prions before reaching the central nervous system via peripheral nerves. Whilst some key players seem to have been identified so far, the mechanisms of prion propagation to the brain are still not fully understood. Seemingly contradictory results have led to some confusion and have provoked discussion.
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PMID:Transmission of prion disease. 1206 58

Despite extensive data supporting their use for non-ST-segment elevation acute coronary syndromes, glycoprotein (GP) IIb/IIIa antagonists are underutilized. This is likely the consequence of confusion as to which patients should receive these agents, as well as to the most appropriate timing and venue for their initiation. We will review the advances in the understanding of GP IIb/IIIa antagonist therapy, emphasizing methods of identifying those most likely to benefit from the use of GP IIb/IIIa receptor blockade. In addition, we will consider appropriate methods/venues for use of GP IIb/IIIa receptor antagonism, including its role in an "early invasive" catheterization strategy.
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PMID:Optimizing glycoprotein IIb/IIIa receptor antagonist use for the non-ST-segment elevation acute coronary syndromes: risk stratification and therapeutic intervention. 1459 24

Although epithelial cells are known to exhibit a polarized distribution of membrane components, the pathways responsible for delivering membrane proteins to their appropriate domains remain unclear. Using an optimized approach to three-dimensional live cell imaging, we have visualized the transport of newly synthesized apical and basolateral membrane proteins in fully polarized filter-grown Madin-Darby canine kidney cells. We performed a detailed quantitative kinetic analysis of trans-Golgi network (TGN) exit, passage through transport intermediates, and arrival at the plasma membrane using cyan/yellow fluorescent protein-tagged glycosylphosphatidylinositol-anchored protein and vesicular stomatitis virus glycoprotein as apical and basolateral reporters, respectively. For both pathways, exit from the TGN was rate limiting. Furthermore, apical and basolateral proteins were targeted directly to their respective membranes, resolving current confusion as to whether sorting occurs on the secretory pathway or only after endocytosis. However, a transcytotic protein did reach the apical surface after a prior appearance basolaterally. Finally, newly synthesized proteins appeared to be delivered to the entire lateral or apical surface, suggesting-contrary to expectations-that there is not a restricted site for vesicle docking or fusion adjacent to the junctional complex.
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PMID:Vectorial insertion of apical and basolateral membrane proteins in polarized epithelial cells revealed by quantitative 3D live cell imaging. 1656 97

A nested polymerase chain reaction (nested-PCR), utilizing glycoprotein B (gB) gene of bovine herpesvirus-1 (BHV-1) as a target, virus isolation (VI), indirect immunofluorescence (IFA) and In situ immuno-peroxidase (IPr) staining in cell culture were conducted for detection of BHV-1 in suspected cattle, buffalo and sheep clinical specimens. The specimens were obtained in the form of nasal swabs, buffy coats and sera from different localities in Egypt (EI-Sharquia, Dumyat and EI-Fayoum). A total of 15/93 (16.1%) of cattle, 4/55 (7.3%) of buffalo and 0/31 (0%) of sheep clinical specimens were BHV-1 positive in this study. Nested-PCR was superior to immunodetection using IFA and IPr after VI procedure. Besides, it was the most discriminative assay that detected BHV-1 viral DNA extracted directly from cattle and buffalo clinical specimens (100%). While, none of the sheep viral isolates (0/3; 0%) could be identified as BHV-1 by nested-PCR, although 2/3 of these isolates (from nasal swabs) tested positive by IFA, IPr and the first round PCR. Also, a buffy coat buffalo viral isolate tested positive with the first round PCR while, it turned repeatedly negative to VI, IFA, IPr and nested-PCR testing. These nested-PCR negative viral isolates were regarded as antigenically related, yet genetically distinct, other ruminant herpes viruses that require further studies. Findings of this study emphasized the preponderant utility of the BHV-1 gB based nested PCR as a sensitive, discriminative and rapid tool for epidemiological studies and control programs of BHV-1 infections, without confusion with other ruminant herpesviruses. Accordingly, it is recommended for routine screening of not only local but also imported animals and biologics for BHV-1 contamination.
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PMID:Molecular and immunological detection of bovine herpesvirus-1 in clinical specimens. 1797 17


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