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

---

Query: EC:2.7.7.48 (transcriptase)
9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of mycosis fungoides (MF) in the tumor stage were treated with intra-lesional interferon-gamma (IFN-gamma) therapy. After systemic chemotherapy, intra-lesional recombinant interferon-gamma was applied to the residual tumors. Intra-lesional IFN-gamma was sufficiently effective in the treatment of MF tumors, especially small-sized ones. Reverse transcriptase polymerase chain reaction (RT-PCR) analysis of messenger RNA expression of cytokines commonly detected interleukin-6 (IL-6) and IFN-gamma in the tumor cells before intra-lesional IFN-gamma. However, in our study, tumor cells in these cases did not exhibit the definitive cytokine patterns of Th1 or Th2.
...
PMID:Cytokine profile of tumor cells in mycosis fungoides: successful treatment with intra-lesional interferon-gamma combined with chemotherapy. 853 50

Tumour-secreted vascular endothelial growth factor (VEGF) exerts a number of effects which are important in tumour pathology, including stimulation of angiogenesis and permeabilisation of tumour-associated vasculature. In this study we have examined the possibility that VEGF may also play an autocrine role in tumour growth. Using reverse-transcriptase polymerase chain reaction (RT-PCR), the expression of VEGF was found in 15/15 human tumour cell lines examined, while the VEGF receptor KDR was detected only in three melanoma cell lines (MeWo and A375, both wild type and metastatic variant). Exogenously added VEGF (10ng/ml) was able to stimulate up to 40% increased proliferation of A375 M melanoma cells following a 48-h period of quiescence, suggesting that VEGF may indeed play a role in autocrine, as well as paracrine, stimulation of melanoma growth.
...
PMID:Melanoma cell lines express VEGF receptor KDR and respond to exogenously added VEGF. 855 90

We investigated the expression of granulocyte colony-stimulating factor (G-CSF), G-CSF mRNA, and G-CSF receptor mRNA in astrocytoma cell lines, G-CSF in astrocytoma cyst fluid, and the effect of recombinant G-CSF on the proliferation of astrocytoma cells in vitro and in vivo. We first examined supernatants from astrocytoma cell lines for the presence of G-CSF by ELISA. G-CSF was expressed by 6 of 14 astrocytoma cell lines constitutively, and, was detected after stimulation with tumor necrosis factor-alpha (TNF-alpha) in four of eight cell lines which did not produce G-CSF constitutively. G-CSF mRNA was detected by reverse-transcriptase polymerase chain reaction (RT-PCR) in all cell lines studied, suggesting that astrocytoma cells have the potential to produce G-CSF. We also analyzed the presence of G-CSF by ELISA in five astrocytoma cyst fluids. G-CSF was detected in one case. Although, in vitro study, the growth of glioma cells was not affected by rG-CSF, in a mouse model, the administration of G-CSF significantly shortened the time to tumor appearance and accelerated tumor growth. These data suggest that G-CSF has a stimulatory effect on the proliferation of astrocytoma cells in vivo through the mediation of host factors.
...
PMID:Granulocyte colony-stimulating factor (G-CSF) production by astrocytoma cells and its effect on tumor growth. 869 23

Twenty-nine children treated for medulloblastoma between 1987 and 1991 were reviewed. Thirteen patients with high-risk medulloblastoma characterized by incomplete resection, diploid tumor or subarachnoid dissemination received chemotherapy following radiation therapy. Three received postoperative chemotherapy. Eight patients who had been treated with postoperative radiation therapy also received chemotherapy for recurrent tumors. After a minimum 3-year follow-up period, 16 were alive but 13 had died from recurrent tumors. In order to evaluate the possible participation of P-glycoprotein (Pgp)-mediated multidrug resistance (MDR) in medulloblastoma therapy and its correlation with prognosis, archival specimens were examined by immuno-histochemistry utilizing 3 monoclonal antibodies against Pgp and 6 cases by reverse-transcriptase polymerase chain reaction (RT-PCR) using MDR1-specific primers. Sixteen patients (55%) had MDR expression detected either by 1 of the 3 antibodies or by RT-PCR. DNA ploidy study was also performed on 18 specimens. We correlated patients' outcome with variable factors (extent of surgical resection, chemotherapy, DNA ploidy) and MDR expression. Patients who were treated with radiation therapy and adjuvant chemotherapy had a significantly better (p = 0.036) survival than those with radiation therapy alone, despite the fact that the former group of patients was considered to be high-risk. The extent of surgical resection and DNA ploidy did not correlate with prognosis. However, a statistically significant association was found between MDR expression and outcome (p = 0.007). Among the patients who received chemotherapy, positive MDR expression significantly correlated with poor outcome (p = 0.036). Our results showed that Pgp-mediated intrinsic MDR in medulloblastomas seems to correlate with an adverse outcome. This information may be used in designing new therapeutic protocols for medulloblastoma.
...
PMID:Multidrug resistance gene expression in childhood medulloblastoma: correlation with clinical outcome and DNA ploidy in 29 patients. 874 96

We analyzed the p16INK4 status of 6 hepatocellular carcinoma (HCC) cell lines and 32 primary HCC tumors, including 9 early-stage tumors, to determine whether p16INK4 tumor-suppressor gene inactivation participates in hepatocarcinogenesis. p16INK4 was studied at its protein level through Western blotting, at its messenger RNA (mRNA) level through reverse-transcriptase polymerase chain reaction analysis (RT-PCR) and Northern blotting, and at its genomic level through Southern blotting and PCR-single-strand conformation polymorphism analysis. The p16 protein was absent from 3 of 6 cell lines (50%) and 11 of 32 primary tumors (34%), but present in noncancerous tissues, indicating that p16INK4 is involved in hepatocarcinogenesis. Furthermore, we suggest that the p16 protein loss may contribute to the following: (1) early-stage hepatocarcinogenesis, because it was observed in 22% of early stage tumors; and (2) tumor progression, because it occurred approximately twice as often in advanced rather than in early stage tumors (40%). It was striking that neither p16INK4 homozygous deletion and mutation nor loss of p16INK4 mRNA expression were observed in HCC cell lines and primary tumors, including those specimens from which the p16 protein was absent except the Li7HM cell line, in which p16INK4 mRNA was not detected. These results suggest that p16INK4 in HCC is inactivated predominantly by posttranscriptional regulation rather than by genomic aberrations and lack of transcription.
...
PMID:Inactivation of p16INK4 in hepatocellular carcinoma. 878 27

The dissemination of cancer cells is a prerequisite in the development of micrometastases and solid metastases. Our previous examinations of these cells were based on immunocytological staining of tumor-associated antigens and cytokeratins. We have now developed a highly sensitive and specific detection method based on a nested reverse-transcriptase-polymerase-chain reaction (RT-PCR) of cytokeratin-20 (CK-20) mRNA. Using this method, we examined the bone marrow of 57 patients with colorectal cancer and detected increasing numbers of CK-20-positive samples, depending on the UICC stage. Some 35% of all bone-marrow samples tested positive for CK-20: none were found in colorectal cancer stage 1, 24% were in stage II, 31% in stage III and 71% in stage IV. Investigation of bone-marrow specimens of patients with pancreatic cancer showed that 4 out of 11 patients were positive for CK-20 mRNA. To confirm that sample positivity for CK-20 expression was due to disseminated tumor cells, we examined bone marrow from a control group (n = 16) without apparent carcinoma. In this group, 15 out of 16 donors were CK-20-negative, while one donor with familial adenomatous polyposis showed a CK-20-specific signal.
...
PMID:The detection of disseminated tumor cells in bone marrow from colorectal-cancer patients by a cytokeratin-20-specific nested reverse-transcriptase-polymerase-chain reaction is related to the stage of disease. 879 68

Reverse transcriptase-polymerase chain reaction (RT-PCR) for detection of occult malignancies in breast cancer patients is evolving as a useful diagnostic tool. However, no reliable molecular mRNA markers are available. We developed an RT-PCR plus Southern blot assay using beta-hCG (beta-subunit of human chorionic gonadotropin) gene expression as a tumor marker for detection of breast malignancies metastatic to tumor-draining lymph nodes and blood. Breast carcinoma cell lines, primary breast malignancies and human placenta were used as positive controls for establishing the beta-hCG RT-PCR assay. Peripheral blood leukocytes (PBL) from normal volunteer donors, normal breast tissue and lymph nodes from cancer-free patients were used as negative controls. beta-hCG RT-PCR was used to assess tumor cell presence in PBL and tumor-draining axillary nodes from patients with AJCC stage I-IV breast cancer. The assay sensitivity and specificity were enhanced by restriction endonuclease digestion of an Sty I site of the RT-PCR cDNA product followed by Southern blot analysis. beta-hCG mRNA was expressed in all breast cancer cell lines and 80% of primary breast cancers; it was not expressed in negative controls. The assay reliably detected one cancer cell in > 10(7) PBL, with a sensitivity of 10(-5) microgram RNA. Eighty percent of PBL and 61% of tumor-draining axillary nodes from breast cancer patients expressed beta-hCG mRNA. The assay is a sensitive and specific method of identifying breast cancer cells in breast tissues, lymph nodes and blood.
...
PMID:Detection of metastatic breast cancer by beta-hCG polymerase chain reaction. 890 Mar 69

The ICP4 homolog of Marek's disease virus (MDV ICP4) is a possible candidate for the transactivator of the early genes. We transfected MDCC-MSB-1 (MSB-1) tumor cells with plasmid including a coding region of MDV ICP4 using cationic liposome. As carriers for intranuclear transport, high mobility group -1 and -2 proteins were bound to the plasmid DNA before forming liposomes. We detected transcripts from the plasmid 2 hr after transfection by quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) analysis. We also detected abundant transcripts of endogenous ICP4 2-96 hr after transfection. These data suggested that expression of introduced MDV ICP4 gene enhanced the expression of endogenous MDV ICP4. On the other hand, quantitative PCR analysis for virus genome DNA indicated no significant alteration of copy number of virus genome in transfected MSB-1 cells, suggesting that reactivation of virus requires more than turning on MDV ICP4 gene.
...
PMID:Expression of the endogenous Marek's disease virus ICP4 homolog (MDV ICP4) gene is enhanced in latently infected cells by transient transfection with the recombinant MDV ICP4 gene. 890 Oct 28

The gastrointestinal peptides gastrin and cholecystokinin (CCK) stimulate growth of human pancreatic cancer through a CCK-B/gastrin- like receptor. In the present study we evaluated whether growth of human pancreatic cancer is endogenously regulated by gastrin. Immunohistomical examination of BxPC-3 cells and tumor xenografts revealed specifc gastrin immunoreactivity. Gastrin was detected by radioimmunoassay in pancreatic cancer cell extracts and in pancreatic cancer cell extracts and in the growth media. With use of reverse-transcriptase polymerase chain reaction gastrin gene expression was detected in both cultured BxPC-3 cancer cells and transplanted tumors, as well as seven addition human pancreatic cancer cell lines. Growth of BxPC-3 human pancreatic cancer cell in serum-free medium was inhibited by the addition of the CCK-B/gastrin receptor antagonist L-365,260, and gastrin treatment reversed the inhibitory effect of the antagonist. A selective gastrin antibody (Ab repressed growth of BxPC-3 cells. Gastrin immunoreactivity was detected in fresh human pancreatic cancer specimens but not in normal human pancreatic tissue. These data provide the first evidence that growth of a human pancreatic cancer is tonically stimulated by the autocrine production of gastrin. Evidence for the ubiquity of this system was provided by the detection of gastrin gene expression in multiple human pancreatic cancer cell lines and detection of gastrin in cell lines and fresh pancreatic tumors.
...
PMID:Gastrin regulates growth of human pancreatic cancer in a tonic and autocrine fashion. 892 9

Primary lung adenocarcinomas originate from the progenitor cells of peripheral airway cells. Alveolar type II cells and Clara cells are the major progenitor cells of peripheral airway cells. Alveolar type II cells produce a lipid-protein complex called surfactant, which contains surfactant proteins SP-A, SP-B, SP-C and SP-D. Phosphatidylcholine (PC) and phosphatidylglycerol (PG) are believed to be essential for the surfactant function. Clara cells also express SP-A, SP-B and SP-D but not SP-C. In this study we examined the properties of the cancer cells isolated from the pleural effusion of a patient with primary lung adenocarcinoma by analyzing lipids, proteins and mRNAs. The cancer cells, designated as LC117 cells, were isolated from the pleural effusion of a patient with primary lung adenocarcinoma. The percent distributions of [14C]-acetate incorporated into PC and PG in the cancer cells were 55.7 and 1.1%, respectively. The disaturated species in total PC was 46.2%. Immunoblotting analysis using anti-SP-D monoclonal antibody revealed that the pleural effusion from a patient with lung adenocarcinoma contained SP-D. We determined the concentrations of SP-A and SP-D by enzyme-linked immunosorbent assay. The pleural effusions from this patient and the media incubated with cancer cells exhibited significant levels of SP-D as well as SP-A. Reverse transcriptase-polymerase chain reaction demonstrated that the tumor cells expressed mRNAs for SP-C as well as the other surfactant proteins. The results demonstrate that tumor cells from lung adenocarcinoma express all of surfactant-associated proteins, indicating that LC117 cells originate from alveolar type II cells. This study indicates that the combination of analyses of lipids, proteins and mRNAs in the cancer cells isolated from pleural effusion is useful to understand the property of lung adenocarcinoma.
...
PMID:Lipid analysis and surfactant-associated protein expression in lung adenocarcinoma cells from pleural effusion. 893 61


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---