HCLSIG BioRDF Subgroup/Data/Pubmed

<?xml version="1.0" encoding="UTF-8"?> <rdf:RDF xmlns:xxx="urn:lsid:uniprot.org:ontology:" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:rdfs="http://www.w3.org/2000/01/rdf-schema#" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/"> <rdf:Description rdf:about="urn:lsid:uniprot.org:pubmed:15143089"> <rdf:Type rdf:resource="urn:lsid:uniprot.org:ontology:Pubmed" /> <dc:date>2004-05-14</dc:date> <dc:identifier>0732-183X</dc:identifier> <dc:volume>22</dc:volume> <dc:issue>10</dc:issue> <dcterms:issued>2004-May-15</dcterms:issued> <dc:title>Diagnosis of deep septic thrombophlebitis in cancer patients by fluorine-18 fluorodeoxyglucose positron emission tomography scanning: a preliminary report.</dc:title> <dc:description>PURPOSE To determine the role of the fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) scan in the diagnosis and management of deep septic thrombophlebitis (STP). PATIENTS AND METHODS We conducted a prospective observational evaluation of FDG-PET in patients with cancer and suspected STP. Retrospective evaluation of patients with cancer and deep venous thrombosis (DVT) who underwent FDG-PET and extremity duplex scan (DS) was also performed. Results Strong venous uptake was observed in FDG-PET of nine STP episodes versus 0 of 27 DVT episodes (P <.001). FDG-PET identified central vein STP in five patients, whereas DS and venography were negative in five and two of these patients, respectively. FDG-PET diagnosis of STP resulted in therapeutic changes in all patients. In four patients, follow-up FDG-PET confirmed resolution. CONCLUSION In cancer patients, FDG-PET identifies STP even in areas not optimally visualized by DS or venography, distinguishes STP from DVT, and leads to significant therapeutic changes.</dc:description> <dc:creator>Miceli, Marisa</dc:creator> <dc:creator>Atoui, Rola</dc:creator> <dc:creator>Walker, Ronald</dc:creator> <dc:creator>Mahfouz, Tahsine</dc:creator> <dc:creator>Mirza, Nadeem</dc:creator> <dc:creator>Diaz, Jose</dc:creator> <dc:creator>Tricot, Guido</dc:creator> <dc:creator>Barlogie, Bart</dc:creator> <dc:creator>Anaissie, Elias</dc:creator> <dc:location>United States</dc:location> <dc:publisher>J Clin Oncol</dc:publisher> </rdf:Description> <rdf:Description rdf:about="urn:lsid:uniprot.org:pubmed:15140540"> <rdf:Type rdf:resource="urn:lsid:uniprot.org:ontology:Pubmed" /> <dc:date>2004-05-13</dc:date> <dc:identifier>0169-5002</dc:identifier> <dc:volume>44</dc:volume> <dc:issue>3</dc:issue> <dcterms:issued>2004-Jun-</dcterms:issued> <dc:title>Lack of association between Caucasian lung cancer risk and O(6)-methylguanine-DNA methyltransferase-codon 178 genetic polymorphism.</dc:title> <dc:description>The formation of DNA adducts is thought to be a critical step for the induction of chemically induced cancer. O(6)-Methylguanine-DNA methyltransferase (MGMT) is a ubiquitously expressed enzyme that repairs DNA adducts formed by alkylating carcinogens. Thus, genetic polymorphisms of the MGMT that could result in differences in MGMT activity are potential risk factors for cancer. In the present study, we established a convenient and reliable genotyping method for the MGMT codon 178 polymorphism, a Lys (AAG) to Arg (AGG) substitution, using restriction fragment length polymorphism (RFLP), and studied differences in the distribution of this polymorphism in 92 Caucasian lung cancer patients and 85 controls. Frequencies of the "A" and "G" alleles (MGMT codon 178, AAG and AGG, respectively) were 0.91 and 0.09, respectively. The genetic polymorphism of the MGMT codon 178 was linked with that of the MGMT codon 143 ( [Formula: see text] ). The distribution of the MGMT codon 178 genetic polymorphism was not significantly different between lung cancer patients and controls. Thus, our study suggests that the MGMT codon 178 (and possibly 143) polymorphisms do not appear to markedly affect lung cancer risk for this population. In addition, we found an apparent 10bp-deletion in the intron before exon 5 by DNA sequencing. Because this "deletion" was observed in all sequenced samples ( [Formula: see text] ), the previously reported human (Caucasian) MGMT gene sequence should be revised to exclude this 10bp segment.</dc:description> <dc:creator>Yang, Mihi</dc:creator> <dc:creator>Coles, Brian F</dc:creator> <dc:creator>Caporaso, Neil E</dc:creator> <dc:creator>Choi, Yunhee</dc:creator> <dc:creator>Lang, Nicholas P</dc:creator> <dc:creator>Kadlubar, Fred F</dc:creator> <dc:location>Ireland</dc:location> <dc:publisher>Lung Cancer</dc:publisher> </rdf:Description> <rdf:Description rdf:about="urn:lsid:uniprot.org:pubmed:15139712"> <rdf:Type rdf:resource="urn:lsid:uniprot.org:ontology:Pubmed" /> <dc:date>2004-05-13</dc:date> <dc:identifier>0003-469X</dc:identifier> <dc:volume>74</dc:volume> <dc:issue>5</dc:issue> <dcterms:issued>--</dcterms:issued> <dc:title>Evaluation of DOWNSTAGING as leading concept in sphincter-saving surgery for rectal cancer after preoperative radio-chemotherapy (Preop RCT).</dc:title> <dc:description>AIM: To evaluate the downstaging of rectal cancer after preop R +/- CT. METHODS: 392 patients (pts) with rectal cancer were observed. Only 172 pts (58%) with II and III stage cancer of middle and lower third were examined. Enrol-led pts were 168: 52 of them received preop R +/- CT (32 RT, 20 R + CT). Preop R +/- CT group included 14 middle third cancers (73%), 38 lower third (17%). In this group, tumor stage was as follows: 44 T3 stage tumors (86.4%), 8 (15.4%) T4. Mean age of this group was 57 years (range 42-67). Patients received 45 Gy for 5 weeks in 25 fractions and continuous administration of 5-FU (300-500 mg/m2/die). Surgery was performed 6 weeks +/- 7 days after the therapy. RESULTS: Downstaging, at least of 1 T-stage level, was detected in 45 patients (86%) (8 middle third; 32 lower third), in 5 (9.6%) (4 middle third, 1 lower third), tumor decreased to pT0N0, while in 7 (13.5%) (2 middle third, 5 lower third), there was no response. An Anterior Resection (AR) was performed in 40 patients (77%) [4 Downstaged to pT0N0 middle third cancers; 36 downstaged but with residual disease (8 middle third, 28 lower third)]; APR was performed in 12 (23%) (7 No responders patients, 1 Downstaged to pT0N0 lower third cancer, 4 downstaged but with residual disease of lower third). CONCLUSIONS: Preop R +/- CT is effective in obtaining a significative downstaging to allow sphincter saving surgery, without compromising oncological results.</dc:description> <dc:creator>Gentile, M</dc:creator> <dc:creator>Bucci, L</dc:creator> <dc:creator>Cerbone, D</dc:creator> <dc:creator>D'Antonio, D</dc:creator> <dc:creator>Guarino, V</dc:creator> <dc:location>Italy</dc:location> <dc:publisher>Ann Ital Chir</dc:publisher> </rdf:Description> <rdf:Description rdf:about="urn:lsid:uniprot.org:pubmed:15138573"> <rdf:Type rdf:resource="urn:lsid:uniprot.org:ontology:Pubmed" /> <dc:date>2004-05-12</dc:date> <dc:identifier>1021-335X</dc:identifier> <dc:volume>11</dc:volume> <dc:issue>6</dc:issue> <dcterms:issued>2004-Jun-</dcterms:issued> <dc:title>The biological basis for the use of an anti-androgen and a 5-alpha-reductase inhibitor in the treatment of recurrentprostate cancer: Case report and review.</dc:title> <dc:description>Although many prostate cancer cases relapse to a hormone-insensitive state, endocrine therapy involving androgen depletion by orchiectomy or by treatment with LHRH-analogue as well as blockade of the androgen receptor (AR) with anti-androgens remains a primary treatment option. Quality of life (QOL) however, is a prime consideration of men choosing such an approach. In this report we discuss a synergistic combination of 150-mg bicaltumide (Casodex) and 5 mg finasteride (Proscar) in the treatment of a 69-year-old patient with a relapsed (biochemical failure) Gleason score 7 prostate cancer, initially treated with external beam radiation therapy. A successful clinical outcome as evidenced by undetectable serum PSA, bone scan density and overall general well-being was accomplished with minimal side effects. Experiments using an established hormone-dependent prostate cancer cell line (LNCaP) showed that the combination of bicaltumide-finasteride at the same ratio as used clinically, produced synergistic effects on the inhibition of cell proliferation and AR expression/phosphorylation. A more complete inactivation of the AR on this regimen may have had the effect of constraining the ability of the AR to mutate, and/or diminishing the ability of androgen independent clones to evolve. Thus, passage to androgen independence may have been slowed or arrested.</dc:description> <dc:creator>Wang, Long G</dc:creator> <dc:creator>Mencher, Simon K</dc:creator> <dc:creator>McCarron, J P</dc:creator> <dc:creator>Ferrari, Anna C</dc:creator> <dc:location>Greece</dc:location> <dc:publisher>Oncol Rep</dc:publisher> </rdf:Description> </rdf:RDF>