bluuebunny/crossref_metadata_2025_split huggingface dataset:
Is there a folate‐related gene‐environment interaction in the etiology of childhood acute lymphoblastic leukemia?
Authors: Milne Elizabeth , de Klerk Nicholas H. , van Bockxmeer Frank , Kees Ursula R. , Thompson Judith R. , Baker David , Armstrong Bruce K. 
Published: January 2006

AbstractAcute lymphoblastic leukaemia (ALL) is the commonest childhood cancer in developed countries. Little is known about its causes, although its early age at diagnosis has focused interest on maternal and perinatal factors. We have previously observed a protective effect of maternal folate supplementation during pregnancy against ALL, and a number of studies have reported protective effects of some common polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) gene. One study has suggested that the effect of MTHFR polymorphisms on risk of ALL may depend on folate status. This study aimed to look for evidence of an interaction between maternal folate supplementation and child's genotype among the cases from our previous study. Bone marrow specimens from 82 of 83 case children were available. DNA was extracted and genotyped for MTHFR C677T and A1298C using standard techniques. We used a case‐only analysis to estimate the case‐only odds ratio (COR) for MTHFR genotype and folate supplementation in association with ALL. None of the CORs indicated a significant departure from a multiplicative model. Adjustment for sex, age or genotype at the other locus had little effect on the results. Other studies of this gene and environment interaction in ALL and other cancers have produced contradictory results, perhaps because of varying definitions of folate exposure. Further research into the interaction of folate intake and genotype in causing ALL and other cancers is needed. We are specifically studying it in an Australian national case‐control study of genetic and environmental causes of ALL. © 2006 Wiley‐Liss, Inc.
Performance of clinical mammography: A nationwide study from Denmark
Authors: Jensen Allan , Vejborg Ilse , Severinsen Niels , Nielsen Susanne , Rank Fritz , Mikkelsen Gerd Just , Hilden Jørgen , Vistisen Dorte , Dyreborg Uffe , Lynge Elsebeth 
Published: January 2006

AbstractClinical mammography is the key tool for breast cancer diagnosis, but little is known about the impact of the organisational set‐up on the performance. We evaluated whether organisatorial factors influence the performance of clinical mammography. Clinical mammography data from all clinics in Denmark in the year 2000 were collected and linked to cancer outcome. Use of the National Institute of Radiation Hygiene register for identification of radiology clinics ensured comprehensive nationwide registration. We used the final mammographic assessment at the end of the imaging work‐up to determine sensitivity, specificity and accuracy, the latter using a receiver‐operating characteristics (ROC) analysis. In 96,534 clinical mammography examinations, sensitivity was 75% and specificity 99%. The presence of at least one high volume‐reading radiologist in the clinic increased accuracy (AUC = 0.91 for <1,000 examinations/year and 0.92 for >2,000 examinations/year, p = 0.017). The examination volume per clinic showed no clear effect on performance, as accuracy was significantly higher in clinics with a medium number of examinations (AUC = 0.93 for 2,000–4,000 examinations/year and 0.90 for >6,000 examinations/year, p = 0.003). Accuracy was significantly lower in regions with high annual utilisation rate of clinical mammography, which means the proportion of examined women in a region (AUC = 0.90 for 3.0–5.0% annual utilisation rate and AUC = 0.93 for 2.0–2.5% annual utilisation rate, and p = 0.001), indicating that clinical mammography worked best in patient populations of purely symptomatic women. Our data indicate that to increase the accuracy of clinical mammography at the community level, the presence of an experienced radiologist should be prioritised ahead of raising the clinic size. © 2006 Wiley‐Liss, Inc.
Molecular characterization of adenocarcinoma and squamous carcinoma of the uterine cervix using microarray analysis of gene expression
Authors: Chao Angel , Wang Tzu‐Hao , Lee Yun‐Shien , Hsueh Swei , Chao An‐Shine , Chang Ting‐Chang , Kung Wei‐Hsiang , Huang Shang‐Lang , Chao Fang‐Yu , Wei Min‐Li , Lai Chyong‐Huey 
Published: January 2006

AbstractIn an attempt to understand the molecular mechanisms for the different clinical features between adenocarcinoma/adenosquamous carcinoma (AC/ASC) and squamous carcinoma (SC) of the uterine cervix, we analyzed gene expression profiles of different histological subtypes of cervical cancer. Cancer specimens and the surrounding normal tissue counterparts were separately collected from cervical cancer patients undergoing type III radical hysterectomy. Paired total RNA (cancer and normal tissues) was isolated and analyzed with cDNA microarrays containing duplicate spots of 7 334 sequence‐verified human cDNA clones. Selected differentially expressed genes specific for AC or SC were further verified using real‐time quantitative polymerase chain reaction (RTQ‐PCR) and immunohistochemistry. Genes, including CEACAM5, TACSTD1, S100P and MSLN were upregulated in AC. Contrarily, genes involved in epidermal differentiation complex such as S100A9 and ANXA8 were upregulated in SC. Cross‐validation of the results using an independent but comparable group of patients with known long‐term outcomes (n = 63, median follow‐up 70.3 months; range, 4–208 months) showed that the correlation between the selected 6 differentially expressed genes and histology was highly significant. CEACAM5 (p < 0.0001) and TACSTD1 (p = 0.009) were significant prognostic factors by multivariate Cox proportional hazards regression analysis. The combination of cDNA microarray, RTQ‐PCR and immunohistochemical results of this study showed that it is possible to define different gene profiles for AC and SC. Moreover, TACSTD1 expression may be a novel poor prognostic factor. © 2006 Wiley‐Liss, Inc.
Regular aspirin use and esophageal cancer risk
Authors: Jayaprakash Vijayvel , Menezes Ravi J. , Javle Milind M. , McCann Susan E. , Baker Julie A. , Reid Mary E. , Natarajan Nachimuthu , Moysich Kirsten B. 
Published: January 2006

AbstractGiven the high mortality rate and the rapidly increasing incidence rate of esophageal carcinoma, chemopreventive agents are highly desirable. Aspirin has been shown to be associated with reduced risk of developing colorectal carcinoma and other cancers. Even though previous studies have shown reduced risk of esophageal cancer associated with aspirin use, results were inconsistent with respect to frequency and duration of use. In this hospital‐based case‐control study, 163 esophageal cancer cases were compared to 482 age‐ and sex‐matched hospital controls with nonneoplastic conditions. Participants were classified as regular aspirin users if they had taken the drug at least once a week for 6 months. Results suggest that esophageal cancer risk is significantly lower for regular aspirin users compared to nonusers [adjusted odds ratio (aOR) 0.54; 95% confidence interval (CI) 0.36–0.86]. Individuals who used an equivalent of at least 1 aspirin a day (≥7 tablets/week) were half as likely to have been diagnosed with esophageal carcinoma (aOR 0.47; 95% CI 0.26–0.85), and a linear trend was noted with increasing frequency of use (ptrend 0.007). Similar protective effects were noted with ≤20 years of use, whereas no risk reduction was noted with >20 years of use. Consistent reduction in risk associated with aspirin use was noted among both the major histological subtypes, but the protective effect appears to be more pronounced in adenocarcinoma compared to squamous cell carcinoma. Overall, results from the current study suggest that regular aspirin use may be associated with reduced risk of esophageal cancer. © 2006 Wiley‐Liss, Inc.
Telomere DNA content and allelic imbalance demonstrate field cancerization in histologically normal tissue adjacent to breast tumors
Authors: Heaphy Christopher M. , Bisoffi Marco , Fordyce Colleen A. , Haaland Christina M. , Hines William C. , Joste Nancy E. , Griffith Jeffrey K. 
Published: January 2006

AbstractCancer arises from an accumulation of mutations that promote the selection of cells with progressively malignant phenotypes. Previous studies have shown that genomic instability, a hallmark of cancer cells, is a driving force in this process. In the present study, two markers of genomic instability, telomere DNA content and allelic imbalance, were examined in two independent cohorts of mammary carcinomas. Altered telomeres and unbalanced allelic loci were present in both tumors and surrounding histologically normal tissues at distances at least 1 cm from the visible tumor margins. Although the extent of these genetic changes decreases as a function of the distance from the visible tumor margin, unbalanced loci are conserved between the surrounding tissues and the tumors, implying cellular clonal evolution. Our results are in agreement with the concepts of “field cancerization” and “cancer field effect,” concepts that were previously introduced to describe areas within tissues consisting of histologically normal, yet genetically aberrant, cells that represent fertile grounds for tumorigenesis. The finding that genomic instability occurs in fields of histologically normal tissues surrounding the tumor is of clinical importance, as it has implications for the definition of appropriate tumor margins and the assessment of recurrence risk factors in the context of breast‐sparing surgery. © 2006 Wiley‐Liss, Inc.
Cytoplasmic melanoma‐associated antigen (CYT‐MAA) serum level in patients with melanoma: A potential marker of response to immunotherapy?
Authors: Reynolds Sandra R. , Vergilis Irene J. , Szarek Michael , Ferrone Soldano , Bystryn Jean‐Claude 
Published: January 2006

AbstractSimple, noninvasive methods are needed to follow effectiveness of new treatments in patients with melanoma. In our study, we examined cytoplasmic melanoma‐associated antigen (CYT‐MAA) serum level in melanoma patients during immunotherapy. Sera of 117 patients were assayed for CYT‐MAA by double‐sandwich ELISA before and during treatment with a polyvalent, shed antigen, melanoma vaccine. Vaccine‐treated patients included 30 with American Joint Committee on Cancer (AJCC) stage IIb or IIIa, 30 with stage IIc, IIIb or IIIc, 30 with resected stage IV and 27 with measurable stage IV disease. Prior to vaccine therapy, 63% of patients had elevated serum CYT‐MAA with high levels of antigen in all disease stages. After initiation of therapy, the level declined in more than 90% of the positive patients and fell below the positive cut‐off in 56% of these patients within 5 months. By contrast, there was no decline in CYT‐MAA serum level in 11 patients who served as untreated controls with melanoma. Multivariate analysis of the treated patients using accelerated failure time Weibull models adjusted for stage and age showed that patients whose CYT‐MAA serum level remained elevated during treatment were ∼3 times more likely to recur or progress than patients who were consistently below the positive cut‐off (hazard ratio = 3.42, 95% CI [1.38, 8.47], p = 0.0079). Measurement of CYT‐MAA serum level appears to show potential as an early marker of prognosis in patients with stages IIb to IV melanoma. Measurement of CYT‐MAA serum level during therapy could provide an intermediate marker of response in these patients. © 2006 Wiley‐Liss, Inc.
SAHA‐sensitized prostate cancer cells to TNFα‐related apoptosis‐inducing ligand (TRAIL): Mechanisms leading to synergistic apoptosis
Authors: Lakshmikanthan Vijayabaskar , Kaddour‐Djebbar Ismail , Lewis Ronald W. , Kumar M. Vijay 
Published: January 2006

AbstractTreatment of cancer cells with histone deacetylase inhibitors (HDACi) such as suberolylanilide hydroxamic acid (SAHA) activates genes that promote apoptosis. To enhance proapoptotic efficiency, SAHA has been used in combination with radiation, kinase inhibitors and cytotoxic drugs. Although several prostate cells respond to TNFα‐Related Apoptosis‐Inducing Ligand (TRAIL), LNCaP are resistant. This model system was utilized to examine the advantages of combined treatment with SAHA and TRAIL. In LNCaP cells, TRAIL induced synergistic apoptosis when combined with even with the lowest dose SAHA. Treatment with caspase inhibitor confirmed that SAHA‐induced apoptosis was mediated through caspases. In addition to induction of apoptosis, SAHA and TRAIL decreased the levels of proapoptotic proteins IKKα, IKKβ and IKKγ, suggesting that SAHA treatment may reduce the activity of NFκB. However, assay for NFκB luciferase reporter activity showed highly significant increase in SAHA‐treated cells, supporting earlier suggestions that HDACi promotes NFκB transcriptional activity. Further analyses to determine the mechanisms by which the combination of SAHA and TRAIL led to synergistic apoptosis indicated that the apoptotic response of LNCaP is due to a complex regulation of death receptor pathway and alterations of NFκB activity at several regulatory steps. © 2006 Wiley‐Liss, Inc.
Optical diagnosis of cervical cancer by fluorescence spectroscopy technique
Authors: Chidananda Siddappa M. , Satyamoorthy Kapaettu , Rai Lavanya , Manjunath Attibele P. , Kartha Vasudevan B. 
Published: January 2006

AbstractIn the present work, we examine normal and malignant stage IIIB cervical tissue by laser induced fluorescence, with 2 different objectives. (i) Development of the fluorescence spectroscopy technique as a standard optical method for discrimination of normal and malignant tissue samples and, (ii) Optimization of the technique by the method of matching of a sample spectrum with calibration sets of spectra of pathologically certified samples. Laser‐induced fluorescence spectra were measured using samples from 62 subjects at different excitation wavelengths. Principal component analysis (PCA) of spectra and intensity ratios of curve‐resolved fluorescence peaks were tested for discrimination. It was found that PCA of total fluorescence at 325 nm excitation gives specificity and sensitivity over 95%. Use of calibration sets of spectra of histo‐pathologically certified samples combined with PCA for matching and pass/fail classification of test samples is shown to have high sensitivity/specificity for routine diagnostic purposes as well as for possible staging of the disease. Further, the multi‐component origin of the fluorescence spectra is illustrated by curve resolution and fluorescence spectra of separated proteins of tissue homogenates. © 2006 Wiley‐Liss, Inc.
Truncated APC is required for cell proliferation and DNA replication
Authors: Schneikert Jean , Behrens Jürgen 
Published: January 2006

AbstractThe tumour suppressor APC is truncated in most colon cancers, which leads to the stabilization of β‐catenin and to the constitutive activation of Wnt signalling. However, it is not clear why colon cancer cells retain the truncated APC fragment. Here, we show that a decrease of APC levels achieved by RNA interference impairs cell proliferation and DNA replication, not only in 293 cells that express a wild‐type protein, but also in SW480 colon cancer cells that express exclusively a truncated APC fragment. This correlates with a reduction of the levels of cyclin A, cyclin A‐dependent kinase activity, p27kip1 and the catalytic subunit of DNA polymerase δ. Thus, our data suggest that colon cancer cells retain a truncated APC fragment because it is essential for cell proliferation. © 2006 Wiley‐Liss, Inc.
Nocardia tartaricans cells immobilized in sodium alginate–cellulose sulfate–poly (methylene‐co‐guanidine)capsules: mechanical resistance and operational stability
Authors: Bučko Marek , Vikartovská Alica , Gemeiner Peter , Lacík Igor , Kolláriková Gabriela , Marison Ian W 
Published: January 2006

AbstractThe stereospecific hydrolysis of cis‐epoxysuccinate (CES) to L‐(+)‐tartrate, catalysed by the action of CES hydrolase activity in whole Nocardia tartaricans bacterial cells, has been chosen as a model biotransformation system. The performance of cells was studied by immobilization in polyelectrolyte complex (sodium alginate–cellulose sulfate–poly(methylene‐co‐guanidine, SA–CS/PMCG) capsules based on sodium alginate and cellulose sulfate as polyanions, poly(methylene‐co‐guanidine) as polycation, CaCl2 as gelling agent and NaCl as antigelling agent. The encapsulated cells showed a preservation of 80% of the initial catalytic activity in encapsulated cells compared with 15% of retained catalytic activity in free cells after 10 repeated biotransformation cycles. Uniformity of batches of capsules was achieved by the use of an air‐stripping extrusion device fitted with a multiloop reactor. The capsules produced using this device had narrow standard deviations for capsule diameter (<3%) and membrane thickness (<6%). Monodisperse capsules are essential to ensure constant properties, including mechanical resistance and diffusional characteristics. Storage of capsules under different conditions revealed an approximate three‐fold decrease in bursting force after long‐term exposure to the highly sequestering CES, compared with capsules stored in 0.9% (w/v) NaCl. The molecular weight cut‐off of the capsular membrane, determined by inverse size exclusion chromatography, is in the range of the size of CES hydrolase. Copyright © 2006 Society of Chemical Industry
Quantitative myocardial infarction on delayed enhancement MRI. Part I: Animal validation of an automated feature analysis and combined thresholding infarct sizing algorithm
Authors: Hsu Li‐Yueh , Natanzon Alex , Kellman Peter , Hirsch Glenn A. , Aletras Anthony H. , Arai Andrew E. 
Published: January 2006

AbstractPurposeTo develop a computer algorithm to measure myocardial infarct size in gadolinium‐enhanced magnetic resonance (MR) imaging and to validate this method using a canine histopathological reference.Materials and MethodsDelayed enhancement MR was performed in 11 dogs with myocardial infarction (MI) determined by triphenyltetrazolium chloride (TTC). Infarct size on in vivo and ex vivo images was measured by a computer algorithm based on automated feature analysis and combined thresholding (FACT). For comparison, infarct size by human manual contouring and simple intensity thresholding (based on two standard deviation [2SD] and full width at half maximum [FWHM]) were studied.ResultsBoth in vivo and ex vivo MR infarct size measured by the FACT algorithm correlated well with TTC (R = 0.95–0.97) and showed no significant bias on Bland Altman analysis (P = not significant). Despite similar correlations (R = 0.91–0.97), human manual contouring overestimated in vivo MR infarct size by 5.4% of the left ventricular (LV) area (equivalent to 55.1% of the MI area) vs. TTC (P < 0.001). Infarct size measured by simple intensity thresholdings was less accurate than the proposed algorithm (P < 0.001 and P = 0.007).ConclusionThe FACT algorithm accurately measured MI size on delayed enhancement MR imaging in vivo and ex vivo. The FACT algorithm was also more accurate than human manual contouring and simple intensity thresholding approaches. J. Magn. Reson. Imaging 2006. Published 2006 Wiley‐Liss, Inc.
HOXD10 M319K mutation in a family with isolated congenital vertical talus
Authors: Dobbs Matthew B. , Gurnett Christina A. , Pierce Brandon , Exner G. Ulrich , Robarge Jason , Morcuende Jose A. , Cole William G. , Templeton Peter A. , Foster Bruce , Bowcock Anne M. 
Published: January 2006

AbstractCongenital vertical talus (CVT) is a primary dislocation of the talonavicular joint that often occurs in neuromusculoskeletal syndromes, but may also be seen as an isolated abnormality. Six families with isolated CVT were ascertained. DNA was isolated from 21 affected individuals and 17 unaffected individuals from these families, as well as from five sporadic patients with CVT. Variable expressivity was noted in three families, manifesting as clubfoot in three individuals. Genome‐wide linkage analysis generated a maximum two‐point logarithm of odds score on chromosome 2q with D2S1353 (Zmax = 1.43 at θmax = 0.1), 17 Mb from the HOXD gene cluster. DNA from one affected individual of each family was subjected to mutational analysis of the HOXD10 gene. A single missense mutation was identified (M319K, 956T > A) in the homeodomain recognition helix of the HOXD10 gene that segregated with disease in one large British family. This mutation was recently described in a family of Italian descent with CVT and Charcot‐Marie‐Tooth deformity HOXD10 gene mutations were not identified in any of the other families or sporadic patients with CVT, suggesting that genetic heterogeneity underlies this disorder. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:448–453, 2006
Particulate endocytosis mediates biological responses of human mesenchymal stem cells to titanium wear debris
Authors: Okafor Chukwuka C. , Haleem‐Smith Hana , Laqueriere Patrice , Manner Paul A. , Tuan Rocky S. 
Published: January 2006

AbstractContinual loading and articulation cycles undergone by metallic (e.g., titanium) alloy arthroplasty prostheses lead to liberation of a large number of metallic debris particulates, which have long been implicated as a primary cause of periprosthetic osteolysis and postarthroplasty aseptic implant loosening. Long‐term stability of total joint replacement prostheses relies on proper integration between implant biomaterial and osseous tissue, and factors that interfere with this integration are likely to cause osteolysis. Because multipotent mesenchymal stem cells (MSCs) located adjacent to the implant have an osteoprogenitor function and are critical contributors to osseous tissue integrity, when their functions or activities are compromised, osteolysis will most likely occur. To date, it is not certain or sufficiently confirmed whether MSCs endocytose titanium particles, and if so, whether particulate endocytosis has any effect on cellular responses to wear debris. This study seeks to clarify the phenomenon of titanium endocytosis by human MSCs (hMSCs), and investigates the influence of endocytosis on their activities. hMSCs incubated with commercially pure titanium particles exhibited internalized particles, as observed by scanning electron microscopy and confocal laser scanning microscopy, with time‐dependent reduction in the number of extracellular particles. Particulate endocytosis was associated with reduced rates of cellular proliferation and cell–substrate adhesion, suppressed osteogenic differentiation, and increased rate of apoptosis. These cellular effects of exposure to titanium particles were reduced when endocytosis was inhibited by treatment with cytochalasin D, and no significant effect was seen when hMSCs were treated only with conditioned medium obtained from particulate‐treated cells. These findings strongly suggest that the biological responses of hMSCs to wear debris are triggered primarily by the direct endocytosis of titanium particulates, and not mediated by secreted soluble factors. In this manner, therapeutical approaches that suppress particle endocytosis could reduce the bioreactivity of hMSCs to particulates, and enhance long‐term orthopedic implant prognosis by minimizing wear‐debris periprosthethic osteolysis. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:461–473, 2006