bluuebunny/crossref_metadata_2025_split huggingface dataset:
Down‐regulation of mitochondrial gene expression by the anti‐tumor arotinoid mofarotene (Ro 40‐8757)
Authors: Uchida Takafumi , Inagaki Naohito , Furuichi Yasuhiro , Eliason James F. 
Published: February 2007

AbstractTo understand the mechanism of action of the antitumor arotinoid mofarotene (Ro 40‐8757), differential screening of cDNA libraries with cDNA probes prepared from treated or untreated breast‐cancer cells was performed. Several genes were identified that appeared to be regulated by mofarotene, including a mitochondrial gene encoding a subunit of NADH dehydrogenase (NDI). This gene was down‐regulated in the breast‐cancer cell line MDA‐MB‐231 after treatment with the arotinoid for 3 to 6 hr. Down‐regulation of NDI was detected in 2 other breast‐carcinoma cell lines (ZR‐75‐1 and MCF‐7) and a pancreatic cancer cell line (BxPC3), but not in the normal fibroblast cell line Wi‐38 or several other tumor cell lines. This effect was blocked by addition of cycloheximide to the medium. The retinoids, all‐trans and 9‐cis retinoic acids, did not affect the expression of NDI in MDA‐MB‐231 cells, demonstrating that mofarotene was not acting through the nuclear retinoic‐acid receptors. In the estrogen‐receptor‐expressing breast‐cancer line ZR‐75‐1, tamoxifen had no effect on NDI expression. The cytotoxic drugs doxorubicin, 5‐FU and vincristine also had no effect on regulation of this gene. Two mitochondrial proteins encoded in the nucleus, ATPase β subunit and mitochondrial transcription factor I, were not down‐regulated by mofarotene. Addition of mofarotene to cells incubated in glucose‐free medium led to their death. These results indicate that down‐regulation of mitochondrial gene transcription is specific to mofarotene and may explain, in part, the anti‐proliferative effects of this compound.
HIV‐associated lymphoma in Africa: An autopsy study in Ĉote D'ivoire
Authors: Lucas Sebastian B. , Diomande Mohenou , Hounnou Anatole , Beaumel Anne , Giordano Christian , Kadio Auguste , Peacock Christopher S. , Honde Michel , De Cock Kevin M. 
Published: February 2007

AbstractHIV infection predisposes to the development of non‐Hodgkin lymphoma (NHL). The frequency of NHL among HIV‐positive adults and children in sub‐Saharan Africa is not known. In 1991–1992, a representative autopsy study of HIV infection was performed in Abidjan, Cǒte d'Ivoire. Of 247 HIV‐positive adult (> 14 years) medical patients dying in hospital, 2.8% had NHL, 1.6% with visceral NHL and 1.2% with primary cerebral lymphoma. The estimated crude incidence of NHL among HIV‐positive adults in Abidjan was 84/ 100,000 per year, 10‐fold greater than the expected pre‐AIDS incidence of NHL but less than the incidence observed among HIV‐positive adults in industrialised countries. None of 78 autopsied HIV‐positive children (median age = 17 months) had NHL. HIV infection augments the incidence of NHL among adults in Africa, but short survival with advanced HIV disease probably prevents the major increase in HIV‐associated NHL seen in industrialised countries. Survival of HIV‐positive children in Africa appears too short to permit the significant development of additional NHL; classic Burkitt lymphoma is not an AIDS‐associated tumour in Africa.
Testicular cancer in nine northern european countries
Authors: Adami Hans‐Olov , Bergström Reinhold , Möhner Matthias , Zatoôski Witold , Storm Hans , Ekbom Anders , Tretli Steinar , Teppo Lyly , Ziegler Hartwig , Rahu Mati , Gurevicius Romualdas , Stengrevics Aivars 
Published: February 2007

AbstractThe incidence of testicular cancer was examined in the Nordic and Baltic countries, Poland and Germany by collaboration among 10 cancer registries. Population‐based registers were used to analyze a total of 34,309 cases, diagnosed from the start of registration (varying from 1943 in Denmark to 1980 in Latvia and Lithuania) through 1989. An approximately 10‐fold geographical variation was found in 1980, with the highest age‐standardized incidence rate (7.8 per 105; world standard population) in Denmark and the lowest (0.9) in Lithuania. During the entire period of registration, incidence increased rapidly in all countries, by 2.3 to 3.4 per cent annually in the Nordic countries and by about 5 per cent in Poland and Germany; there was some evidence of a slower increase in Denmark and Poland after 1975. The rising trend was more pronounced for ages below 30. The age‐specific incidence peaked in all countries at ages 25 to 34, but the geographical variation was considerable. Our data indicate that environmental influences on testicular cancer are strong. Exposure to causal factors mostly takes place early in life, shows substantial geographical variation, and increases over time, so that the age‐standardized incidence doubles every 15 to 25 years. New aetiological hypotheses are needed to accommodate these salient features of the descriptive epidemiology, since risk factors considered so far cannot explain the observed pattern.
Mutations of the adenomatous polyposis coli gene in the mutation cluster region: Comparison of human pancreatic and colorectal cancers
Authors: Yashima Kazuo , Nakamori Shouji , Murakami Yoshinori , Yamaguchi Akio , Hayashi Kenshi , Ishikawa Osamu , Konishi Youichi , Sekiya Takao 
Published: February 2007

AbstractWe analyzed the adenomatous polyposis coli (APC) tumorsuppressor gene as one of the possible genes mutated in human pancreatic carcinomas. DNAs from 39 surgical specimens were subjected to single‐strand conformation polymorphism analysis of polymerase chain reaction products and the mutation cluster region (MCR) of the gene was examined. We also examined the same region of DNAs from 27 surgical specimens of sporadic colon carcinomas and detected mutations in 11 carcinomas (41%). This mutation frequency in colon carcinomas was similar to those reported previously. Using this system, we detected a mutated APC gene in one of 39 pancreatic carcinomas. The results indicated that mutation of the MCR in the APC gene is involved in genesis of some of human pancreatic carcinomas, but its frequency is much lower than in colorectal carcinomas.
Inhibitory effects of analogs of luteinizing hormone‐releasing hormone on the growth of the androgen‐independent dunning R‐3327‐AT‐1 rat prostate cancer
Authors: Pinski Jacek , Reile Herta , Halmos Gabor , Groot Kate , Schally Andrew V. 
Published: February 2007

AbstractThe effects of treatment with the luteinizing hormone‐releasing hormone (LH‐RH) antagonist SB‐75 and agonist [D‐Trp6] LH‐RH were investigated in Copenhagen rats bearing the anaplastic, androgen‐independent Dunning R‐3327‐AT‐1 pros‐tatic adenocarcinoma implanted orthotopically into the ventral lobes of prostate glands. The LH‐RH antagonist SB‐75 and the LH‐RH agonist [D‐Trp6] LH‐RH were administered from osmotic minipumps and the survival time of animals bearing this cancer was evaluated. Treatment with SB‐75 and [D‐Trp6] LH‐RH significantly prolonged the mean survival time of rats by 4.1 days and 4.5 days, respectively. In cell cultures, proliferation of the AT‐1 cell line was strongly inhibited by the antagonist SB‐75, but only a moderate suppression of tumor cell growth in vitro was observed with the agonist [D‐Trp6] LH‐RH. Receptor assays on Dunning R‐3327‐AT‐1 tumor membranes showed high‐affinity binding sites for LH‐RH, epidermal growth factor (EGF) and insulin‐like growth factor‐1 (IGF‐1). Receptors for EGF were significantly down‐regulated by treatment with SB‐75. Therapy with SB‐75 also decreased EGF levels in tumor tissue to non‐detectable levels, as measured by specific RIA. Our results demonstrate that the LH‐RH antagonist SB‐75 and agonist [D‐Trp6] LH‐RH inhibit the growth of androgen‐independent Dunning R‐3327‐AT‐1 prostatic cancer in vivo and in vitro.
Circumvention of acquired tetraplatin resistance in a human ovarian carcinoma cell line by a novel Trans platinum complex, JM335 [Trans ammine (cyclohexylamine) dichloro dihydroxo platinum (IV)]
Authors: Mellish Kirste J. , Barnard Chris F. J. , Kelland Lloyd R. , Harrap Ken R. 
Published: February 2007

AbstractAcquired resistance to tetraplatin [d, I ‐trans‐1,2‐diaminocyclohexane tetrachloroplatinum (IV)] has been generated in vitro in the human ovarian carcinoma cell line PXN94; the derived line, PXN94tetR, was 24‐fold resistant to tetraplatin. Intracellular tetraplatin accumulation was reduced in PXN94tetR compared with PXN94 by an average of 1.3‐fold across the concentration range 1–100 μM (2 hr exposure). There was no significant difference in glutathione levels between the 2 cell lines. PXN94tetR was 1.6‐fold more resistant to cadmium chloride than PXN94, suggesting that metallothionein levels may be elevated. However, no significant difference was observed between PXN94 and PXN94tetR in the levels of total platinum bound to DNA or DNA interstrand cross‐links immediately after tetraplatin exposure (10–100 μM x 2 hr). There was also no significant difference between the 2 cell lines in the rate of removal of total platinum or interstrand cross‐links from DNA following 2 hr exposure to 25 μM tetraplatin. Hence the major mechanism of acquired tetraplatin resistance in PXN94tetR appears to be increased tolerance of platinum‐DNA adducts. PXN94tetR was partially cross‐resistant to the bifunctional alkylating agents melphalan, chlorambucil and mitomycin C. Partial cross‐resistance was also observed to Adriamycin, bleomycin, etoposide, 5‐fluorouracil and vinblastine; however, no elevation in P‐glycoprotein levels was apparent in PXN94tetR. No cross‐resistance was observed to taxotere. PXN94tetR was partially cross‐resistant to cisplatin, carboplatin and several novel cis platinum complexes. In contrast, resistance was completely circumvented by the novel trans platinum complex JM335 [trans ammine (cyclohexylamine) dichloro dihydroxo platinum (IV)].
Inhibition of tumorigenic potential and prostate‐specific antigen expression in LNCaP human prostate cancer cell line by 13‐cis‐retinoic acid
Authors: Dahiya Rajvir , Park Hae Duck , Cusick John , Vessella Robert L. , Fournier George , Narayan Perinchery 
Published: February 2007

AbstractProstate‐specific antigen (PSA) is a member of the kallikrein family and has been an important biological marker for prostate cancer. The mechanisms regulating PSA expression in prostatic cancer cells are unclear. The present study was designed to elucidate the role of 13‐cis‐retinoic acid (RA) in regulation of PSA and the tumorigenic potential of the human prostate cancer cell line LNCaP. The growth regulation of LNCaP cells was examined by DNA synthesis and doubling time. The tumorigenic potential of prostate cancer cells was analyzed by soft agar colony‐forming assay, in vitro invasion assay, type IV collagenase assay and binding to extracellular matrix assay. The nuclear receptors for retinoic acid (RARα, ‐β, ‐γ and RXRα, ‐β,‐γ) as well as PSA mRNA were determined by Northern blot using specific oligonucleotide probes. Our results suggest that 13‐cis‐RA significantly inhibits PSA secretion and expression both at the mRNA and protein levels compared with untreated cells. Electron microscopic studies suggest that after 13‐cis‐RA treatment, cells become more differentiated as they contain lumina, lined by plasma membrane and microvilli. Prostate cancer cell growth and tumorigenic potential after 13‐cis‐RA treatment was significantly decreased compared with controls. Nude mice tumorigenicity studies showed that 13‐cis‐RA‐treated cells produced significantly smaller tumors compared with untreated cell tumors. There was also a significant increase in the expression of RXRa mRNA after 13‐cis‐RA treatment compared with untreated cells.
Volatile N‐nitrosamines and their precursors in chinese salted fish—a possible etological factor for NPC in China
Authors: Zou Xiao Nong , Lu Shih Hsin , Liu Bin 
Published: February 2007

AbstractEpidemiological studies show that the consumption of Chinese salted fish is a causative factor for nasopharyngeal carcinoma (NPC) in southern China. In the present study, N‐nitrosamines and their precursors were analyzed in 145 samples of cooked, salted fish collected from various areas in China. The results show that N‐dimethylnitrosamine (NDMA), N‐diethylnitrosamine (NDEA), N‐nitrosopyrrolidine (NPYR) and N‐nitrosopiperidine (NPIP) were present in the salted fish. Total volatile N‐nitrosamines (TVN) in the salted fish were 0.028 to 4.54 mg/kg. The samples from areas with higher NPC risk showed a higher average level of TVN than those from areas of lower NPC risk. Positive correlations were found between the levels of NDMA, NDEA and TVN and mortality from NPC. Although neither the nitrates nor the nitrites in the salted fish were present at significantly high levels, in vitro data regarding nitrosation of salted fish showed that the N‐nitrosamine content had increased substantially. The results support the conclusion that the high NPC risk in southern Chinese may be attributed to consumption of salted fish containing high levels of N‐nitrosamines.
Lung cancer and cigarette smoking in women: A case‐control study in barcelona (Spain)
Authors: Agudo Antonio , Barnadas Agusti , Pallares Cinta , Martinez Ignacio , Fabregat Xavier , Rosello Josep , Estape Jordi , Planas Josep , Gonzalez Carlos A. 
Published: February 2007

AbstractA case‐control study on lung cancer and the habit of cigarette smoking was carried out in Barcelona (Spain). Cases were 103 women newly diagnosed with primary lung cancer in 10 hospitals from the study area. Histologic confirmation was given in 101 cases, of which 53 were adenocarcinoma, 19 squamous‐cell carcinoma, 9 small‐cell carcinoma and 20 other types. Two controls per case were selected, matched by age, residence and hospital. Compared with the never‐smokers, the odds ratios (OR), with corresponding 95% confidence intervals (CI), were 1.61 (0.4 to 6.9) for ex‐smokers and 3.61 (1.6 to 8.3) for current smokers. The risk of lung cancer showed a good dose‐response relationship with duration of the habit, average number of cigarettes smoked daily and cumulative cigarette consumption. The risk of lung cancer increased by 62% for each 10 pack‐years. Depth of inhalation also showed a remarkable effect, independently of the intensity of the habit. Although mortality and incidence rates of lung cancer among women in Spain are lower than in other developed countries, the risk of lung cancer is that which would be expected according to the pattern of the smoking habit in Spanish women.
The tyrosine kinase activity of the C‐erbB‐2 gene product (p185) is required for growth inhibition by anti‐p185 antibodies but not for the cytotoxicity of an anti‐p185‐ricin‐a chain immunotoxin
Authors: Xu Feng Ji , Boyer Cinda M. , Bae Duk Soo , Wu Shu , Greenwald Marilee , O'Briant1 Kathy , Yu Yin Hua , Mills Gordon B. , Bast Robert C. 
Published: February 2007

AbstractOur previous studies have demonstrated that 7 of 10 lgG antibodies against distinct epitopes on the extracellular domain of the c‐erbB‐2 gene product (p185) inhibit the anchorage‐independent growth of SKBr3 human breast‐cancer cells that overexpress this transmembrane tyrosine kinase growth‐factor receptor. Two of 7 growth‐inhibitory antibodies also block the binding and function of the gp30 and p75 c‐erbB‐2 ligands. In this report we have studied phosphorylation of p185 and different intracellular substrates after binding of antibodies that do or do not inhibit tumor‐cell growth. A correlation has been found between antibodies that inhibit growth and the intensity of tyrosine phosphorylation of p185. At late intervals, serine phosphorylation of at least 3 intracellular substrates is increased preferentially by growth‐inhibitory antibodies. To test the importance of p185 kinase activity more critically, NIH3T3 cells were transfected with an expression vector containing the full‐length human c‐erbB‐2 gene (cell line 17313), c‐erbB‐2 with deletion of the kinase region from codons 751–979 (cell line 9309) or c‐erbB‐2 with deletion of most of the intracellular domain from codons 684–1255 (cell line 9310). Unconjugated antibodies inhibited anchorage‐independent growth of 17313 cells as well as SKBr3 cells, but did not inhibit growth of either 9309 or 9310 cells. In contrast, the cytotoxic effect of anti‐p185‐ricin A chain (RTA) conjugates was comparable for 17313, 9309 and 9310. The tyrosine‐kinase activity of p185 is required for growth inhibition mediated by unconjugated anti‐p185 antibodies, but not for the cytotoxic activity of anti‐p185‐RTA immunotoxins.
Suppressed expression of insulin‐like growth factor binding protein‐1 mRNA in the endometrium: A molecular mechanism associating endometrial cancer with its risk factors
Authors: Rutanen Eeva‐Marja , Nyman Tuulikki , Lehtovirta Pentti , Ämmälä Martti , Pekonen Fredrika 
Published: February 2007

AbstractThe insulin‐like growth factor (IGF) system is thought to function as a mediator of steroid hormone actions in the endometrium. IGFs (IGF‐I and IGF‐II) are also potent mitogens in endometrial cancer. The biological actions of IGFs are modulated by specific binding proteins (IGFBP)—6 cloned and sequenced so far—which may either inhibit or enhance the effects of IGF at the cellular level. In the endometrium, IGFBP‐1 gene expression is stimulated by progesterone and inhibited by insulin, while IGFBP‐1 inhibits the mitogenic action of IGF‐I. In this study, we used a quantitative reverse transcriptase polymerase chain reaction (RT‐PCR) to investigate IGFBP‐I, IGFBP‐2, IGFBP‐4, IGFBP‐5 and IGFBP‐6 gene expression in endometrial cancer tissues. Endometrial cancer tissue samples were collected from 20 women (aged 54–79 yrs) with stage I to II well‐differentiated endometrial adenocarcinoma. Samples of normal endometrium (n = 14) obtained from women undergoing tubal ligation in various phases of the menstrual cycle, and normal early‐pregnancy endometrium (decidua) were studied for comparison. In endometrial cancer tissues, the IGFBP‐I mRNA was undetectable or minimally expressed when studied by RT‐PCR. The mean (+SD) levels of IGFBP‐2 and IGFBP‐4 and IGFBP‐5 mRNAs in endometrial cancer tissues did not differ from those in normal endometrium, in which no cyclic variation was observed, suggesting that the genes encoding IGFBP‐2, IGFBP‐4 and IGFBP‐5 are not hormonally regulated in the endometrium. The IGFBP‐6 mRNA expression showed a significant cyclic variation in normal endometrium, with low levels in late‐prolitferative and early‐ to mid‐secretory phases and high expression in late‐secretory and early‐prolitferative phases. In endometrial cancer tissues, the mean IGFBP‐6 mRNA level was similar to that in cycling endometrium during the peri‐ovulatory period. In summary, a continuous stimulation of the endometrial epithelial cells by IGFs with suppressed IGFBP‐1 expression may lead to an imbalance in the IGF system of the endometrium and trigger an uncontrolled cell proliferation, ultimately resulting in malignant transformation. © 1994 Wiley‐Liss, Inc.
Estrogen and progesterone receptor mrna levels in primary breast cancer: Association with patient survival and other clinical and tumor features
Authors: Nagai M. A. , Marques L. A. , Yamamoto L. , Fujiyama C. T. , Brentani M. M. 
Published: February 2007

AbstractThe relative expression of estrogen receptor (ER) and progesterone receptor (PR) mRNA transcripts was measured in 71 primary breast‐cancer biopsies. ER and PR binding activity were estimated in parallel by the dextran‐coated‐charcoal method. There was a close correlation between the amount of ER mRNA and estradiol binding activity. Tumors from post‐menopausal patients contained higher levels of ER mRNA than those from pre‐menopausal patients. Northern‐blot analysis indicated the presence of a major band of 6.3 kb in all ER mRNA‐positive tumors. Some tumors showed, in addition, 3,7‐ and 2.4‐kb transcripts. PR binding activity and overall PR mRNA levels correlated moderately. PR mRNA and ER mRNA were associated. Four PR mRNA species with estimated sizes of 11.4, 4.5, 3.7 and 2.5 kb were detected in 14% of the PR mRNA‐positive tumors. The 3.7‐kb transcript was detected to varying degrees in all PR mRNA‐positive biopsies, accompanied in some tumors by the 2.5‐kb species. ER and PR mRNA levels < 50 pg/5 μg total RNA correlated with prolonged survival of the patients. In addition, high ER mRNA levels were associated with absence of necrosis and vascular invasion together with absence or minimal level of tumor lymphocytic infiltration, but not with age, clinical stage, tumor size or overexpression of c‐myc or c‐erbB‐2 mRNA. PR mRNA was not statistically associated with any of the above clinicopathological features. A bivariate analysis showed that both ER and PR mRNA levels were able to predict overall survival independently of the lymph‐node status. © 1994 Wiley‐Liss, Inc.
Dietary factors and the risk of glioma in adults: Results of a case‐control study in melbourne, Australia
Authors: Giles Graham G. , McNeil John J. , Donnan Geoffrey , Webley Carole , Staples Margaret P. , Ireland Paul D. , Hurley Susan F. , Salzberg Michael 
Published: February 2007

AbstractIn a population‐based case‐control study of 416 incident gliomas in adults carried out in Melbourne, Australia, between 1987 and 1991, 409 age‐sex‐matched case‐control pairs (243 male and 166 female) had adequate data available to examine associations between the dietary intake of N‐nitroso compounds, N‐nitroso precursors, other nutrients including N‐nitroso inhibitors, and the risk of glioma. Dietary intakes were based on the reported frequency of consumption of 59 food items. Increased odds ratio (OR) were observed in males who consumed high levels of bacon, corned meats, apples, melons and oil. OR less than unity were observed in men consuming cabbage and cola drinks, and in women who consumed wholegrain bread, pasta, corned meat, bananas, cauliflower, broccoli, cola drinks and nuts. Generally, N‐nitroso associations were greater in men and micronutrient associations were greater in women. Elevated OR in men, but not women, were associated with the intake of N‐nitroso dimethylamine (NDMA), retinol and vitamin E. The intake of nitrate (largely of vegetable origin) was protective in women but not in men. When analyzed using multiple logistic regression, the association with NDMA intake in males was not modified by dietary micronutrient intakes. In females, beta carotene alone, though not directly associated with risk, modified the effect of NDMA. On balance, this study added only limited support to the N‐nitroso hypothesis of glial carcinogenesis. © 1994 Wiley‐Liss, Inc.
Oncostatin M, interleukin 2, interleukin 6 and interleukin 8 in breast cyst fluid
Authors: Lai Leslie C. , Kadory Sana , Siraj Abdul K. , Lennard Thomas W. J. 
Published: February 2007

AbstractWomen with breast cysts lined by apocrine epithelium (intracystic Na/K <3) may have a higher risk of developing breast cancer than those whose breast cysts are lined by “flattened” epithelium (intracystic Na/K <3). In this study, the concentrations of the cytokines, oncostatin M (OSM), interleukin 2 (IL‐2), interleukin 6 (IL‐6) and interleukin 8 (IL‐8) were measured in breast cyst fluid, OSM, IL‐2 and IL‐6 having been shown to have growth‐inhibitory actions on tumour cells. All cytokines were measured by “sandwich” enzyme immunoassays. IL‐2 was not detectable in breast cyst fluid. OSM, IL‐6 and IL‐8 concentrations were significantly higher in the high‐electrolyte‐ratio group. Although significant positive correlations were found between OSM and IL‐6, OSM and IL‐8, OSM and Na/K, IL‐6 and IL‐8, IL‐6 and Na/K and IL‐8 and Na/K when all samples were analysed together, analysis of the correlations between these analytes in each subgroup separately suggests that the control of production of these cytokines or the mechanism of entry into cyst fluid is likely to be different for the 2 cyst types. The significantly higher intracystic concentrations of OSM and IL‐6 in the high‐electrolyte‐ratio group may partly explain the lower risk of breast cancer in this group of women. © 1994 Wiley‐Liss, Inc.