bluuebunny/crossref_metadata_2025_split huggingface dataset:
Risk factors for squamous intraepithelial lesions (SIL) of the cervix among women residing at the US‐Mexico border
Authors: Giuliano Anna R. , Papenfuss Mary , Mendez Brown de Galaz Elena , Feng Janine , Abrahamsen Martha , Denman Catalina , Guernsey de Zapien Jill , Navarro Henze Jose Luis , Garcia Francisco , Hatch Kenneth 
Published: January 2004

AbstractIt is now well established that cervical cancer is caused by oncogenic human papillomavirus (HPV) infections that commonly infect women worldwide. What remains to be understood are the factors that contribute to cervical cancer in the presence of HPV infection. We conducted a case‐control analysis of women recruited at the US‐Mexico border to simultaneously evaluate factors associated with 3 cytologic outcomes: atypical squamous cells of undetermined significance or atypical glandular cells of undetermined significance (ASCUS/AGUS), low grade squamous intraepithelial lesions (LSIL) and high grade squamous intraepithelial lesions (HSIL). A cross‐sectional binational study of 2,059 women ages 15–79 years was conducted between 1997 and 1998. A significant difference in the distribution of cytologic categories by country was observed (3.0% vs. 0.7% HSIL among Mexican vs. US women, respectively). The only factors independently associated with all 3 cytologic outcomes were HPV infection and viral load. A linear increase in risk with increasing viral load was observed for each of the 3 outcome variables, with the strength of this association increasing with cytology abnormality. In addition to HPV infection, parity and Mexico as a country of residence appear to be associated with LSIL and HSIL, respectively. Factors associated with cytologic outcomes in analyses limited to women with HPV infection were similar to results obtained in models where HPV infection was included as a covariate. Future work is needed to evaluate the predictive value of HPV viral load utilizing more specific and quantitative measures. © 2003 Wiley‐Liss, Inc.
DNA polymerase θ is preferentially expressed in lymphoid tissues and upregulated in human cancers
Authors: Kawamura Kiyoko , Bahar Rumana , Seimiya Mika , Chiyo Masako , Wada Akihiko , Okada Seiji , Hatano Masahiko , Tokuhisa Takeshi , Kimura Hideki , Watanabe Satoshi , Honda Ichiro , Sakiyama Shigeru , Tagawa Masatoshi , O‐Wang Jiyang 
Published: January 2004

AbstractDNA polymerase θ (Pol θ) is a recently identified family A polymerase that contains an intrinsic helicase domain. Drosophila Pol θ mutants are hypersensitive to bifunctional DNA crosslinking agents and exhibit an elevated frequency of spontaneous chromosomal aberrations, suggesting a role for Pol θ in repair of DNA interstrand crosslinks and in the general maintenance of genome stability. To investigate a possible involvement of Pol θ in tumorigenesis, we have examined its expression in various normal and malignant tissues. Paired tumor and adjacent nontumorous tissues from patients with lung (n = 27), stomach (n = 28) and colon (n = 26) cancer, as well as 26 normal human tissues, were examined for Pol θ expression by RT‐PCR, Northern or Western blot analysis. Pol θ was predominantly expressed in primary lymphoid organs including the fetal liver, thymus and bone marrow where lymphocyte progenitors undergo V(D)J rearrangements of their antigen receptor genes. In addition, Pol θ expression was upregulated in germinal center B cells, in which class switch recombination of the immunoglobulin genes occurs. Examination of Pol θ expression in matched cancer specimens revealed that Pol θ was barely detectable in the nontumorous tissues but was upregulated in 17 of 27 (63%) lung, 11 of 28 (39%) stomach and 20 of 26 (77%) colon cancers. Moreover, patients with high levels of Pol θ expression had a significantly poorer clinical outcome compared with those expressing low levels of Pol θ. These results implicate that Pol θ may have a specialized function in lymphocytes and that its overexpression may contribute to tumor progression. © 2003 Wiley‐Liss, Inc.
Obesity and colon cancer: Does leptin provide a link?
Authors: Stattin Pär , Lukanova Annekatrin , Biessy Carine , Söderberg Stefan , Palmqvist Richard , Kaaks Rudolf , Olsson Tommy , Jellum Egil 
Published: January 2004

AbstractObesity, a risk factor for colorectal cancer, is associated with elevated serum levels of leptin, the adipocyte‐derived hormone, and insulin. Experimental and epidemiologic studies have indicated a role for insulin in the pathogenesis of colon cancer, and recent experimental studies have suggested a similar role for leptin. In a case‐control study nested in the Janus Biobank, Norway, we measured serum levels of leptin and C‐peptide (a marker of pancreatic insulin secretion) in cryopreserved prediagnostic sera from men (median age, 45 years) who were diagnosed with cancer of the colon (n = 235) or rectum (n = 143) after blood collection (median time, 17 years), and among 378 controls matched for age and date of blood collection. Conditional logistic regression analyses showed an approximately 3‐fold increase in colon cancer risk with increasing concentrations of leptin up to an odds ratio (OR) of 2.72 (95% CI = 1.44–5.12) for top vs. bottom quartile (ptrend = 0.008). The corresponding OR for C‐peptide was 1.81 (95% CI = 0.67–4.86; ptrend = 0.19). The risk estimates remained unchanged after mutual adjustment. No association of hormone levels with rectal cancer risk was found. Reproducibility of hormone measurements assessed by intraclass coefficients (ICCs) for paired samples taken 1 year apart was high for leptin (ICC = 0.82) but lower for C‐peptide (ICC = 0.30). Our results suggest that leptin is a risk factor for colon cancer, and that leptin may provide a link between obesity and colon cancer. Leptin may be directly involved in colon tumorigenesis or it may serve as a sensitive and robust marker of an obesity‐induced adverse endocrine environment. Only weak support for an association of insulin with colon cancer was found. © 2003 Wiley‐Liss, Inc.
Fruits and vegetables and prostate cancer: No association among 1,104 cases in a prospective study of 130,544 men in the European Prospective Investigation into Cancer and Nutrition (EPIC)
Authors: Key Timothy J. , Allen Naomi , Appleby Paul , Overvad Kim , Tjønneland Anne , Miller Anthony , Boeing Heiner , Karalis Dimitrios , Psaltopoulou Theodora , Berrino Franco , Palli Domenico , Panico Salvatore , Tumino Rosario , Vineis Paolo , Bueno‐de‐Mesquita H.B. , Kiemeney Lambertus , Peeters Petra H.M. , Martinez Carmen , Dorronsoro Miren , González Carlos A. , Chirlaque M.D. , Quiros J. Ramon , Ardanaz Eva , Berglund Göran , Egevad Lars , Hallmans Göran , Stattin Pär , Bingham Sheila , Day Nicholas , Gann Peter , Kaaks Rudolf , Ferrari Pietro , Riboli Elio 
Published: January 2004

AbstractWe examined the association between self‐reported consumption of fruits and vegetables and prostate cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Data on food consumption and complete follow‐up for cancer incidence were available for 130,544 men in 7 countries recruited into EPIC between 1993 and 1999. After an average of 4.8 years of follow‐up, there were 1,104 incident cases of prostate cancer. The associations of consumption of total fruits, total vegetables, cruciferous vegetables and combined total fruits and vegetables with prostate cancer risk were examined using Cox regression, stratified for recruitment center and adjusted for height, weight and energy intake. There was a wide range in consumption of fruits and vegetables: mean intakes (g/day) in the bottom and top fifths of the distribution, as estimated from 24‐hr recalls in a subsample of participants, were 53.2 and 410.7 for fruits, 97.1 and 242.1 for vegetables and 169.0 and 633.7 for fruits and vegetables combined. No significant associations between fruit and vegetable consumption and prostate cancer risk were observed. Relative risks (95% confidence intervals) in the top fifth of the distribution of consumption, compared to the bottom fifth, were 1.06 (0.84–1.34) for total fruits, 1.00 (0.81–1.22) for total vegetables and 1.00 (0.79–1.26) for total fruits and vegetables combined; intake of cruciferous vegetables was not associated with risk. These results suggest that total consumption of fruits and vegetables is not associated with the risk for prostate cancer. © 2003 Wiley‐Liss, Inc.
Cyclin E expression in papillary thyroid carcinoma: Relation to staging
Authors: Brzeziński Jan , Migodziński Adam , Gosek Aleksandra , Tazbir Józef , Dedecjus Marek 
Published: January 2004

AbstractCyclin E plays a pivotal role in the regulation of G1‐S transition and relates to malignant transformation of the cells. However, the clinical significance of cyclin E expression in patients with papillary thyroid carcinoma (PTC) remains unknown. We examined by immunohistochemistry the expression of cyclin E in 41 resected PTCs in pathologic stages from pT1a to pT4 and analyzed its relation to clinicohistopathologic factors. The positive staining was divided into 3 grades: no expression if less than 10%, expression if 11–50% and overexpression if more than 50% of the nuclei of tumor cells were stained positively. Cylin E expressions were observed in 75.6% of analyzed PTCs but only 60% of papillary microcarcinomas (PMCs) were immunopositive for cyclin E expression. However, cyclin E staining was observed in 90.4% of PTCs in a group with TNM higher than pT1a. The staining index was significantly different between the PMCs and the rest of the cancers investigated (14.91% ± 14.4% vs. 34.03% ± 23.44%, respectively; p < 0.005) and we observed positive relation between the staining index and factor T of staging of PTCs. All the lymph node metastases coexisted with cyclin E expression and most, but not all, of them coexisted with cyclin E overexpression. These findings indicate that cyclin E may play a key role for the oncogenesis and biologic behavior of PTC. If our results are confirmed in a larger study, a high level of cyclin E expression may become a new prognostic marker for PTCs. © 2003 Wiley‐Liss, Inc.
Bcl‐xL inhibits p53‐ but not apoptin‐induced apoptosis in head and neck squamous cell carcinoma cell line
Authors: Schoop Remilio A.L. , Kooistra Klaas , Baatenburg de Jong Robert J. , Noteborn Mathieu H.M. 
Published: January 2004

AbstractNonfunctional p53 and especially upregulation of Bcl‐xL result in advanced disease and poor prognosis of patients suffering head and neck squamous cell carcinoma (HNSCC). Aberrancies of Bcl‐xL and/or p53 in HNSCC lead to inability of anticancer drugs to induce apoptosis. Bcl‐xL and/or mutated p53 inhibit the apoptotic process by preventing the mitochondrial release of cytochrome c and/or activation of execution caspases. Here, we report that expression of the avian virus‐derived apoptin protein resulted in induction of apoptosis in the HNSCC‐derived cell line UMSSC‐14B despite the presence of nonfunctional p53. Apoptin activated the execution caspase 3 and induced the release of mitochondrial cytochrome c. Upregulation of Bcl‐xL in UMSCC‐14B cells did not interfere with the apoptin‐induced apoptosis, whereas it clearly negatively affected the p53‐induced one. Bcl‐xL significantly decreased the p53‐induced cytochrome c release, but not the apoptin‐triggered one. Our data demonstrate that apoptin induces apoptosis independent of Bcl‐xL and p53 and may constitute a potential therapeutic agent for treatment of HNSCC. © 2003 Wiley‐Liss, Inc.
Expression profile of genes associated with antimetastatic gene: nm23‐Mediated metastasis inhibition in breast carcinoma cells
Authors: Zhao Hui , Jhanwar‐Uniyal Meena , Datta Prasun K. , Yemul Srishailam , Ho Lap , Khitrov Gregory , Kupershmidt Ilya , Pasinetti Giulio M. , Ray Tarun , Athwal Raghbir S. , Achary Mohanrao P. 
Published: January 2004

AbstractMetastases of various malignancies have been shown to be inversely related to the abundance of nm23 protein expression. However, the downstream pathways involved in nm23‐mediated suppression of metastasis have not been elucidated. In the present investigation, we used cDNA microarrays to identify novel genes and functional pathways in nm23‐mediated spontaneous breast metastasis. Microarray experiments were performed in a pair of cell lines, namely, C‐100 (only vector transfected; highly metastatic) and H1‐177 (nm23 transfected; low metastatic), derived from human mammary carcinoma cell line MDA‐MB‐435. The cDNA microarray analysis using GeneSpring software revealed significant as well as consistent alterations in the expression (up‐ and downregulation) of 2,158 genes in a total of 18,889 genes between high and low metastatic cells. Some of these genes were grouped into 6 functional categories, namely, invasion and metastasis, apoptosis and senescence, signal transduction molecules and transcription factors, cell cycle and repair, adhesion, and angiogenesis to extrapolate an association between these genes and different functional pathways involved in nm23‐regulated metastasis. The results suggest that nm23 gene plays a major role in metastasis and its mechanism of action of metastasis suppression may involve downregulation of genes associated with cell adhesion, motility (integrins α2, ‐8, ‐9, ‐L and ‐V, collagen type VIII α1, fibronectin 1, catenin, TGF‐β2, FGF7, MMP14 and 16, ErbB2) and possibly certain tumor/metastasis suppressors (2 members of SWI/SNF‐related matrix‐associated proteins 2 and 5 and PTEN). © 2003 Wiley‐Liss, Inc.
Expression of LDL receptor‐related protein 5 (LRP5) as a novel marker for disease progression in high‐grade osteosarcoma
Authors: Hoang Bang H. , Kubo Tadahiko , Healey John H. , Sowers Rebecca , Mazza BethAnne , Yang Rui , Huvos Andrew G. , Meyers Paul A. , Gorlick Richard 
Published: January 2004

AbstractThe Wingless‐type (Wnt) family of proteins and its coreceptor LRP5 have recently been implicated in human skeletal development. Wnt pathway modulates cell fate and cell proliferation during embryonic development and carcinogenesis through activation of receptor‐mediated signaling. Osteosarcoma (OS) is a bone‐forming tumor of mesenchymal origin whose growth control has been linked to autocrine or paracrine stimulation by several growth factor families. We examined 4 OS cell lines for WNT1, WNT4, WNT5A, WNT7A, WNT11, FZD1‐10 and LRP5 expression by reverse transcription polymerase chain reaction (RT‐PCR). In addition, RT‐PCR for LRP5 expression was performed in 44 OS patient samples and the findings were correlated with clinical data. Expression profiling of Wnts and their receptors revealed the presence of several isoforms in OS cell lines. Overall, 22/44 (50%) of OS patient samples showed evidence of LRP5 expression. Presence of LRP5 correlated significantly with tumor metastasis (p = 0.005) and the chondroblastic subtype of OS (p = 0.045). In addition, patients whose tumors were positive for LRP5 showed a trend toward decreased event‐free survival (p = 0.066). No significant association was found between LRP5 expression and age, gender, site of disease, site of metastasis or degree of chemotherapy‐induced tumor necrosis. Sequencing of exon 3 of LRP5 in 10 OS patient‐derived cell cultures showed no activating mutation of LRP5. These results showed that expression of LRP5 is a common event in OS and strongly suggest a role for LRP and Wnt signaling in the pathobiology and progression of this disease. © 2003 Wiley‐Liss, Inc.
Progression of chronic atrophic gastritis associated with Helicobacter pylori infection increases risk of gastric cancer
Authors: Ohata Hiroshi , Kitauchi Shintaro , Yoshimura Noriko , Mugitani Kouichi , Iwane Masataka , Nakamura Hideya , Yoshikawa Akiyoshi , Yanaoka Kimihiko , Arii Kenji , Tamai Hideyuki , Shimizu Yasuhito , Takeshita Tatsuya , Mohara Osamu , Ichinose Masao 
Published: January 2004

AbstractWe conducted a longitudinal cohort study to determine the association of Helicobacter pylori infection and the progression of chronic atrophic gastritis (CAG) with gastric cancer. A cohort of 4,655 healthy asymptomatic subjects was followed for a mean period of 7.7 years. H. pylori infection was established by serum specific antibodies and the presence of CAG was confirmed by serum pepsinogen. During the follow‐up period, 45 gastric cancer cases were detected (incidence rate, 126/100,000 person‐years). A univariate analysis after adjustment for age showed that both H. pylori and CAG were significantly associated with gastric cancer. To clarify the interaction between H. pylori and CAG, an analysis stratified by H. pylori‐ and CAG–status was performed. No cancer developed in the H. pylori(−)/CAG(−) group during the study period. This supports the theory that it is quite rare for any type of gastric cancer to develop in an H. pylori‐free healthy stomach. With the progression of H. pylori‐induced gastritis, the risk of gastric cancer increased in a stepwise fashion from CAG‐free gastritis [H. pylori(+)/CAG(−) group] (HR=7.13, 95%CI=0.95‐53.33) to CAG [H. pylori(+)/CAG(+) group] (HR=14.85, 95%CI=1.96–107.7) and finally to severe CAG with extensive intestinal metaplasia [H. pylori(−)/CAG(+) group] (HR=61.85, 95%CI=5.6–682.64) in which loss of H. pylori from the stomach is observed. Therefore, it is probable that H. pylori alone is not directly associated with stomach carcinogenesis. Instead, H. pylori appears to influence stomach carcinogenesis through the development of CAG. The observed positive correlation between the extent of H. pylori‐induced gastritis and the development of cancer was strong, especially for the intestinal type. These results are compelling evidence that severe gastritis with extensive intestinal metaplasia is a major risk factor for gastric cancer, and they confirm the previously described model of stomach carcinogenesis: the gastritis‐metaplasia‐carcinoma sequence. © 2003 Wiley‐Liss, Inc.
Secondhand smoke exposure in adulthood and risk of lung cancer among never smokers: A pooled analysis of two large studies
Authors: Brennan Paul , Buffler Patricia A. , Reynolds Peggy , Wu Anna H. , Wichmann H. Erich , Agudo Antonio , Pershagen Göran , Jöckel Karl‐Heinz , Benhamou Simone , Greenberg Raymond S. , Merletti Franco , Winck Carlos , Fontham Elizabeth T.H. , Kreuzer Michaela , Darby Sarah C. , Forastiere Francesco , Simonato Lorenzo , Boffetta Paolo 
Published: January 2004

AbstractThe interpretation of the evidence linking exposure to secondhand smoke with lung cancer is constrained by the imprecision of risk estimates. The objective of the study was to obtain precise and valid estimates of the risk of lung cancer in never smokers following exposure to secondhand smoke, including adjustment for potential confounders and exposure misclassification. Pooled analysis of data from 2 previously reported large case‐control studies was used. Subjects included 1,263 never smoking lung cancer patients and 2,740 population and hospital controls recruited during 1985–1994 from 5 metropolitan areas in the United States, 11 areas in Germany, Italy, Sweden, United Kingdom, France, Spain and Portugal. Odds ratios (ORs) of lung cancer were calculated for ever exposure and duration of exposure to secondhand smoke from spouse, workplace and social sources. The OR for ever exposure to spousal smoking was 1.18 (95% CI = 1.01–1.37) and for long‐term exposure was 1.23 (95% CI = 1.01–1.51). After exclusion of proxy interviews, the OR for ever exposure from the workplace was 1.16 (95% CI = 0.99–1.36) and for long‐term exposure was 1.27 (95% CI = 1.03–1.57). Similar results were obtained for exposure from social settings and for exposure from combined sources. A dose‐response relationship was present with increasing duration of exposure to secondhand smoke for all 3 sources, with an OR of 1.32 (95% CI = 1.10–1.79) for the long‐term exposure from all sources. There was no evidence of confounding by employment in high‐risk occupations, education or low vegetable intake. Sensitivity analysis for the effects of misclassification (both positive and negative) indicated that the observed risks are likely to underestimate the true risk. Clear dose‐response relationships consistent with a causal association were observed between exposure to secondhand smoke from spousal, workplace and social sources and the development of lung cancer among never smokers. © 2003 Wiley‐Liss, Inc.
Risk of lung cancer and residential radon in China: Pooled results of two studies
Authors: Lubin Jay H. , Wang Zuo Yuan , Boice John D. , Xu Zhao Yi , Blot William J. , De Wang Long , Kleinerman Ruth A. 
Published: January 2004

AbstractStudies of radon‐exposed underground miners predict that residential radon is the second leading cause of lung cancer mortality; however, case‐control studies of residential radon have not provided unambiguous evidence of an association. Owing to small expected risks from residential radon and uncertainties in dosimetry, large studies or pooling of multiple studies are needed to fully evaluate effects. We pooled data from 2 case‐control studies of residential radon representing 2 large radon studies conducted in China. The studies included 1,050 lung cancer cases and 1,996 controls. In the pooled data, odds ratios (OR) increased significantly with greater radon concentration. Based on a linear model, the OR with 95% confidence intervals (CI) at 100 Becquerel/cubic‐meter (Bq/m3) was 1.33 (1.01,1.36). For subjects resident in the current home for 30 years or more, the OR at 100 Bq/m3 was 1.32 (1.07,1.91). Results across studies were consistent with homogeneity. Estimates of ORs were similar to extrapolations from miner data and consistent with published residential radon studies in North American and Europe, suggesting long‐term radon exposure at concentrations found in many homes increases lung cancer risk. © 2003 Wiley‐Liss, Inc.
Prognosis of dermal lymphatic invasion with or without clinical signs of inflammatory breast cancer
Authors: Gruber Guenther , Ciriolo Michele , Altermatt Hans Joerg , Aebi Stefan , Berclaz Gilles , Greiner Richard H. 
Published: January 2004

AbstractIt is still an open debate whether tumor emboli in dermal lymphatics without inflammatory signs represent a similar bad prognosis like inflammatory breast cancer. We evaluated the prognostic role of dermal lymphatic invasion (DLI) in breast cancer with (DLI + ID) or without (DLI w/o ID) inflammatory disease (ID). From August 1988 to January 2000, 42 patients with DLI were irradiated. Twenty‐five were classified as pT4, 13 out of them as pT4d (inflammatory disease); the 17 remaining patients had 1 T1c, 12 T2 and 4 T3 cancers with DLI. Axillary dissection revealed node‐positive disease in 39/41 patients (median, 9 positive nodes). Thirty‐eight out of 42 patients received adjuvant systemic treatment(s). After a mean follow‐up of 33 months, 22/42 patients (52%) are disease‐free. The actuarial 3‐year disease‐free survival is 50% (DLI w/o ID, 61%; DLI + ID, 31%; p < 0.03); the corresponding overall survival was 69% (DLI w/o ID, 87%; DLI + ID, 37%; p = 0.005). The presence or absence of ID was the only significant parameter for all endpoints in multivariate analyses. Dissemination occurred in 19 (45%), local relapse in 7 (n = 17%) and regional failure in 4 (10%). Nine patients (21%) had contralateral breast cancer/relapse. Despite the same histopathologic presentation, DLI w/o ID offered a significantly better disease‐free survival and overall survival than ID. The finding of dermal lymphatic tumor invasion predicts a high probability for node‐positive disease. © 2003 Wiley‐Liss, Inc.