bluuebunny/crossref_metadata_2025_split huggingface dataset:
Validation of a diabetic foot surgery classification
Authors: Armstrong David G , Lavery Lawrence A , Frykberg Robert G , Wu Stephanie C , Boulton Andrew JM 
Published: September 2006

AbstractThe purpose of this project was to evaluate associations of increasing diabetic foot surgery stage with postoperative outcome. This project, designed as a retrospective cohort model, was conducted at three large, urban referral‐based diabetic foot clinics. The investigators abstracted medical records from 180 patients with diabetes, 76·1% male, aged 57·8 ± 11·2 years, falling equally into four classes of a previously reported diabetic foot surgery classification system. These classes included class 1 (elective), class 2 (prophylactic), class 3 (curative) and class 4 (emergency). There was a significant trend towards increasing risk of ulceration/reulceration (χ2trend= 17·8,P= 0·0001), peri‐postoperative infection (χ2trend= 96·9,P= 0·0001), all‐level amputation (χ2trend= 41·7P= 0·001) and major amputation (χ2trend= 8·6,P= 0·003), with increasing class of foot surgery. The results of this study suggest that a non vascular foot surgery classification system including variables such as the presence or absence of neuropathy, an open wound and acute infection may be predictive of peri‐ and postoperative complications. This may assist the surgeon in better identifying risk when determining a rationale for and type of surgery in persons with diabetes.
Healing of large midline wounds in infants: unlike in adults, does conservative approach give better results? Two case reports and review of the literature
Authors: Suliman M Taifour 
Published: September 2006

AbstractThe case of two infants with large midline wounds, one with an omphalocele and the other with a lumbosacral wound secondary to ruptured meningocele, is reported wherein the advantages of leaving such wounds in infants to heal spontaneously over surgical intervention are shown. In this report, the cases are discussed and the literature is reviewed. It is concluded that the midline wounds in infants yield better results if left to heal spontaneously.
CHARACTERIZATION OF A LAMB HAM: FATTY ACIDS AND VOLATILE COMPOUNDS COMPOSITION
Authors: PALEARI MARIA ANTONIETTA , MORETTI VITTORIO MARIA , BERETTA GIUSEPPE , CAPRINO FABIO 
Published: September 2006

ABSTRACT The study presents and characterizes a little‐known product that is processed manually on the cottage industry scale. The product, called “violino” of lamb, is a cured and matured lamb thighbone of sheep of the Lamon × Bergamasca breed. The sheep graze on pasturelands, and the lambs are weaned at 60–70 days of age. They are then raised out in the field and the pasture feeding is supplemented with a commercial concentrate based on maize and soybean. At 7–8 months the lambs are slaughtered, and the thighs are cured with a curing mixture and ripened for 60 days. The study determined, on the fresh thighs, the proximate composition and fatty acid profile; and on the cured thighs (violino), the proximate composition, fatty acid profile and the volatile composition influenced by curing, salting and spicing. The results revealed the cured ham lamb to have a reduced fat content, a high polyunsaturated fatty acids/saturated fatty acids ratio and a high protein content. The processing, performed completely manually, resulted in a niche product that has the possibility of being produced on a bigger scale, which would favor breeders in that they would profit from being able to sell not just the fresh lamb meat but also a cured end‐product. Given the consumer demand for typical products, this lamb ham, known as lamb violino, could be a sought‐after product.
Use of Analgesics and Nonsteroidal Anti-inflammatory Drugs, Genetic Predisposition, and Bladder Cancer Risk in Spain
Authors: Fortuny Joan , Kogevinas Manolis , Garcia-Closas Montserrat , Real Francisco X. , Tardón Adonina , Garcia-Closas Reina , Serra Consol , Carrato Alfredo , Lloreta Josep , Rothman Nat , Villanueva Cristina , Dosemeci Mustafa , Malats Núria , Silverman Debra 
Published: September 2006

Abstract
Background: We assessed use of nonaspirin nonsteroidal anti-inflammatory drugs (NSAID), aspirin, paracetamol (acetaminophen), phenacetin, and metamizol (dipyrone) and risk of bladder cancer and their interaction with polymorphisms in drug-metabolizing genes.
Methods: We analyzed personal interview data from 958 incident bladder cancer cases and 1,029 hospital controls from a multicenter case-control study in Spain. A drug matrix was developed to estimate cumulative lifetime dose of active ingredients. Polymorphisms in GSTP1, SULT1A1, CYP2E1, CYP2C9, and NAT2 were examined.
Results: A significant reduction in bladder cancer risk [adjusted odds ratio (OR), 0.4; 95% confidence interval (95% CI), 0.2-0.9] was observed for regular users of nonaspirin NSAIDs compared with never users. Regular users of aspirin experienced no reduction in risk (OR, 1.0; 95% CI, 0.7-1.5). Regular users of paracetamol had no overall increased risk of bladder cancer (OR, 0.8; 95% CI, 0.4-1.3), but our data suggested a qualitative interaction with the GSTP1 I105V genotype. Subjects with at least one copy of the 359L or 144C variant alleles in the NSAID-metabolizing gene CYP2C9 had a slightly decreased risk of bladder cancer (OR, 0.8; 95% CI, 0.7-1.0; P = 0.037); however, having at least one copy of the 359L or 144C variant alleles did not significantly modify the protective effect of nonaspirin NSAID use.
Conclusion: Regular use of nonaspirin NSAIDs was associated with a reduced risk of bladder cancer, which was not modified by polymorphisms in the NSAID-metabolizing gene CYP2C9. We found no evidence of an overall effect for paracetamol or aspirin use. (Cancer Epidemiol Biomarkers Prev 2006;15(9):1696–703)
Genomic Instability and Prognosis in Breast Carcinomas
Authors: Kronenwett Ulrike , Ploner Alexander , Zetterberg Anders , Bergh Jonas , Hall Per , Auer Gert , Pawitan Yudi 
Published: September 2006

Abstract
Background: We recently reported that DNA content of breast adenocarcinomas, cytometrically assessed by diploid (D), tetraploid (T), and aneuploid (A) categories, can be further divided into genomically stable and unstable subtypes by means of the stemline scatter index (SSI). The aim of the present study was to survey the clinical correlates and the prognostic value of the SSI in a consecutive series of 890 breast cancer patients.
Results: Genomically stable subtype had a significantly better survival compared with the unstable subtype within each ploidy category: D (P = 0.04), T (P = 0.008), and A (P = 0.004). By contrast, no statistically significant difference in survival was observed between the D, T, and A categories within the stable (P = 0.23) and unstable subtypes (P = 0.12). Among A tumors, the unstable subtype tended to be larger, more frequently estrogen- and progesterone-receptor negative, and to be of higher grade compared with the stable subtype. Stable D tumors tended to have lower grade than the unstable subtype, but among the D and T tumors, genomic instability was not associated with receptor status. Within the Elston grade 3, lymph node–positive or estrogen receptor–positive subgroups, patients with stable tumors had significantly better survival compared with unstable tumors (P = 0.01, 0.002, and 7.2E−5, respectively).
Conclusions: The SSI contributes supplementary biological and clinical information in addition to ploidy information alone. Objective classification of breast adenocarcinomas into stable and unstable subtypes is a useful prognostic indicator independent of established clinical factors. (Cancer Epidemiol Biomarkers Prev 2006;15(9):1630–5)
Up-to-Date Estimates of Cancer Patient Survival Even with Common Latency in Cancer Registration
Authors: Brenner Hermann , Hakulinen Timo 
Published: September 2006

Abstract
In an era of ongoing improvement in cancer patient survival, available long-term survival figures from cancer registries are often outdated and too pessimistic for two reasons: first, delay in availability of cancer registry data, typically in the order of a few years, and, second, application of cohort-based methods of survival analysis, which provide survival estimates for patients diagnosed many years ago. We developed a model-based period analysis approach aimed to overcome both problems. We provide extensive empirical evaluation of our approach by comparing its performance with that of previously available methods for monitoring of 5- and 10-year relative survival, with the use of data from the nationwide Finnish Cancer Registry of 490,279 patients ages ≥15 years and diagnosed with one of 20 common forms of cancer between 1953 and 1997. We show that, in most cases, the model-based approach predicts 5- and 10-year relative survival expectations of newly diagnosed patients quite closely and much better than any of the previously available methods, including standard period analysis. We conclude that the model-based approach may enable deriving up-to-date cancer survival rates even with the common latency in availability of cancer registry data. (Cancer Epidemiol Biomarkers Prev 2006;15(9):1727–32)
Interleukin-1β and Interleukin-1 Receptor Antagonist Gene Polymorphisms and Gastric Cancer: A Meta-analysis
Authors: Camargo M. Constanza , Mera Robertino , Correa Pelayo , Peek Richard M. , Fontham Elizabeth T.H. , Goodman Karen J. , Piazuelo M. Blanca , Sicinschi Liviu , Zabaleta Jovanny , Schneider Barbara G. 
Published: September 2006

Abstract
Background: Polymorphisms of interleukin-1B (IL1B) and its receptor antagonist (IL1RN) genes have been inconsistently associated with gastric cancer risk. We examined these associations by performing meta-analyses.
Materials and Methods: Twenty-five studies testing the association between IL1B and/or IL1RN gene polymorphisms and gastric cancer were examined: 14 studies of IL1B-511, 14 studies of IL1B-31, 8 studies of IL1B+3954, and 23 studies of IL1RN. Overall and ethnicity-specific summary odds ratios and corresponding 95% confidence intervals for gastric cancer associated with these polymorphisms were estimated using fixed- and random-effects models. Heterogeneity and publication bias were evaluated.
Results: IL1B-511T and IL1RN*2 were associated with gastric cancer risk in Caucasians, but not in Asians. For IL1B-511T, the association in Caucasians was stronger when intestinal-subtype and noncardia gastric cancer cases were examined. A nonsignificant trend was observed between IL1B-31C and gastric cancer in Caucasians. No significant association of IL1B+3954T and gastric cancer risk was detected. Studies with better methodologic characteristics reported stronger effects. There was no evidence of publication bias.
Conclusion: IL1B-511T is associated with gastric cancer susceptibility in Caucasians. The meta-analyses suggest that the conflicting results among studies may be explained by variation in allele frequencies among the ethnic groups and variation in tumor types, as well as by the methodologic quality of the studies. (Cancer Epidemiol Biomarkers Prev 2006;15(9):1674–87)
Endometrial Cancer Risk Is Associated with Variants of the Mismatch Repair Genes MLH1 and MSH2
Authors: Beiner Mario E. , Rosen Barry , Fyles Anthony , Harley Ian , Pal Tuya , Siminovitch Kathy , Zhang Shiyu , Sun Ping , Narod Steven A. 
Published: September 2006

Abstract
Women with germ-line mutations in the mismatch repair genes (responsible for hereditary nonpolyposis colorectal cancer) face an increased risk of colonic and endometrial cancer. However, these germ-line mutations are rare and are responsible for fewer than 1% of endometrial cancers. Therefore, we examined whether or not common variants of the hereditary nonpolyposis colorectal cancer–associated genes might also be associated with an increased risk of endometrial cancer. Three single-nucleotide polymorphisms were selected in the MLH1 and MSH2 mismatch repair genes. All the various 672 women with endometrial cancer and 880 controls were genotyped. Each of these three single-nucleotide polymorphisms was associated with an increased risk of endometrial cancer. Carriers of the MLH1 nt-93 A allele were at a 1.5-fold increased risk of developing endometrial cancer compared with controls [95% confidence interval (95% CI), 1.2-2.0; P = 0.001]. The risk was higher for homozygote carriers [odds ratio (OR), 1.9; 95% CI, 1.2-3.2; P = 0.009]. For carriers of the MSH2 rs2303428 C allele, the OR was 1.4 (95% CI, 1.0-1.9; P = 0.05), and for carriers of the MSH2 rs2059520 G allele, the OR was 1.3 (95% CI, 1.0-1.7; P = 0.03). More than 9% of endometrial cancer cases carried a variant allele in both MLH1 and MSH2. For these women, the risk of endometrial cancer was particularly high (OR, 2.1; 95% CI, 1.2-3.6; P = 0.005). For patients younger than 50 years at diagnosis who carried both variants, the risk was even higher (OR, 3.4; 95% CI, 1.7-6.6; P = 0.0005). In summary, two common variant alleles of the MLH1 and MSH2 genes make a substantial contribution to endometrial cancer incidence in Ontario. (Cancer Epidemiol Biomarkers Prev 2006;15(9):1636–40)
Clonal Origin of Metastatic Testicular Teratomas
Authors: Jones Timothy D. , Wang Mingsheng , Sung Ming-Tse , Zhang Shaobo , Ulbright Thomas M. , Eble John N. , Beck Stephen D. , Foster Richard S. , Anagnostou John J. , Conner Clay , Cheng Liang 
Published: September 2006

Abstract
Purpose: Testicular teratomas in adult patients are histologically diverse tumors that frequently coexist with other germ cell tumor (GCT) components. These mixed GCTs often metastasize to retroperitoneal lymph nodes where multiple GCT elements are frequently present in the same metastatic lesion. Neither the genetic relationships among the different components in metastatic lesions nor the relationships between primary and metastatic GCT components have been elucidated.
Experimental Design: We examined metastases from 31 patients who underwent primary retroperitoneal lymph node dissection for metastatic testicular GCT. All patients had metastatic mature teratoma with one or more other GCT components. This study included a total of 72 metastatic GCT components and 16 primary GCT components from 31 patients. Genomic DNA samples from each component were prepared from formalin-fixed, paraffin-embedded tissue sections using laser-assisted microdissection. Loss of heterozygosity (LOH) assays for seven microsatellite polymorphic markers on chromosomes 1p36 (D1S1646), 9p21 (D9S171 and IFNA), 9q21 (D9S303), 13q22-q31 (D13S317), 18q22 (D18S543), and 18q21 (D18S60) were done to assess clonality.
Results: Twenty-nine of 31 (94%) cases showed allelic loss in one or more components of the metastatic GCTs. Twenty-nine of 31 mature teratomas showed allelic loss in at least one of seven microsatellite polymorphic markers analyzed. The frequency of allelic loss in informative cases of metastatic mature teratoma was 27% (8 of 30) with D1S1646, 34% (10 of 29) with D9S171, 37% (10 of 27) with IFNA, 27% (8 of 30) with D9S303, 46% (13 of 28) with D13S317, 26% (7 of 27) with D18S543, and 36% (10 of 28) with D18S60. Completely concordant allelic loss patterns between the mature teratoma and all of the other metastatic GCT components were seen in 26 of 29 cases in which the mature teratoma component showed LOH. Nearly identical allelic loss patterns were seen in the three remaining cases. In six cases analyzed, LOH patterns of each metastatic component were compared with each GCT component of the primary testicular tumor. In all six cases, each primary and metastatic component showed an identical pattern of allelic loss.
Conclusion: Our data support the common clonal origin of metastatic mature teratomas with other components of metastatic testicular GCTs and with each component of the primary tumor.
Antiangiogenic activity of 4′-thio-β-d-arabinofuranosylcytosine
Authors: Roy Anshu M. , Tiwari Kamal N. , Parker William B. , Secrist John A. , Li Rongbao , Qu Zhican 
Published: September 2006

Abstract
4′-Thio-β-d-arabinofuranosylcytosine (T-araC), a new-generation deoxycytidine nucleoside analogue, showed significant efficacy against numerous solid tumors in preclinical studies and entered clinical development for cancer therapy. It is a structural analogue of cytarabine (araC), a clinically used drug in the treatment of acute myelogenous leukemia, which has no or very limited efficacy against solid tumors. In comparison with araC, the excellent in vivo activity of T-araC against solid tumors suggests that, in addition to inhibition of DNA synthesis, T-araC may target cellular signaling pathways, such as angiogenesis, in solid tumors. We studied T-araC and araC for their antiangiogenic activities in vitro and in vivo. Both compounds inhibited human endothelial cell proliferation with similar IC50s. However, only T-araC inhibited endothelial cell migration and differentiation into capillary tubules. T-araC also abrogated endothelial cell extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, a key signaling molecule involved in cellular processes of angiogenesis. Results from chick chorioallantoic membrane angiogenesis assays revealed that T-araC significantly inhibited the development of new blood vessels in vivo, whereas araC showed much less effect. The findings of this study show a role of T-araC in antiangiogenesis and suggest that T-araC combines antiproliferative and antiangiogenic activity in one molecule for a dual mechanism of drug action to achieve the excellent in vivo efficacy against several solid tumors. This study also provides important information for optimizing dosage and sequence of T-araC administration in clinical investigations by considering T-araC as both an antiproliferative and an antiangiogenic agent. [Mol Cancer Ther 2006;5(9):2218–24]
Therapeutic value of glycosaminoglycans in cancer
Authors: Yip George W. , Smollich Martin , Götte Martin 
Published: September 2006

Abstract
Glycosaminoglycans are unbranched polysaccharides composed of repeating units of alternating uronic acids and amino sugars. Most glycosaminoglycans are covalently attached to core proteins to form proteoglycans. Posttranslational modifications result in specific motifs that bind to a large variety of ligands, thus regulating growth factor signaling, cellular behavior, inflammation, angiogenesis, and the proteolytic environment. Dysregulated expression of glycosaminoglycans is present in cancer and reported to correlate with clinical prognosis in several malignant neoplasms. Recent knowledge on the biological roles of these molecules in cancer biology, tumor angiogenesis, and metastasis has promoted the development of drugs targeting them. Pharmaceutical approaches include the use of chemically modified heparins and glycosaminoglycans with defined structures, combination of inhibitors of glycosaminoglycan biosynthesis and polyamine depletion, and biologically active glycosaminoglycan-binding peptides. In addition, glycosaminoglycans are used as tumor-specific delivery and targeting vehicles for toxins and chemotherapeutics. Encouraging results in animal studies and clinical trials show the clinical relevance of glycosaminoglycan-based drugs and the use of glycosaminoglycans as therapeutic targets. [Mol Cancer Ther 2006;5(9):2139–48]
A non–RGD-based integrin binding peptide (ATN-161) blocks breast cancer growth and metastasis in vivo
Authors: Khalili Parisa , Arakelian Ani , Chen Gaoping , Plunkett Marian L. , Beck Ivy , Parry Graham C. , Doñate Fernando , Shaw David E. , Mazar Andrew P. , Rabbani Shafaat A. 
Published: September 2006

Abstract
Purpose: Integrins are expressed by numerous tumor types including breast cancer, in which they play a crucial role in tumor growth and metastasis. In this study, we evaluated the ability of ATN-161 (Ac-PHSCN-NH2), a 5-mer capped peptide derived from the synergy region of fibronectin that binds to α5β1 and αvβ3 in vitro, to block breast cancer growth and metastasis. Experimental design: MDA-MB-231 human breast cancer cells were inoculated s.c. in the right flank, or cells transfected with green fluorescent protein (MDA-MB-231-GFP) were inoculated into the left ventricle of female BALB/c nu/nu mice, resulting in the development of skeletal metastasis. Animals were treated with vehicle alone or by i.v. infusion with ATN-161 (0.05–1 mg/kg thrice a week) for 10 weeks. Tumor volume was determined at weekly intervals and tumor metastasis was evaluated by X-ray, microcomputed tomography, and histology. Tumors were harvested for histologic evaluation. Result: Treatment with ATN-161 caused a significant dose-dependent decrease in tumor volume and either completely blocked or caused a marked decrease in the incidence and number of skeletal as well as soft tissue metastases. This was confirmed histologically as well as radiographically using X-ray and microcomputed tomography. Treatment with ATN-161 resulted in a significant decrease in the expression of phosphorylated mitogen-activated protein kinase, microvessel density, and cell proliferation in tumors grown in vivo. Conclusion: These studies show that ATN-161 can block breast cancer growth and metastasis, and provides a rationale for the clinical development of ATN-161 for the treatment of breast cancer. [Mol Cancer Ther 2006;5(9):2271–80]
Real-time gene expression analysis in human xenografts for evaluation of histone deacetylase inhibitors
Authors: Beliën Ann , De Schepper Stefanie , Floren Wim , Janssens Boud , Mariën Ann , King Peter , Van Dun Jacky , Andries Luc , Voeten Jan , Bijnens Luc , Janicot Michel , Arts Janine 
Published: September 2006

Abstract
Real-time analysis of gene expression in experimental tumor models represents a major tool to document disease biology and evaluate disease treatment. However, monitoring gene regulation in vivo still is an emerging field, and thus far it has not been linked to long-term tumor growth and disease outcome. In this report, we describe the development and validation of a fluorescence-based gene expression model driven by the promoter of the cyclin-dependent kinase inhibitor p21waf1,cip1. The latter is a key regulator of tumor cell proliferation and a major determinant in the response to many anticancer agents such as histone deacetylase inhibitors. In response to histone deacetylase inhibitors, induction of fluorescence in A2780 ovarian tumors could be monitored in living mice in a noninvasive real-time manner using whole-body imaging. Single p.o. administration of the histone deacetylase inhibitor MS-275 significantly induces tumor fluorescence in a time- and dose-dependent manner, which accurately predicted long-term antitumoral efficacy in individual mice following extended treatment. These findings illustrate that this technology allows monitoring of the biological response induced by treatment with histone deacetylase inhibitors. In addition to providing experimental pharmacokinetic/pharmacodynamic markers for investigational drugs, this model provides insight into the kinetics of in vivo regulation of transcription, which plays a key role in causing and maintaining the uncontrolled proliferation of tumor tissue. [Mol Cancer Ther 2006;5(9):2317–24]