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:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

BRCA1 and BRCA2 mRNA expression in sporadic breast cancers was quantified by a real-time reverse transcriptase-polymerase chain reaction (RT-PCR), and the relationship of their expression with various clinicopathological factors was studied. BRCA2 mRNA levels (0.993 +/- 1.395, mean +/- SD (BRCA2 / beta-glucuronidase mRNA ratios)) were significantly (P < 0.01) higher than BRCA1 mRNA levels (0.519 +/- 0.570 (BRCA1 / beta-glucuronidase mRNA ratios)), and a weak but significant (r = 0.390, P < 0.01) correlation was observed between BRCA1 and BRCA2 mRNA expression levels. There was no significant association between BRCA1 mRNA expression and clinicopathological factors such as menstrual status, tumor size, lymph node status, estrogen and progesterone receptor status, and histological grade. On the other hand, there was a significant association between higher BRCA2 mRNA expression and estrogen receptor (ER) negativity (P < 0.01) or progesterone receptor (PR) negativity (P < 0.01) or high histological grade (P < 0.01). These results suggest a differential contribution of BRCA1 and BRCA2 in the pathogenesis of sporadic breast cancers. BRCA2 mRNA is speculated to be up-regulated in response to proliferation and genomic instability in high histological grade tumors.
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PMID:Quantitative analysis of BRCA1 and BRCA2 mRNA expression in sporadic breast carcinomas and its relationship with clinicopathological characteristics. 1142 50

We addressed the clinicopathological significance of the oestrogen receptor (ER) beta protein, including an ERbeta variant, ERbetacx, in normal human breast and breast cancer. The reverse transcriptase-polymerase chain reaction (RT-PCR) showed that wild-type ERbeta (ERbetaw) mRNA expression was higher in normal than cancer tissues, and that ERbetacx mRNA was higher in cancer than in normal tissues. Immunohistochemistry of 22 normal breast tissues and 57 breast cancers was performed with three different ERbeta antibodies and one ERbetacx antibody. All normal breast samples showed staining with the three ERbeta antibodies, suggesting that ERbetaw might have a physiological role in oestrogen signalling in the normal breast. In breast cancer, expression of the ERbetaw protein correlated well with the expression of the ERalpha and progesterone receptor (PgR), as well as histological grade (HG), and tended to indicate a better prognosis than when ERbetaw was absent. Thirty-one (54%) breast cancer samples contained ERbetacx, whereas the corresponding tissue for normal breast samples stained positive in only two (9%).
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PMID:Evaluation of oestrogen receptor beta wild-type and variant protein expression, and relationship with clinicopathological factors in breast cancers. 1181 3

Estrogen induction of progesterone receptor (PR) expression may be important to bone physiology because progesterone has been implicated in the control of bone formation and resorption. Although PR gene expression can be induced in osteoblasts by estrogen signaling through the estrogen receptor (ER) a isoform, it is unknown whether the ER-beta isoform is involved in this regulation. The effect of estrogen on PR expression was examined in human fetal osteoblast (hFOB) cell lines stably transfected with either ER-alpha or ER-beta. Estrogen treatment of hFOB/ER-a cells induced PR messenger RNA (mRNA) steady-state levels after 24 h and protein levels after 48 h, as established by competitive reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. Interestingly, no induction of PR expression was observed in the hFOB/ER-beta cells during this period. However, PR mRNA was induced progressively after 48 h of treatment with estrogen with maximum levels achieved at 12 days posttreatment. ER protein also was increased after 12 days of treatment. Both A and B isoforms of PR (PRA and PRB) were induced by estrogen in the hFOB/ER-a cells as well as much later in hFOB/ER-beta cells. The pure antiestrogen ICI 182,780 prevented PR induction by estrogen in both cell lines. An ER-beta-selective antagonist R, R-tetrahydrochrysene (THC) abolished the induction of PR mRNA in hFOB/ER-beta but not in hFOB/ER-a cells, verifying that the response in the former cell line was ER-beta-mediated. Transient cotransfection of hFOB cells with ER-a or ER-beta together with either a human PRA or PRB promoter linked to a reporter plasmid revealed that although the PRB promoter was stimulated equally by estrogen activation of either ER isoform, PRA was activated preferentially by ER-alpha. Together, these results show that although estrogen can up-regulate endogenous PR gene expression in osteoblasts via both ER isoforms, ER-alpha is the predominant inducer.
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PMID:Estrogen receptor isoform-specific induction of progesterone receptors in human osteoblasts. 1191 16

Primary hypoxic tolerance and preconditioning are gender dependent and modulated in females during the estrus cycle. The underlying mechanisms, however, remain to be determined. mRNA of estrogen receptor-alpha (EAR), progesterone receptor (PR), and adenosine receptor subtypes A1 and A3 (A1R and A3R) were investigated with reverse transcriptase-PCR in hippocampi from control male and female mice and animals treated in vivo with a single i.p. injection of 20 mg/kg body weight 3-nitropropionate (3NP) 1 or 24 hr prior to preparation. Results were analyzed relative to expression in hippocampi from untreated males. mRNA levels of EAR and A1R were alike in males and females and unaltered by preconditioning with 3NP. In contrast, PR mRNA levels were alike in males and females during proestrus but lower during estrus and diestrus (85% +/- 15%, P < 0.05; and 80% +/- 10%, P < 0.05, respectively). Upon preconditioning, PR mRNA decreased to 67% +/- 19% (P < 0.05) and 56% +/- 13% (P < 0.05) during proestrus and diestrus, respectively, but was unaltered during estrus and in males. On preconditioning, A3R mRNA decreased from 115% +/- 16% to 86% +/- 29% (P < 0.05) during diestrus but remained at the control level during proestrus and estrus. With low-level expression of PRs, as achieved upon preconditioning, hypoxic tolerance is increased. Other than in males, adenosine A3 receptors are not up-regulated upon preconditioning in females. Thus, not only is net hypoxic tolerance gender dependent but mechanisms conferring hypoxic tolerance are gender specific.
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PMID:Gender-dependent hypoxic tolerance mediated via gender-specific mechanisms. 1193 52

Kallikreins are a group of serine proteases with diverse physiological functions. KLK13 (previously known as KLK-L4) is a novel kallikrein gene located on chromosome 19q13.4 and shares a high degree of homology with other kallikrein family members. Many kallikrein genes were found to be differentially expressed in various malignancies, and their regulation is controlled by steroid hormones in prostate and breast cancer cell lines. We studied the expression of KLK13 by quantitative reverse transcriptase-polymerase chain reaction in 173 patients with epithelial breast carcinoma. An optimal cutoff point equal to the 40th percentile was defined, based on the ability of KLK13 to predict disease-free survival. KLK13 values were then associated with other established prognostic factors and with disease-free survival and overall survival. Higher positivity for KLK13 expression was found in older, oestrogen receptor positive patients. In univariate analysis, KLK13 expression is a significant predictor of improved disease-free survival and overall survival (P<0.001 and P=0.009, respectively). Cox multivariate analysis indicated that KLK13 was an independent prognostic variable in the subgroups of patients with Grade I-II tumours and in patients who were oestrogen receptor and progesterone receptor positive, and node positive. Hazard ratios derived from Cox analysis, related to disease-free survival and overall survival were 0.22 (P=0.001) and 0.24 (P=0.008), respectively, for the Grade I-II group; 0.36 (P=0.008) and 0.44 (P=0.038), respectively, for the node positive group and 0.36 (P=0.008) and 0.18 (P=0.008), respectively, for the oestrogen receptor positive group. The adjusted hazard ratio for progesterone receptor positive patients for disease-free survival was 0.25 (P=0.012). For patients in the node positive and oestrogen receptor positive subgroup (n=51) the adjusted hazard ratio was 0.25 (P=0.006) and for the node positive and progesterone receptor positive subgroup (n=46) the hazard ratio was 0.24 (P=0.008). Taken together, these data suggest that higher KLK13 expression in these subgroups of breast cancer patients is associated with an approximately 55 to 80% reduction in the risk of relapse or death. We conclude that KLK13 expression, as assessed by quantitative reverse transcriptase-polymerase chain reaction, is an independent favourable prognostic marker for breast carcinoma.
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PMID:Human kallikrein gene 13 (KLK13) expression by quantitative RT-PCR: an independent indicator of favourable prognosis in breast cancer. 1198 81

The identification of a second oestrogen receptor, oestrogen receptor (ER) beta, has led to a need to assess the relative importance of the classical ERalpha and ERbeta in human breast and breast carcinomas. ERalpha and ERbeta mRNA was assessed in 61 carcinomas, 8 benign breast lesions, and 30 samples of normal breast using reverse transcriptase (RT)-nested polymerase chain reaction (PCR). Immunohistochemical analysis of ERalpha and ERbeta was performed in 62 carcinomas, the 38 non-malignant breast tissues, and 32 normal breast samples with menstrual cycle data. ERalpha mRNA was detected in 92% of breast cancers, with ERbeta mRNA (wild-type and/or variant form) in 85%; 72% had ERalpha protein, 62% progesterone receptor (PgR), and 32% ERbeta. ERalpha protein had a strong correlation with grade; ERbeta did not, although it was present in three of four grade I carcinomas and in special types. There was no correlation between the presence of ERalpha and ERbeta protein. In non-malignant breast, similar expression of ERalpha and beta was observed, apart from expression of ERbeta in stromal cells and myoepithelium, the latter being confirmed by RT-PCR and western blotting. There were differences in ERalpha in relation to the menstrual cycle but not PgR or ERbeta. The findings indicate a need to understand the role and regulation of ERbeta in normal breast and the reason for its down-regulation in mammary carcinogenesis.
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PMID:Oestrogen receptors alpha and beta differ in normal human breast and breast carcinomas. 1243 14

Many kallikrein genes were found to be differentially expressed in various malignancies, and prostate specific antigen (encoded by the KLK3 gene) is the best tumour marker for prostate cancer. Prostate specific antigen has recently been shown to be an independent favourable prognostic marker for breast cancer. KLK15 is newly discovered kallikrein gene that is located adjacent to KLK3 on chromosome 19q13.4. KLK15 has 41% similarity to KLK3 and the encoded protein, hK15, can activate pro-prostate specific antigen. We studied the expression of KLK15 by real-time quantitative reverse transcriptase-polymerase chain reaction in 202 tissues from patients with breast carcinoma of various stages, grades and histological types. KLK15 expression was found to be a significant predictor of progression-free survival (hazard ratio of 0.41 and P=0.011) and overall survival (hazard ratio of 0.34 and P=0.009). When all other known confounders were controlled in the multivariate analysis, KLK15 retained its prognostic significance. Higher concentrations of KLK15 mRNA were found more frequently in node negative patients (P=0.042). No association was found between KLK15 expression and any other clinicopathological variable. Further, KLK15 is an independent prognostic factor of progression-free survival and overall survival in the subgroup of patients with lower grade and those with oestrogen receptor and progesterone receptor negative tumours in both univariate and multivariate analysis. KLK15 levels of expression were slightly higher (although not statistically significant) in the oestrogen receptor negative and progesterone receptor negative subgroups of patients. KLK15 is up-regulated by androgens in breast cancer cell lines. Time-course and blocking experiments suggest that this regulation is mediated through the androgen receptor.
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PMID:The androgen-regulated gene human kallikrein 15 (KLK15) is an independent and favourable prognostic marker for breast cancer. 1243 20

Telomerase is a ribonucleoprotein enzyme that synthesises telomeres after cell division and maintains chromosomal length and stability thus leading to cellular immortalisation. hTERT (human telomerase reverse transcriptase) gene is the rate-limiting determinant of telomerase reactivation. The present study aims to quantitatively measure the expression of hTERT mRNA in human breast cancer, adjacent non-cancerous tissue (ANCT) and benign breast lesions, examine the association between hTERT and the clinicopathological characteristics of the cancer specimens and to explore the relationship between c-Myc and hTERT expressions. RNA was extracted from 49 breast carcinomas, 46 matched ANCT, and eight fibroadenomas. hTERT and c-Myc mRNA expressions were estimated by reverse transcriptase-PCR (RT-PCR) and Taqman methodology. hTERT mRNA was present in all of the cancerous and most of ANCT specimens with levels being much higher in the cancerous tissue than in ANCT. The ratio of hTERT mRNA in tumour to that in ANCT was 2011 (95% confidence interval 373-10,853, P < 0.0001). There was no significant association between tumour hTERT expression and patient's age, tumour size, grade, nodal metastasis, estrogen receptor (ER) positivity, lymphovascular (LVI) or c-Myc expression. However, there was a weak but significant negative correlation between hTERT expression and progesterone receptor (PR) status (p = 0.04) in tumours. hTERT mRNA expression was also significantly higher in carcinomas (median = 2.61 x 10(6)) than in fibroadenomas (median = 424).We conclude that hTERT mRNA expression is significantly higher in human breast cancer than in non-cancerous breast tissue suggesting that hTERT has a potential role in breast cancer diagnosis. The hTERT mRNA levels in tumour do not seem to be associated with the patient's age or advanced tumour stage. Furthermore, hTERT mRNA expression does not correlate with c-Myc mRNA expression in breast cancer.
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PMID:hTERT expression in human breast cancer and non-cancerous breast tissue: correlation with tumour stage and c-Myc expression. 1260 27

The distribution of progesterone receptor isoform B may have important clinical significance. The aim of this study was to compare the expression, localization and regulation of progesterone receptor isoform B in the human Fallopian tube and endometrium following mifepristone in a dose effective for contraception. Fertile women were treated with a single dose of 200 mg mifepristone on day luteinizing hormone (LH)+2. Biopsies were obtained from the Fallopian tube on day LH+4 to LH+6 and from the endometrium on day LH+6 to LH+8. Progesterone receptor isoform B expression was analyzed by immunohistochemistry and reverse transcriptase polymerase chain reaction. Treatment with mifepristone increased progesterone receptor isoform B concentration in epithelial and stromal cells in the Fallopian tube and also increased progesterone receptor isoform B concentration in the glandular cells of the endometrium. These results further support the hypothesis that the contraceptive effect of mifepristone when given postovulatory is primarily due to alteration of the peri-implantation milieu influencing endometrial receptivity.
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PMID:Progesterone receptor isoform B in the human fallopian tube and endometrium following mifepristone. 1268 55

There is a large and increasing body of experimental and clinical data supporting the involvement of estrogen on the proliferation of hormone-dependent breast tumors. Estrogen acts via its receptor (ER) stimulating cellular proliferation. ER and progesterone receptor (PR), which is regulated by estrogen via ER, have been used as prognostic markers in the clinical management of breast cancer patients. The aim of the present study was the identification of tumor-associated genes differentially expressed in breast tumors regarding the presence or absence of ER and PR. Using the technique of differential display reverse transcriptase-polymerase chain reaction (DDRT-PCR) we have isolated and cloned 127 cDNA fragments that showed differential expression in either ER+/PR+ or ER-/PR- breast tumors. Sequencing analysis of these clones revealed that 119 cDNAs had homology with known sequences in the National Center of Biotechnology Information (NCBI) and 8 were novel, showing no homology to known genes. Among these differentially expressed transcripts are metabolic enzymes, ribosomal proteins, transcription factors, hypothetical proteins, cell cycle regulators, cytoskelectum related genes, cell adhesion and motility genes. Differences in gene expression profiles are likely to explain the phenotypic differences between hormone-responsive and hormone-unresponsive breast tumors.
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PMID:Differentially expressed genes and estrogen receptor status in breast cancer. 1453 86


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