bluuebunny/crossref_metadata_2025_split huggingface dataset:
Occupation and risk of hodgkin's disease in north‐east Italy
Authors: Franceschi Silvia , Serraing Diego , Bidoli Ettore , La Vecchia Carlo , Tirelli Umberto 
Published: February 2007

AbstractThe relationship between occupation and exposure to several occupational agents and Hodgkin's disease (HD) was investigated in a case‐control study of 152 cases and 613 controls with acute diseases admitted to all hospitals in Pordenone province, north‐east Italy. Among cases, there was a significant excess of individuals occupied in agriculture (odds ratio, OR for > 10 years = 2.2, 95% confidence interval, CI:1.3‐3.7), Who were exposed to livestock and meat processing (OR‐3.4, 95% CI:1.7‐6.6), herbicides and pesticides (OR = 3.2, 95% CI:1.6‐6.5). When the relationship between agriculture and specific exposures was assessed, it appeared that contact with some still unidentified animal‐related agent involved in livestock farming and meat processing may be at least as important in determining HD risk as exposure to herbicides and pesticides and, probably, more important than occupation in agriculture per se.
in vitro “progression” of bovine papillomavirus‐transformed cells: Loss of contact sensitivity after multiple rounds of selection
Authors: Naito A. , Kitamura Y. , Yoshikura H. , Sudoh K. 
Published: February 2007

AbstractThe transformed phenotype of C127 cells harboring bovine papillomavirus shuttle vector pdBPVMMTneo(342–12) was suppressed by direct contact with untransformed C127 cells. By repeated selections of rare foci developing on untransformed cell monolayers, we obtained a cellular clone of BPV transformants which formed foci on the untransformed C127 cells as efficiently as on plastic surface. The BPV genome in the mutant cells showed extensive genetic rearrangements, duplication of upstream regulatory region and deletion of pBR322‐derived sequence and its flanking. There was an increase in BPV transcripts per cell. Culture of the parental BPV‐transformant in contact with the untransformed C127 cells resulted in a marked reduction of the BPV transcripts, while in the case of the mutant transformant the reduction was much slighter. This indicates that the transcription level of the BPV genome was controlled by a cell‐cell contact signal.
Inhibition of DNA repair and the enhancement of cytotoxicity of alkylating agents
Authors: Frankfurt Oskar S. 
Published: February 2007

AbstractDNA damage was evaluated by flow cytometric (FCM) analysis of cells treated with L‐phenylalanine mustard (L‐PAM) and stained with anti‐DNA monoclonal antibody (MAb) F7–26. DNA damage was rapidly repaired, as indicated by the loss of DNA immunoreactivity after removal of L‐PAM. Two types of drug combinations were found to inhibit DNA repair. Combinations containing inhibitors of DNA polymerase (ara‐C, aphidicolin) or these inhibitors and hydroxyurea inhibited DNA repair in A2780/PAM and A549 cells. The inhibition of DNA repair by combinations of DNA‐damaging agents thloTEPA or cisplatln and DNA polymerase inhibitors is a novel observation based on the specificity of DNA damage assay with MAb F7–26. Combinations containing thioTEPA or cisplatin inhibited DNA repair in A549 but not in A2780/PAM cells. Drug combinations which inhibited DNA repair also significantly enhanced cell killing by L‐PAM. Cell survival in cultures treated with L‐PAM and efficient inhibitors was 2 to 3 orders of magnitude lower than was expected for additive survival. ThioTEPA and cisplatin play a dual role in combination chemotherapy by inducing DNA damage and inhibiting repair of DNA damage. FCM analysis of DNA repair may be a useful component of drug evaluation and could be applied to determine cell‐type specific sensitivity to inhibitors of DNA repair.
The interrelationship between the anti‐mitotic action of the somatostatin analog octreotide and that of cytostatic drugs and suramin
Authors: Lamberts S. W. J. , Van Koetsveld P. , Hofland L. J. 
Published: February 2007

AbstractIn the present study we used the model of cultured somatostatin‐receptor‐positive prolactin (PRL)‐secreting rat pituitary tumor cells to investigate the possible interrelationships between the anti‐mitotic and hormone‐release‐inhibitory effects of the somatostatin analog octreotide (SMS 201–955) and the effects of vincristine, methotrexate, fluo‐ uracil and suramin. Dose‐dependent inhibitory effects of all compounds were shown both on the DNA content and on PRL release. Octreotide and these cytostatic compounds were slightly additive in their anti‐proliferative and anti‐secretory effects. The somatostatin analog did not alter drug sensitivity in these tumor cells, however. The data obtained in this tumor model suggest that octreotide can be effectively administered in combination with cytostatic drugs and/or suramin.
Human papillomavirus infection and other risk factors for cervical neoplasia: A case‐control study
Authors: Morrison Ellen A. B. , Ho Gloria Y. F. , Vermund Sten H. , Goldberg Gary L. , Kadish Anna S. , Kelley Karen F. , Burk Robert D. 
Published: February 2007

AbstractA case control design has been used to investigate risk factors associated with the development of cervical squamous intraepithelial lesions (SIL) in a population of urban women in which non‐affluent minority groups were heavily represented. Eighty‐five women with histologically confirmed SIL were compared to a control group of 70 cytologically normal women. HPV infection was determined using both Southern blot hybridization and polymerase chain reaction (PCR) amplification specific for HPV types 16, 18, and 33. When Southern blot was used to detect HPV, logistic regression analysis identified HPV infection (odds ratio (OR) = 17.9, 95% confidence interval (CI) = 6.2‐51.6) and low educational achievement (OR = 3.4, 95% CI = 1.2‐10.1) as major independent risk factors. When PCR was employed to detect HPV, the logistic regression model suggested that HPV infection (OR = 10.4, 95% CI = 3.6‐30.4) and Hispanic ethnicity (OR = 5.0, 95% CI = 1.2‐20.5) represented independent risk factors; low educational achievement and Black ethnicity were risk factors of borderline significance. PCR detection of simultaneous co‐infection with more than one HPV type was associated with a very high risk of SIL (OR for one type = 7.2, 95% CI = 2.4‐21.9; OR for >1 type = 43.0, 95% CI = 6.9‐266.6). Furthermore, increased viral load determined by either method carried an increased risk of disease. HPV infection with viral types previously reported to be related to neo‐plastic or dysplastic lesions carried the highest risk of SIL. The association of HPV detected by Southern blot and SIL in women < 35 years old had an OR of 10.1, whereas in women ≦35 the OR was 74.5 (p = 0.09 for homogeneity of ORs). We conclude that infection with HPV is the major risk factor for cervical SIL and suggest that targeted HPV screening of women over age 35 may represent an innovative strategy to detect women at high risk of cervical neoplasia.
Functional characterization of tumor‐infiltrating lymphocytes, lymph‐node lymphocytes and peripheral‐blood lymphocytes from patients with breast cancer
Authors: Rubbert Andrea , Manger Bernhard , Lang Norbert , Kalden Joachim R. , Platzer Erich 
Published: February 2007

AbstractMononuclear cell infiltration is frequently seen within human solid tumors. Effector cells within the tumor site usually fail to exhibit cytotoxic or natural killer activity when freshly isolated; however, they develop potent and sometimes specific cytotoxicity after expansion in IL2. Thus, local tumor environment may influence lymphocyte function. In our study, we disaggregated human breast‐cancer and lymph‐node tissue to obtain lymphocyte‐enriched cell fractions. Besides phenotypic analysis, functional characterization with regard to proliferation and cytokine production of tumor‐infiltrating lymphocytes (TIL), peripheral‐blood lymphocytes (PBL) and lymph‐node lymphocytes (LNL) was the aim of our study. TIL showed an enrichment of CD8+ cells with a corresponding decrease in CD4+ cells in comparison with PBL and LNL. In response to PHA, TIL showed decreased 3H‐thymidine uptake, but TIL were significantly stimulated by rhlL2. TIL produced low levels of ID, TNF and IFNγ upon mitogen/phorbol ester stimulation, while PBL produce high levels of TNF and IFNγ but low levels of IL2. Under the same experimental conditions, LNL produce high levels of TNF and IL2 but low levels of IFNγ. Mitogen‐mediated TNF secretion was increased after addition of autologous tumor cells in TIL and LNL, whereas IFNγ secretion tended to be suppressed. Our results indicate different patterns of activities of TIL, LNL and PBL from breast‐cancer patients.
A population‐based case‐control study of endometrial cancer in shanghai, china
Authors: Shu Xiao‐Ou , Brinton Louise A. , Zheng Wei , Gao Yu Tang , Fan Jin , Fraumeni Joseph F. 
Published: February 2007

AbstractA case‐control study of 268 patients with endometrial cancer and 268 population controls was conducted during 1988–1990 in Shanghai, China, to evaluate etiologic factors in a population whose risk had not been substantially altered by the use of exogenous estrogens. In spite of this, the major risk factors resembled those found in other studies. The risk of endometrial cancer was significantly elevated among nulli‐gravidas (OR = 5.4, 95% CI = 2.0‐14.6) and decreased with number of pregnancies (p < 0.01). Late age at menopause was associated with increased risk, while early age at menarche was unrelated. Use of oral contraceptives for more than 2 years was associated with a reduction in endometrial cancer risk (OR = 0.4, 95% CI = 0.1‐1.2). while short‐term use of oral contraceptives and other methods of contraception were unrelated. Obesity was a strong predictor of risk, with women in the highest quartile of weight having 2.5 times the risk of those in the lowest quartile. In contrast to many other studies, cigarette smokers were at elevated risk (OR = 1.7. 95% CI = 0.9‐3.0). Risk was also elevated among women reporting a history of gall‐bladder disease, polycystic ovaries, menstrual symptoms, and non‐estrogen hormone use.
Pooled analysis of 3 european case‐control studies: I. Reproductive factors and risk of epithelial ovarian cancer
Authors: Negri Eva , Franceschi Silvia , Tzonou Anastasia , Booth Margaret , La Vecchia Carlo , Parazzini Fabio , Beral Valerie , Boyle Peter , Trichopoulos Dimitrios 
Published: February 2007

AbstractThe role of reproductive factors in the aetiology of epithelial ovarian cancer has been re‐assessed in a meta‐analysis of 3 hospital‐based case‐control studies conducted in Europe (i.e. Italy, the United Kingdom and Greece), providing a total dataset of 1,140 cases and 2,724 controls. Multiple logistic regression models were used to obtain relative risk (RR) estimates adjusted for study centre, age, socio‐cultural indicators, age at menopause, and oral contraceptive use. The risk decreased with increasing number of births and the trend in risk was significant (X = 7.50, p < 0.01). In comparison to nulliparous women, those who reported 4 or more births had a 40% reduction in risk of ovarian cancer (RR = 0.6, 95% confidence interval, CI: 0.4‐0.8). An RR estimate of 1.4 (95% CI: 1.1‐1.7) was found, overall, for age of 35 or more at first birth compared to age of 25 or less at first birth. In each stratum and overall, nulliparous women did not appear to be at increased risk compared to those who delayed birth of their first child until age 35 or more. In each study, as well as in the overall dataset, an inverse association between number of abortions and ovarian cancer risk emerged. Overall, the inverse relationship was highly significant, RR estimates for 1 and 2 or more abortions, as compared to none, being 0.9 (95% CI: 0.8 and 1.1) and 0.7 (95% CI: 0.60.9) respectively. The effects of parity, age at first birth and number of abortions emerged consistently in various strata of study centre and age.
Derivatives of butyric acid as potential anti‐neoplastic agents
Authors: Rephaeli Ada , Rabizadeh Ester , Aviram Adina , Shaklai Mati , Ruse Margaretta , Nudelman Abraham 
Published: February 2007

AbstractA novel derivative of butyric acid, pivalyloxymethyl butyrate (AN‐9) has been shown, in vitro, to: (a) induce cytodifferentiation and inhibit the proliferation of leukemic cells; (b) inhibit the growth and formation of Lewis lung carcinoma colonies in semi‐solid agar. AN‐9 affect cells at about 10‐fold lower concentration and at a faster rate than does butyric acid. The pivalyloxymethyl esters of propionic, isobutyric and valeric acids do not elicit effects similar to those of AN‐9, while the isobutyryloxymethyl butyrate does, which strongly suggests that the activity of AN‐9 stems from intracellular metabolic degradation of the pro‐drug to butyric acid. In vivo, AN‐9, increased the survival of mice in Lewis lung carcinoma primary cancer model and significantly decreased the number of lung lesions of the animals inoculated with highly meta‐static cells, but did not affect their life span. Acute LD50, studies have shown that AN‐9 possesses low toxicity. These results suggest that AN‐9 is a potential anti‐neoplastic agent ar well as a tool for investigation of the differentiation induction mechanism.
Epidermal growth factor reduces resistance to doxorubicin
Authors: Kwok Tim T. , Sutherland Robert M. 
Published: February 2007

AbstractEpidermal growth factor (EGF) increased the sensitivity to doxorubicin (DOX) of a human squamous carcinoma cell line, A431. The relative enhancement of sensitivity by EGF was greater in 2 DOX‐resistant sublines, A431/A5 and A431/A10, established by growing cells from surviving colonies after treatment of A43I cells with DOX. A greater number of EGF receptors (both high‐ and low‐affinity binding sites) was found for resistant A431/A5 and A431/A10 cells than for parental cells. The enhanced drug responsiveness is not directly related to EGF effects on growth, as growth inhibition by EGF appears to be similar among the 3 sublines.
Induction of mammary adenocarcinomas in metallothionein promoter‐human growth hormone transgenic mice
Authors: Törnell Jan , Rymo Lars , Isaksson Olle G. P. 
Published: February 2007

AbstractTo develop transgenic mice, a mouse metallothionein promoter–human growth hormone (Mt‐hGH) gene fragment was injected into the pronucleus of C57BI × DBN/2J F2 one‐cell embryos. Six founder animals grew larger (1.3‐2.2 times) than littermate controls and had higher levels of hGH in plasma (4.6‐279 mU/I). At 27‐43 weeks of age, 3 of the 4 female transgenic founders developed malignant papillary adenocarcinomas of mammary origin. One of the male trantgenic founders was successfully mated and 2 of 3 female transgenic offspring developed mammary tumors. Forty‐two female mice with the same genetic background as the transgenic animals and older than 43 weeks served as controls. No palpable tumor was found in this group. Five of the control animals were killed and examined histologically, revealing only normal mammary tissue. Earlier studies have shown that GH is important for growth and development of the mammary gland. Our study suggests that markedly elevated endogenous levels of GH cause mammary carcinoma in a specific strain of transgenic mice. The present animal model might be useful for studying molecular mechanisms that are involved in the development of hormonally induced mammary tumors.
Characterization of the new bladder cancer cell line HOK‐I: Expression of transitional, squamous and glandular differentiation patterns
Authors: Offner Felix Albert , Ott German , Povey Susan , Knuechel Ruth , Preisler Verena , Fuezesi Laszlo , Klosterhalfen Bemd , Ruebben Herbert , Hofstaedter Ferdinand , Kirkpatrick Charles James 
Published: February 2007

AbstractThe new continuous cell line HOK‐I derived from a grade‐III transitional‐cell bladder carcinoma with foci of squamous and glandular differentiation was shown to retain this pheno‐typical heterogeneity for more than 45 passages in vitro. Electron microscopy revealed transitional as well as a considerable proportion of squamous carcinoma and adenocarcinoma cells. PAS‐positive mucus was detected in numerous cells. These features were principally maintained when grown as multicellular spheroids and in nude mice. More pronounced signs of differentiation (i.e., expression of cytokeratins 10 and 11, formation of glandular structures) were found in xenograft tumours. Independently, cytokeratins 13, 18 and 19 were detected in vitro and in vivo, reflecting the urothelial origin. The line forms distinct colonies in soft agar, expresses Lewis‐x and Lewis‐y antigens and reacts with monoclonal antibodies (MAbs) against CEA, β‐HCG and URO‐5. Cytogenetic analysis revealed several related clones with a rearrangement at chromosome I and loss of one X chromosome as common karyotypic changes in all clones. DNA content, as quantified by image analysis, showed a DNA stemline close to 2c. The new cell line HOK‐I can be used as an in vitro model to study the mechanisms of heterogeneous differentiation patterns in bladder cancer.
Nad(P)H:Quinone oxidoreductase (DT‐Diaphorase) activity and mRNA content in normal and neoplastic mouse lung epithelia
Authors: Thaete Larty G. , Siegel David , Malkinson Alvin M. , Forrest Gerald L. , Ross David 
Published: February 2007

AbstractDT‐diaphorase (DTD) is a flavoprotein which catalyzes obligate two‐electron reduction of a diverse group of substrates. We have reported previously that non‐tumorigenic mouse lung alveolar type‐II pneumocytes have high DTD activity, while cell lines derived from lung tumors do not. In contrast, other investigators, using human lung tissue, reported increased DTD activity in tumors compared with normal tissue. We therefore investigated DTD associated with mouse lung neoplasia in vivo as well as in vitro. Pulmonary tumors had far less DTD activity compared with normal mouse lung. Correspondingly, a tumorigenic mouse lung cell line which arose as a spontaneous transformant of a normal cell line had very low DTD activity compared with non‐tumorigenic lung cells. DTD‐specific mRNA levels were also much higher in normal cell lines than in neoplastic ones. DTD was localized histo‐chemically in type‐ll pneumocytes in situ, but was not observed by this technique in normal bronchiolar epithelia or in tumor cells. These data show that, unlike what has been observed in human lung cancer, a marked decrease in DTD content and activity accompanied mouse lung tumorigenesis in vivo and neoplastic transformation in vitro.
Incidence and prognostic significance of vascular invasion in 529 gastric‐cancer patients
Authors: Gabbert H. E. , Meier S. , Gerharz C. D. , Hommel G. 
Published: February 2007

AbstractThe prognostic significance of blood‐vessel invasion (BVI) and lymphatic‐vessel invasion (LVI) was evaluated in a retrospective series of 529 gastric‐cancer patients who underwent potentially curative surgery. Evidence for BVI was found in 127 patients (24.0%), while LVI was demonstrated in 245 patients (46.3%). The incidence of both BVI and LVI run parallel to increasing tumor size and tumor stage as well as to decreasing grade of tumor differentiation. The incidence of BVI and LVI was higher in lymph‐node‐positive patients than in lymph‐node‐negative patients. The 5‐year‐survival rate was significantly lower (p < 0.0001) in patients with BVI or LVI (14.9% and 22.2% respectively) than in patients without BVI or LVI (54.7% and 64.1% respectively). Both BVI and LVI were shown to be prognostic factors independent of tumor stage, grade of differentiation or lymph‐node involvement. In a multivariate Cox regression analysis, the gain of prognostic information provided by the evidence of BVI and LVI was shown to exceed the information obtained by the combination of tumor stage, grade of differentiation and lymph‐node involvement. A careful search for vascular invasion in gastric cancer may therefore provide additional useful information for identifying patients who are at high risk and who may be candidates for adjuvant therapy in future clinical trials.
Leanness and lung‐cancer risk
Authors: Knekt Paul , Heliövaara Markku , Rissanen Aila , Aromaa Arpo , Seppänen Ritva , Teppo Lyly , Pukkala Eero 
Published: February 2007

AbstractBody mass index (weight/height2) was studied for its prediction of lung cancer in Finnish men examined by the Social Insurance Institution's Mobile Clinic and followed up by the Finnish Cancer Registry. Among 25,994 participants aged 20 to 75 years and free from cancer at the start of the study, 504 lung‐cancer cases were diagnosed during a maximum follow‐up of 19 years. There was a significant inverse gradient between body mass index and the incidence of lung cancer. This association was not due to confounding by age, smoking, social class, self‐perceived general health, history of stress symptoms, chronic cough or chest X‐ray findings, although these factors correlated with body mass index and were also significantly predictive of lung cancer. After adjustment for these factors, the relative risks of lung cancer were 1.0, 1.4, 1.5 and 1.8 (pfor trend < 0.001) from the highest to the lowest quartiles of body mass index. The association was noted among current smokers, but it was most obvious among men who had never smoked, the relative risk of lung cancer between the lowest and highest quartiles of body mass index being 7.6 (95% confidence interval = 2.0 to 29.4). The inverse gradient persisted throughout the entire follow‐up period, and was most distinct after the first 10 years of follow‐up, the relative risks for the quartiles of body mass index being 1.0, 1.9, 2.3 and 2.6 (p< 0,001). The present study shows that the thinner the man, the more liable he is to develop lung cancer. Leanness, or some factor or cluster of factors closely correlated to it, may play an aetiological role in lung cancer.
The biological effects of macrophage‐colony‐stimulating factor induced by progestin on growth and differentiation of endometrial adenocarcinoma cells
Authors: Kimura Tadashi , Azuma Chihiro , Saji Fumitaka , Tokugawa Yoshihio , Takemura Masahiko , Miki Mariko , Ono Masaaki , Tanizawa Osamu 
Published: February 2007

AbstractProgestins have biological effects of regression and differentiation on human endometrial adenocarcinoma. We investigated the effects of progestin on the induction of macrophage‐colony‐stimulating factor (M‐CSF) and its receptor messenger RNAs in the human endometrial adenocarcinoma cell line Ishikawa which has receptors for both estrogen and progesterone. Poly(A)+RNA extracted from lshikawa cells cultured with or without synthetic progestin R5020 was subjected to Northern blot hybridization using M‐CSF and c‐fms cDNA probes. The expression of M‐CSF mRNA in Ishikawa cells increased about 2.3 times following treatment with R5020 at 10−7 M. Induction of M‐CSF mRNA by RS020 was antagonized by anti‐progestin RU486 in a dose‐dependent manner. However, c‐fms mRNA, coding the M‐CSF receptor, was expressed constitutively in Ishikawa cells and its expression was not affected by hormonal treatment. We further examined the biological effects of M‐CSF on endometrial cancer cells. Colony formation of Ishikawa cells in soft agar, which represents anchorage‐independent cell growth, was inhibited by M‐CSF treatment. On the other hand, accumulation of glycogen granules in cytoplasm detected by periodicacid‐Schiff staining was observed in lshikawa cells treated with M‐CSF. These results indicate that M‐CSF, whose gene expression was enhanced by progestin, suppressed growth and induced differentiation of endometrial adenocarcinoma cells. These effects of M‐CSF on endometrial cancer cells are similar to those of progestins, so the effects of progestins on these cells are, at least in part, probably mediated by M‐CSF in an autocrine or paracrine manner.