bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prediction of Rotator Cuff Repair Failure by Histological Analysis
Authors: Matthews Timothy , Brinsden Mark , Athanasou Nicolas , Rees Jonathan , Carr Andrew 
Published: June 2009

Background We aimed to determine if recognised histological features seen in specimens taken during rotator cuff repair could predict which tendon repairs were at risk of re-rupture. Methods Forty rotator cuff tendon edge specimens from 40 patients were analysed histologically following routine mini-open rotator cuff repair. Thirty-two patients returned at a mean follow up of 35 months for an ultrasound examination to determine repair integrity. Results Overall there were 8 small tears, 13 medium tears, 15 large tears and 4 massive tears. Of the 32 patients followed up with ultrasound scan (USS) the overall re-rupture rate was 46%. Small and medium tears had a re-rupture rate of 35% while 60% of the large and massive tears suffered a re-rupture. Comparison of histological features and repair integrity revealed that the rotator cuff repairs which remained intact demonstrated a greater reparative response, in terms of increased fibroblast cellularity, cell proliferation and a thickened synovial membrane, than those repairs that re-ruptured. The larger tears that did remain intact also showed a higher degree of vascularity and a significant inflammatory component than the larger tears that re-ruptured. Conclusion These results indicate the importance of good tissue quality at the time of surgery but that larger tears can heal if the tissue quality is favourable. Post-operative histological analysis of tendon tear edge can aid prognosis and has the potential to guide post-operative immobilization and subsequent physiotherapy.
A Prospective Randomized Placebo Controlled Clinical Trial of a Rehabilitation Programme for Patients with a Diagnosis of Massive Rotator Cuff Tears of the Shoulder
Authors: Ainsworth Roberta , Lewis Jeremy , Conboy Veronica 
Published: June 2009

Background This article compares an exercise regime with a control treatment for the physiotherapy management of patients with massive rotator cuff tears. Methods The study design was a randomized placebo controlled trial of 60 patients with radiologically confirmed massive rotator cuff tears evaluating the change from baseline to 3 months, 6 months and 12 months in shoulder function. The primary outcome measure was the Oxford shoulder score. Results Both the control and the intervention groups had an improvement in their Oxford shoulder scores at 3 months, 6 months and 12 months. The mean improvement at 3 months was statistically significant in favour of the experimental group (p = 0.002). The mean improvement at 6 months was also statistically significant (p = 0.008) but by 12 months there was no statistically significant difference between the two groups (p = 0.16). Discussion The rehabilitation programme for patients with massive rotator cuff tears significantly improved shoulder pain and function in the short term. These improvements in shoulder pain and function were sustained over time although the advantage of intervention against control were not.
Human Schwannomas Express Activated Platelet-Derived Growth Factor Receptors and c-kit and Are Growth Inhibited by Gleevec (Imatinib Mesylate)
Authors: Mukherjee Joydeep , Kamnasaran Deepak , Balasubramaniam Anand , Radovanovic Ivan , Zadeh Gelareh , Kiehl Tim-Rasmus , Guha Abhijit 
Published: June 2009

AbstractSchwannomas, although benign, can be fatal or give rise to significant morbidity due to an unpredictable growth rate. They can reoccur after surgery or radiation, current treatments each with significant inherent risks. These risks are further amplified in neurofibromatosis type 2 (NF2), a germ line predisposition syndrome characterized by multiple schwannomas, underlying the need for biological targeted therapies. Gleevec (STI571, imatinib mesylate), in addition to the bcr-abl oncogene in chronic myelogenous leukemia, inhibits c-kit and platelet-derived growth factor receptor (PDGFR) signaling, thereby expanding its use to several malignant and benign human diseases. In the present study, we show that human sporadic and NF2-associated schwannomas have increased expression along with activation of PDGFR-α, PDGFR-β, and c-kit receptors, compared with normal or traumatic nerve. Using the human NF2-null HEI-193 schwannoma cell line, Gleevec inhibited schwannoma viability, proliferation, and anchorage-independent growth, as well as induced apoptosis in a dose-dependent manner (IC50 5–10 μmol/L). These antitumorigenic effects were correlated to inhibition of PDGFR-α, PDGFR-β, and c-kit activation/phosphorylation and major downstream signaling pathways. Lack of robust xenograft or transgenic models of schwannomas prevents extension of these studies in vivo. However, the established long track record and tolerable toxicity of Gleevec already in clinical use and our preclinical data lead us to propose that Gleevec should be evaluated in human schwannomas with shown progressive growth. [Cancer Res 2009;69(12):5099–107]
Bispecific T-Cell Engaging Antibodies for Cancer Therapy
Authors: Baeuerle Patrick A. , Reinhardt Carsten 
Published: June 2009

Abstract
There is increasing evidence that T cells are able to control tumor growth and survival in cancer patients, both in early and late stages of the disease. However, tumor-specific T-cell responses are difficult to mount and sustain in cancer patients, and are limited by numerous immune escape mechanisms of tumor cells selected during immunoediting. An alternative approach to engage T cells for cancer therapy are antibodies, which are bispecific for a surface target antigen on cancer cells, and for CD3 on T cells. These are capable of connecting any kind of cytotoxic T cell to a cancer cell, independently of T-cell receptor specificity, costimulation, or peptide antigen presentation. Here, we review the principle of a new class of bispecific antibodies called BiTE (for “bispecific T-cell engager”) antibodies. Recent results from clinical studies with a CD19/CD3-bispecific BiTE antibody suggest that this therapeutic paradigm is finally showing promise for treatment of both bulky and minimal residual disease. [Cancer Res 2009;69(12):4941–4]
Fecal Cyclooxygenase 2 Plus Matrix Metalloproteinase 7 mRNA Assays as a Marker for Colorectal Cancer Screening
Authors: Takai Tetsunari , Kanaoka Shigeru , Yoshida Ken-ichi , Hamaya Yasushi , Ikuma Mutsuhiro , Miura Naoyuki , Sugimura Haruhiko , Kajimura Masayoshi , Hishida Akira 
Published: June 2009

Abstract
We previously reported that fecal cyclooxygenase 2 (COX-2) mRNA assay, detecting COX-2 mRNA in feces, is useful for identifying subjects with colorectal cancer (CRC). To further improve the sensitivity, we evaluated the usefulness of the combination of COX-2 mRNA and matrix metalloproteinase 7 (MMP-7) mRNA assays as a marker of CRC. The study cohort included 62 patients with CRC and 29 control patients without colorectal neoplasia. RNA was isolated from routinely collected fecal samples. The expression levels of COX-2 and MMP-7 mRNAs were determined by nested reverse transcription-PCR. PCR conditions were optimized where the specificity of fecal COX-2 and MMP-7 mRNA assay result in 100%. The sensitivity of each fecal assay was 87% [95% confidence interval (95% CI), 76-94%] and 65% (95% CI, 51-76%) for CRC, respectively. The sensitivity of fecal RNA test (either marker being positive) was high for CRC (90%; 95% CI, 80-96%). The sensitivity of the fecal RNA test was also high (93%; 95% CI, 80-98%) in patients with stage I or II who are often cured by surgical resection. The fecal RNA test using COX-2 and MMP-7 mRNAs improved the sensitivity to detect CRC without decreasing the specificity. These results suggest that the fecal RNA test would be a promising approach for CRC screening, although larger clinical investigations are indicated. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1888–93)
Cytokine and Cytokine Receptor Single-Nucleotide Polymorphisms Predict Risk for Non–Small Cell Lung Cancer among Women
Authors: Van Dyke Alison L. , Cote Michele L. , Wenzlaff Angie S. , Chen Wei , Abrams Judith , Land Susan , Giroux Craig N. , Schwartz Ann G. 
Published: June 2009

AbstractStudies on the relationships between inflammatory pathway genes and lung cancer risk have not included African-Americans and have only included a handful of genes. In a population-based case-control study on 198 African-American and 744 Caucasian women, we examined the association between 70 cytokine and cytokine receptor single-nucleotide polymorphisms (SNPs) and risk of non–small cell lung cancer (NSCLC). Unconditional logistic regression was used to estimate odds ratios and 95% confidence intervals in a dominant model adjusting for major risk factors for lung cancer. Separate analyses were conducted by race and by smoking history and history of chronic obstructive pulmonary disease among Caucasians. Random forest analysis was conducted by race. On logistic regression analysis, IL6 (interleukin 6), IL7R, IL15, TNF (tumor necrosis factor), and IL10 SNP were associated with risk of non–small cell lung cancer among African-Americans; IL7R and IL10 SNPs were also associated with risk of lung cancer among Caucasians. Although random forest analysis showed IL7R and IL10 SNPs as being associated with risk for lung cancer among African-Americans, it also identified TNFRSF10A SNP as an important predictor. On random forest analysis, an IL1A SNP was identified as an important predictor of lung cancer among Caucasian women. Inflammatory SNPs differentially predicted risk for NSCLC according to race, as well as based on smoking history and history of chronic obstructive pulmonary disease among Caucasian women. Pathway analysis results are presented. Inflammatory pathway genotypes may serve to define a high risk group; further exploration of these genes in minority populations is warranted. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1829–40)
Novel Fucosylated Biomarkers for the Early Detection of Hepatocellular Carcinoma
Authors: Wang Mengjun , Long Ronald E. , Comunale Mary Ann , Junaidi Omer , Marrero Jorge , Di Bisceglie Adrian M. , Block Timothy M. , Mehta Anand S. 
Published: June 2009

Abstract
Changes in glycosylation, most notably fucosylation, have been associated with the development of hepatocellular carcinoma (HCC). In this report, the levels of fucosylated kininogen (Fc-Kin) and fucosylated α-1-antitrypsin were analyzed individually and in combination with the currently used marker, α-fetoprotein, and a previously identified biomarker, Golgi protein 73 (GP73), for the ability to distinguish between a diagnosis of cirrhosis and HCC. This analysis was done on serum from 113 patients with cirrhosis and 164 serum samples from patients with cirrhosis plus HCC. The levels of Fc-Kin and fucosylated α-1-antitrypsin were significantly higher in patients with HCC compared with those with cirrhosis (P &lt; 0.0001). Greatest performance was achieved through the combination of Fc-Kin, α-fetoprotein, and GP73, giving an optimal sensitivity of 95%, a specificity of 70%, and an area under the receiver operating characteristic of 0.94. In conclusion, the altered glycosylation of serum glycoproteins can act as potential biomarkers of primary HCC when used independently or in combination with other markers of HCC. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1914–21)
Two Independent Prostate Cancer Risk–Associated Loci at 11q13
Authors: Zheng S. Lilly , Stevens Victoria L. , Wiklund Fredrik , Isaacs Sarah D. , Sun Jielin , Smith Shelly , Pruett Kristen , Wiley Kathleen E. , Kim Seong-Tae , Zhu Yi , Zhang Zheng , Hsu Fang-Chi , Turner Aubrey R. , Johansson Jan-Erik , Liu Wennuan , Kim Jin Woo , Chang Bao-Li , Duggan David , Carpten John , Rodriguez Carmen , Isaacs William , Grönberg Henrik , Xu Jianfeng 
Published: June 2009

Abstract
Single nucleotide polymorphisms (SNP) at 11q13 were recently implicated in prostate cancer risk by two genome-wide association studies and were consistently replicated in multiple study populations. To explore prostate cancer association in the regions flanking these SNPs, we genotyped 31 tagging SNPs in a ∼110 kb region at 11q13 in a Swedish case-control study (Cancer of the Prostate in Sweden), including 2,899 cases and 1,722 controls. We found evidence of prostate cancer association for the previously implicated SNPs including rs10896449, which we termed locus 1. In addition, multiple SNPs on the centromeric side of the region, including rs12418451, were also significantly associated with prostate cancer risk (termed locus 2). The two groups of SNPs were separated by a recombination hotspot. We then evaluated these two representative SNPs in an additional ∼4,000 cases and ∼3,000 controls from three study populations and confirmed both loci at 11q13. In the combined allelic test of all four populations, P = 4.0 × 10−11 for rs10896449 at locus 1 and P = 1.2 × 10−6 for rs12418451 at locus 2, and both remained significant after adjusting for the other locus and study population. The prostate cancer association at these two 11q13 loci was unlikely confounded by prostate-specific antigen (PSA) detection bias because neither SNP was associated with PSA levels in controls. Unlike locus 1, in which no known gene is located, several putative mRNAs are in close proximity to locus 2. Additional confirmation studies at locus 2 and functional studies for both loci are needed to advance our knowledge on the etiology of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1815–20)
Intakes of Fruit, Vegetables, and Carotenoids and Renal Cell Cancer Risk: A Pooled Analysis of 13 Prospective Studies
Authors: Lee Jung Eun , Männistö Satu , Spiegelman Donna , Hunter David J. , Bernstein Leslie , van den Brandt Piet A. , Buring Julie E. , Cho Eunyoung , English Dallas R. , Flood Andrew , Freudenheim Jo L. , Giles Graham G. , Giovannucci Edward , Håkansson Niclas , Horn-Ross Pamela L. , Jacobs Eric J. , Leitzmann Michael F. , Marshall James R. , McCullough Marjorie L. , Miller Anthony B. , Rohan Thomas E. , Ross Julie A. , Schatzkin Arthur , Schouten Leo J. , Virtamo Jarmo , Wolk Alicja , Zhang Shumin M. , Smith-Warner Stephanie A. 
Published: June 2009

AbstractFruit and vegetable consumption has been hypothesized to reduce the risk of renal cell cancer. We conducted a pooled analysis of 13 prospective studies, including 1,478 incident cases of renal cell cancer (709 women and 769 men) among 530,469 women and 244,483 men followed for up to 7 to 20 years. Participants completed a validated food-frequency questionnaire at baseline. Using the primary data from each study, the study-specific relative risks (RR) were calculated using the Cox proportional hazards model and then pooled using a random effects model. We found that fruit and vegetable consumption was associated with a reduced risk of renal cell cancer. Compared with &lt;200 g/d of fruit and vegetable intake, the pooled multivariate RR for ≥600 g/d was 0.68 [95% confidence interval (95% CI) = 0.54-0.87; P for between-studies heterogeneity = 0.86; P for trend = 0.001]. Compared with &lt;100 g/d, the pooled multivariate RRs (95% CI) for ≥400 g/d were 0.79 (0.63-0.99; P for trend = 0.03) for total fruit and 0.72 (0.48-1.08; P for trend = 0.07) for total vegetables. For specific carotenoids, the pooled multivariate RRs (95% CIs) comparing the highest and lowest quintiles were 0.87 (0.73-1.03) for α-carotene, 0.82 (0.69-0.98) for β-carotene, 0.86 (0.73-1.01) for β-cryptoxanthin, 0.82 (0.64-1.06) for lutein/zeaxanthin, and 1.13 (0.95-1.34) for lycopene. In conclusion, increasing fruit and vegetable consumption is associated with decreasing risk of renal cell cancer; carotenoids present in fruit and vegetables may partly contribute to this protection. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1730–9)
Human Papillomavirus Infections and Vulvar Disease Development
Authors: Garland Suzanne M. , Insinga Ralph P. , Sings Heather L. , Haupt Richard M. , Joura Elmar A. 
Published: June 2009

Abstract
Background: We describe the prevalence of 14 common types [human papillomavirus (HPV)-6/11/16/18/31/33/35/39/45/51/52/56/58/59] in vulvar intraepithelial neoplasia grades 1 to 3 (VIN 1-3) and HPV genotype–specific infection in relation to the development of VIN 1-3.
Methods: Data were analyzed from women enrolled in the placebo arms of three randomized double-blind trials. Anogenital examinations, including collection of labial/vulvar/perineal/perianal swabs, occurred at day 1 and every 6 to 12 months through 48 months. Lesions that were possibly, probably, or definitely HPV related or of unknown etiology were biopsied. Biopsies and swabs were HPV typed. Biopsies were read for endpoint determination (VIN 1-3) by up to four pathologists.
Results: Incident infection with HPV-16 was the most common (6.0/100 person-years). The mean time from incident infection to the development of VIN 1-3 was 18.5 months (95% confidence interval, 13.4-23.6). HPV-6 or -11 was observed in 64.5% of VIN 1 and 29.0% of VIN 2/3, whereas HPV-16 was observed in 6.5% of VIN 1 and 64.5% of VIN 2/3.
Conclusion: A vaccine that includes both low- and high-risk types could prevent more than half of VIN 1-3 lesions, including the precursor lesions to HPV-related vulvar carcinoma. Understanding the incidence and duration of vulvar HPV infection and risk for progression to VIN 1-3 may inform therapeutic decisions for vulvar disease and mathematical models that assess the cost-effectiveness of vaccination. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1777–84)
Mammographic Density and Breast Cancer Risk: Evaluation of a Novel Method of Measuring Breast Tissue Volumes
Authors: Boyd Norman , Martin Lisa , Gunasekara Anoma , Melnichouk Olga , Maudsley Gord , Peressotti Chris , Yaffe Martin , Minkin Salomon 
Published: June 2009

Abstract
Background: Mammographic density has been found to be strongly associated with risk of breast cancer. We have assessed a novel method of assessing breast tissue that is fully automated, does not require an observer, and measures the volume, rather than the projected area, of the relevant tissues in digitized screen-film mammogram.
Methods: Sixteen mammography machines in seven locations in Toronto were calibrated to allow the estimation of the proportion of radiologically dense (stromal and epithelial tissue) and nondense (fatty) tissue represented in each pixel of the mammographic image. This information was combined with a measurement of breast thickness to calculate the volumes of these tissues. Women with newly diagnosed breast cancer (cases) identified on these mammography machines during the years 2000 to 2003 were compared with other women of the same age who did not have breast cancer (controls).
Results: Three hundred sixty-four cases and 656 controls were recruited, epidemiologic data were collected, screen-film mammograms were digitized and measured using both a computer-assisted thresholding method, and the new measure of the volume of density. After adjustment for other risk factors, the odds ratio for those in the 5th quintile compared with the 1st quintile was 1.98 (95% confidence interval, 1.3-3.1) for the volume measure and 1.86 (95% CI, 1.1-3.0) for the area measurement. After inclusion of the volume and area measures in a predictive model, the volume measure lost significance, whereas the area measure remained significant.
Conclusions: Contrary to our expectations, measurement of the volume of breast tissue did not improve prediction of breast cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1754–62)
No Breast Cancer Association for Transforming Growth Factor-β Pathway Colorectal Cancer Single Nucleotide Polymorphisms
Authors: Gibson Lorna , Johnson Nichola , Fraser Agnes , dos Santos Silva Isabel , Houlston Richard , Peto Julian , Fletcher Olivia 
Published: June 2009

Abstract
SMAD7 and GREM1 are signaling components on the transforming growth factor-β pathway, which regulates normal mammary gland development and has been implicated in breast tumor invasion and metastasis. Three variants within SMAD7 and two variants in CRAC1 (a colorectal cancer–associated region on chromosome 15 in which GREM1 is located) have been associated with colorectal cancer risks [odds ratios (OR), 0.85-1.26; all P &lt; 10−7]. We genotyped these five variants in a series of 1,267 bilateral breast cancer cases and 900 controls to determine whether they are associated with breast as well as colorectal cancer risk. None of these single nucleotide polymorphisms were associated with breast cancer risk in our study and the 95% confidence limits of our data, pooled with data from the Cancer Genetic Markers of Susceptibility study, exclude per allele ORs of &lt;0.94 or &gt;1.08. One or more of these variants may be associated with a very small OR for breast cancer, but our data suggest that the effects of these alleles are cancer site–specific. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1934–6)
IGF2R Missense Single-Nucleotide Polymorphisms and Breast Cancer Risk: The Multiethnic Cohort Study
Authors: Cheng Iona , Stram Daniel O. , Burtt Noël P. , Gianniny Lauren , Garcia Rachel R. , Pooler Loreall , Henderson Brian E. , Le Marchand Loïc , Haiman Christopher A. 
Published: June 2009

Abstract
IGF2R has been proposed to be a tumor suppressor gene given its antagonist role on cellular growth and evidence of loss of heterozygosity in several cancers, including breast cancer. To investigate whether inherited differences in potentially functional IGF2R variants influence the risk of breast cancer, we sequenced 46 exons of IGF2R to identify novel missense single-nucleotide polymorphisms (SNP) and tested 12 missense SNPs for their associations with breast cancer risk among 1,614 breast cancer cases and 1,960 controls from the Multiethnic Cohort. None of these missense SNPs were significantly associated with breast cancer risk. Our findings provide no evidence that missense SNPs in IGF2R influence breast cancer susceptibility.(Cancer Epidemiol Biomarkers Prev 2009;18(6):1922–4)
Dietary Acrylamide Intake and Prostate Cancer Risk in a Prospective Cohort of Swedish Men
Authors: Larsson Susanna C. , Åkesson Agneta , Wolk Alicja 
Published: June 2009

Abstract
Background: Acrylamide is a probable human carcinogen that can be formed in foods prepared at high temperatures. Whereas evidence indicates that acrylamide causes cancer in laboratory animals, epidemiologic data on dietary acrylamide intake in relation to cancer risk are limited and mainly null. We examined the association between dietary acrylamide intake and risk of prostate cancer in a cohort of men.
Methods: The Cohort of Swedish Men is a population-based prospective study of 45,306 men who were cancer-free and completed a food frequency questionnaire at enrollment in 1997. Cox proportional hazards models were used to estimate relative risks adjusted for potential confounders.
Results: During a mean follow-up of 9.1 years, we ascertained 2,696 incident cases of prostate cancer. We observed no association between acrylamide intake and risk of prostate cancer. Compared with the lowest quintile of acrylamide intake (mean, 23.7 μg/d), the multivariable relative risks (95% confidence interval) for the highest quintile (mean, 49.8 μg/d) were 0.88 (0.70-1.09) for total prostate cancer, 1.07 (0.87-1.32) for localized prostate cancer (n = 1,088), and 0.98 (0.78-1.22) for advanced prostate cancer (n = 951).
Conclusions: Results from this prospective study provide no evidence that dietary acrylamide in amounts typically consumed by Swedish men is associated with risk of prostate cancer.(Cancer Epidemiol Biomarkers Prev 2009;18(6):1939–41)