bluuebunny/crossref_metadata_2025_split huggingface dataset:
Histologic characteristics of skin cancer in Hiroshima and Nagasaki: Background incidence and radiation effects
Authors: Kishikawa Masao , Koyama Kojiro , Iseki Masachika , Kobuke Toshihiro , Yonehara Shuji , Soda Midori , Ron Elaine , Tokunaga Masayoshi , Preston Dale L. , Mabuchi Kiyohiko , Tokuoka Shoji 
Published: May 2005

AbstractSkin cancers, though rare in Japan, have reportedly been on the rise, but little else is known about epidemiologic features of different histologic types of skin cancer. The Life Span Study cohort, which consists of 93,700 atomic‐bomb survivors, many of whom were exposed to negligibly low radiation doses, and 26,600 people not exposed to radiation, enables a population‐based study of spontaneous as well as radiation‐related cancer risk. Skin tumor incident cases diagnosed between 1958 and 1987 were ascertained by linkage to the Hiroshima and Nagasaki tumor registries augmented by searches of other data sources. Study pathologists reviewed tumor specimens and pathology reports and classified tumors using the World Health Organization classification scheme. They identified 274 primary incident skin cancers, of which 106 were basal cell carcinoma (BCC), 81 were squamous cell carcinoma (SCC), and 14 were malignant melanomas. Background incidence rates and radiation effects were assessed by Poisson regression models allowing for the effects of demographic and other covariates. BCC and SCC background incidence rates were both about 3 per 100,000 per year. BCCs were mainly on the head/neck (81%), whereas SCCs occurred most frequently on the arms/legs (45%) and head/neck (29%), consistent with the presumed role played by solar UV exposure in skin cancer. The BCC rates increased significantly between 1958 and 1987, whereas the SCC rates remained unchanged. The excess absolute risk of BCC per unit skin surface area related to atomic‐bomb radiation exposure did not differ between UV‐exposed and shielded parts of the body, suggesting the additivity of the radiation‐related and background BCC risks. © 2005 Wiley‐Liss, Inc.
Total loss of MHC class I is an independent indicator of good prognosis in breast cancer
Authors: Madjd Zahra , Spendlove Ian , Pinder Sarah E. , Ellis Ian O. , Durrant Lindy G. 
Published: May 2005

AbstractTumours can be recognised by CTL and NK cells. CTL recognition depends on expression of MHC Class I loaded with peptides from tumour antigens. In contrast, loss of MHC Class I results in NK activation. In our study a large set of samples from patients with primary operable invasive breast cancer was evaluated for the expression of MHC Class I heavy and light by immunohistochemical staining of 439 breast carcinomas in a tissue microarray. Forty‐seven percent (206 of 439) of breast carcinomas were considered negative for HLA Class I heavy chain (HC10), whereas lack of anti‐β2m‐antibody staining was observed in 39% (167 of 424) of tumours, with only 3% of the β2m‐negative tumours expressing detectable HLA Class I heavy chain. Correlation with patient outcome showed direct relationship between patient survival and HLA‐negative phenotype (log rank = 0.004). A positive relationship was found between the intensity of expression of MHC Class I light and heavy chains expression and histological grade of invasive tumour (p < 0.001) and Nottingham Prognostic Index (p < 0.001). To investigate whether HLA Class I heavy and light chains expression had independent prognostic significance, Cox multivariate regression analysis, including the parameters of tumour size, lymph node stage, grade and intensity of HC10 and anti‐β2m staining, was carried out. In our analysis, lymph node stage (p < 0.001), tumour grade (p = 0.005) and intensity of MHC Class I light and heavy chains expression were shown to be independent prognostic factors predictive of overall survival (p‐values HC10 = 0.047 and β2m = 0.018). © 2005 Wiley‐Liss, Inc.
Adenoviral modulation of the tumor‐associated system L amino acid transporter, LAT1, alters amino acid transport, cell growth and 4F2/CD98 expressionwith cell‐type specific effects in cultured hepatic cells
Authors: Storey Bill T. , Fugere Celine , Lesieur‐Brooks Anne , Vaslet Charles , Thompson Nancy L. 
Published: May 2005

AbstractAltered expression of metabolite transporters is observed frequently in tumor cell lines and primary neoplasms. The extent to which these may to contribute to the growth autonomy associated with cancer is not clear. LAT1 is a major L‐type amino acid transporter over‐expressed in a variety of cancer types and a light chain component of the CD98 heterodimer. We utilized an adenoviral expression system to modulate the level of LAT1 in a hepatic in vitro model to examine phenotypic changes associated with short‐term exogenous and blocked expression. LAT1 levels were increased three fold and resulted in increased L‐type amino acid transport as a result of adenoviral expression in murine hepatocytes. The protein was expressed on the cell surface and complexed with the CD98 heavy chain known as 4F2. Surprisingly, levels of the total CD98 protein complex were increased 2.4‐fold as a result of adenoviral expression of light chain only, suggesting coordinate regulation. Exogenous overexpression was less effective in normal rat liver cells relative to mouse. LAT1 antisense expression in hepatic tumor cells resulted in a modest though statistically significant decrease in cell number, viability and S‐phase cells over a 5‐day period relative to controls despite the absence of a significant decrease in L‐type transport over this period. These studies are preparatory to in vivo efforts focusing on LAT1/CD98 as a potential therapeutic target. © 2005 Wiley‐Liss, Inc.
Identification of postoperative adjuvant chemotherapy responders in non‐small cell lung cancer by novel biomarker
Authors: Hirano Takashi , Kato Harubumi , Maeda Masahiro , Gong Yunbo , Shou Yanning , Nakamura Miho , Maeda Junichi , Yashima Koichi , Kato Yasufumi , Akimoto Shingo , Ohira Tatsuo , Tsuboi Masahiro , Ikeda Norihiko 
Published: May 2005

AbstractCisplatin‐based (CDDP‐based) adjuvant chemotherapy of non‐small cell lung cancer (NSCLC) was reported to yield 5–15% improvement in 5‐year survival compared to complete resection alone. The importance of information concerning preselection of good responders has become increasingly evident. The purpose of our study is the establishment of a preselection of good responders for CDDP‐based adjuvant chemotherapy. We investigated protein expressions comparing intensity between parent strains (H69 and PC14 lung cancer cultured cells) and resistant strains against CDDP using 2‐dimensional polyacrylamide gel electrophoresis (2‐DE). Immunohistochemically, we evaluated the relationship between protein expression associated with CDDP‐resistance and the clinical effects of platinum‐based postoperative adjuvant chemotherapy using 126 surgically‐resected NCLC materials. We detected 2 kinds of polypeptides that changed expression levels on 2‐DE gels. The analyses of the amino acid sequence showed that these polypeptides were reticulocalbin (RCN) and glutathione‐S‐transferase‐π (GST‐π). The 2‐DE analysis showed decreased expression in RCN and overexpression in GST‐π with the acquisition of CDDP‐drug resistance. RCN‐transfectant of H69 CDDP‐resistant strain showed intermediate sensitivity between the parent strain and the CDDP‐resistant strain. RCN‐positive cases showed a statistically significant better disease‐free survival only in the cases receiving postoperative platinum‐based adjuvant chemotherapy after curative resection (p = 0.007). In addition, cases that were both RCN‐positive and GST‐π‐negative showed a statistically significantly better outcome (p = 0.0150). In the cases without postoperative adjuvant chemotherapy no relationship between the outcome and these expressions was seen. The evaluation of RCN and GST‐π might provide valuable information concerning postoperatively therapeutic strategy from the standpoint of individualized postoperative therapy. © 2005 Wiley‐Liss, Inc.
Genomewide loss of heterozygosity and its clinical associations in non small cell lung cancer
Authors: Tseng Ruo‐Chia , Chang Jer‐Wei , Hsien Feng‐Jen , Chang Ya‐Hui , Hsiao Chin‐Fu , Chen Jung‐Ta , Chen Chih‐Yi , Jou Yuh‐Shan , Wang Yi‐Ching 
Published: May 2005

AbstractWe extensively allelotyped a panel of 71 microdissected primary surgically resected non small cell lung cancer (NSCLC) tumors to identify chromosomal regions that are likely to contain tumor suppressor genes (TSGs) or associated with clinicopathologic and prognostic effects. Loss of heterozygosity (LOH) was detected by genotyping of 177 microsatellite markers and correlation of LOH with clinicopathologic parameters and prognosis was analyzed. Twenty markers showed an LOH frequency greater than 48%, and 8 of them (2p23.3, 2p24.3, 2q35, 6p22.2, 7p14.3, 7p22.2, 17q24.3 and 21q22.3) were novel in NSCLC. The high LOH regions were confirmed by further aligning continuous LOH regions from another set of 24 NSCLC tissues and defining 7 minimal deletion regions ranging from 1.29 to 12.26 cM. The aberrations of 8 markers showed a significant correlation with alteration of p16 and Rb proteins, suggesting the gene(s) located in the chromosomal loss that may interact with p16/Rb pathway. In addition, markers specifically associated with smoking, histology types and tumor stages were identified and the linked candidate TSGs were suggested. For example, marker D1S1612 closely linked with Mig‐6 gene was associated with smoking patients, squamous cell carcinoma patients and late‐stage patients. Furthermore, 3 markers, D2S2968, D6S2439 and D7S1818, were significantly associated with poor prognosis of NSCLC patients using both univariate and multivariate Cox's regression analyses (p = 0.035, 0.022 and 0.006, respectively). These markers can potentially be used for early lung cancer detection, outcome measurement and the positional cloning of new TSGs whose loss of function contributes to NSCLC tumorigenesis. © 2005 Wiley‐Liss, Inc.
International lung cancer trends by histologic type: Male:Female differences diminishing and adenocarcinoma rates rising
Authors: Devesa Susan S. , Bray Freddie , Vizcaino A. Paloma , Parkin D. Max 
Published: May 2005

AbstractLung cancer rates have peaked among men in many areas of the world, but rates among women continue to rise. Most lung cancers are squamous cell carcinoma, small cell carcinoma, or adenocarcinoma; trends vary according to type. We compiled population‐based morphology‐specific incidence data from registries contributing to the International Agency for Research on Cancer (IARC) databases. Unspecified cancers and carcinomas were reallocated based on a registry, time period, sex and age group‐specific basis. Where available, data from several registries within a country were pooled for analysis. Rates per 100,000 person‐years for 1980–1982 to 1995–1997 were age‐adjusted by the direct method using the world standard. Squamous cell carcinoma rates among males declined 30% or more in North America and some European countries while changing less dramatically in other areas; small cell carcinoma rates decreased less rapidly. Squamous and small cell carcinoma rates among females generally rose, with the increases especially pronounced in the Netherlands and Norway. In contrast, adenocarcinoma rates rose among males and females in virtually all areas, with the increases among males exceeding 50% in many areas of Europe; among females, rates also rose rapidly and more than doubled in Norway, Italy and France. Rates of all lung cancer types among women and adenocarcinoma among men continue to rise despite declining cigarette use in many Western countries and shifts to filtered/low‐tar cigarettes. Renewed efforts toward cessation and prevention are mandatory to curb the prevalence of cigarette smoking and to reduce lung cancer rates eventually. © 2005 Wiley‐Liss, Inc.
A novel mouse model for segmental orthotopic colon cancer
Authors: Alencar Herlen , King Ray , Funovics Martin , Stout Charles , Weissleder Ralph , Mahmood Umar 
Published: May 2005

AbstractSpontaneous colon tumor mouse strains offer numerous advantages in modeling disease. However, the wide temporal window in which lesions form and the stochastic nature of lesion location require larger cohorts for assessment of disease modulation. Reliable, reproducible and inexpensive mouse models of early‐stage and invasive cancer would add to existing transgenic models. We show a new method for the creation of orthotopic murine tumors centered in the mucosal and submucosal layers anywhere in the colon, allowing creation of lesions of known age, location and extent. The system overcomes the disadvantages of heterotopic implantation and allows evaluation of lesions distally in the colon as well as proximally, thereby providing an additional method to study the effects of regionality. Invasion, host vascularization and application to disparate cell lines are demonstrated. Noninvasive imaging with magnetic resonance and colonoscopy, allowed in part by the tumor location, show potential applications of this approach. © 2005 Wiley‐Liss, Inc.
Etiologic factors associated with p53 immunostaining in cutaneousmalignant melanoma
Authors: Purdue Mark P. , From Lynn , Kahn Harriette J. , Armstrong Bruce K. , Kricker Anne , Gallagher Richard P. , McLaughlin John R. , Klar Neil S. , Marrett Loraine D. ,   The Genes, Environment and Melanoma Working Group
Published: May 2005

AbstractFindings from a case‐control study of cutaneous malignant melanoma (CMM) in Queensland, Australia, suggest that melanomas exhibiting p53 immunostaining possess different risk factors from those of other melanomas. To further explore this hypothesis, a case‐only analysis of risk factors for p53 immunostaining with anti‐p53 MAb DO‐7 was undertaken in 523 people diagnosed with CMM in Canada and Australia. Phenotypic factors and past sun exposure were measured using a self‐administered questionnaire and telephone interview. The presence of strong p53 staining (>10% of cell nuclei positively stained vs. <1% staining) was positively associated with some indicators of high cumulative sun exposure: lentigo maligna melanoma subtype (OR = 3.2 vs. superficial spreading subtype), melanoma location on the head and neck (OR = 2.8 vs. back), histopathologic evidence of solar elastosis (OR = 2.1) and previous diagnosis of nonmelanoma skin cancer (OR = 2.4). Strong staining was negatively associated with high nevus density on the back (OR = 0.2 for >25 nevi vs. 0–3 nevi) and histologic evidence of a coexisting nevus (OR = 0.3). Other factors associated with strong p53 immunostaining include greater Breslow thickness (OR = 7.4 for >4.00 vs. <0.76 mm), male sex (OR = 2.2) and dense freckling (OR = 6.6 vs. few freckles). Of these, thickness, male sex, dense freckling, low nevus density on the back, histologic subtype and history of nonmelanoma skin cancer appeared to be independently associated with strong p53 staining. Our findings are consistent with the Queensland study in suggesting that variables indicating high accumulated sun exposure are positively associated with p53 staining and that an increased number of nevi is positively associated with its absence; they may reflect etiologic and pathogenetic heterogeneity in melanoma. © 2005 Wiley‐Liss, Inc.
Dendritic cell maturation by CD11c− T cells and Vα24+ natural killer T‐cell activation by α‐Galactosylceramide
Authors: Ishikawa Eiichi , Motohashi Shinichiro , Ishikawa Aki , Ito Toshihiro , Uchida Tetsuro , Kaneko Takaaki , Tanaka Yuriko , Horiguchi Shigetoshi , Okamoto Yoshitaka , Fujisawa Takehiko , Tsuboi Koji , Taniguchi Masaru , Matsumura Akira , Nakayama Toshinori 
Published: May 2005

AbstractHuman invariant Vα24+ natural killer T (NKT) cells display potent antitumor activity upon stimulation. Activation of endogenous Vα24+ NKT cells would be one strategy for the treatment of cancer patients. For example, dendritic cells (DCs) loaded with a glycolipid NKT cell ligand, α‐galactosylceramide (αGalCer, KRN7000), are a possible tool for the activation and expansion of functional Vα24+ NKT cells in vivo. In this report, we demonstrate that the levels of expansion and the ability to produce IFN‐γ of Vα24+ NKT cells induced by αGalCer‐loaded whole PBMCs cultured with IL‐2 and GM‐CSF (IL‐2/GM‐CSF‐cultured PBMCs) were superior to those of cells induced by monocyte‐derived CD11c+ DCs (moDCs) developed with IL‐4 and GM‐CSF. Interestingly, CD11c+ cells in the IL‐2/GM‐CSF‐cultured PBMCs showed a mature phenotype without further stimulation and exerted potent stimulatory activity on Vα24+ NKT cells to enable them to produce IFN‐γ preferentially at an extent equivalent to mature moDCs induced by stimulation with LPS or a cytokine cocktail. Cocultivation with CD11c− cells in the IL‐2/GM‐CSF‐cultured PBMCs induced maturation of moDCs. In particular, CD11c−CD3+ T cells appeared to play important roles in DC maturation. In addition, TNF‐α was preferentially produced by CD11c−CD3+ T cells in IL‐2/GM‐CSF‐cultured PBMCs and was involved in the maturation of moDCs. Thus, the maturation of DCs induced by CD11c− T cells through TNF‐α production appears to result in the efficient expansion and activation of Vα24+ NKT cells to produce IFN‐γ preferentially. © 2005 Wiley‐Liss, Inc.
Androgen receptor modifications in prostate cancer cells upon long‐termandrogen ablation and antiandrogen treatment
Authors: Marques Rute B. , Erkens‐Schulze Sigrun , de Ridder Corrina M. , Hermans Karin G. , Waltering Kati , Visakorpi Tapio , Trapman Jan , Romijn Johannes C. , van Weerden Wytske M. , Jenster Guido 
Published: May 2005

AbstractTo study the mechanisms whereby androgen‐dependent tumors relapse in patients undergoing androgen blockade, we developed a novel progression model for prostate cancer. The PC346C cell line, established from a transurethral resection of a primary tumor, expresses wild‐type (wt) androgen receptor (AR) and secretes prostate‐specific antigen (PSA). Optimal proliferation of PC346C requires androgens and is inhibited by the antiandrogen hydroxyflutamide. Orthotopic injection in the dorsal‐lateral prostate of castrated athymic nude mice did not produce tumors, whereas fast tumor growth occurred in sham‐operated males. Three androgen‐independent sublines were derived from PC346C upon long‐term in vitro androgen deprivation: PC346DCC, PC346Flu1 and PC346Flu2. PC346DCC exhibited androgen‐insensitive growth, which was not inhibited by flutamide. AR and PSA were detected at very low levels, coinciding with background AR activity in a reporter assay, which suggests that these cells have bypassed the AR pathway. PC346Flu1 and PC346Flu2 were derived by culture in steroid‐stripped medium supplemented with hydroxyflutamide. PC346Flu1 strongly upregulated AR expression and showed 10‐fold higher AR activation than the parental PC346C. PC346Flu1 proliferation was inhibited in vitro by R1881 at 0.1 nM concentration, consistent with a slower tumor growth rate in intact males than in castrated mice. PC346Flu2 carries the well‐known T877A AR mutation, causing the receptor to become activated by diverse nonandrogenic ligands including hydroxyflutamide. Array‐based comparative genomic hybridization revealed little change between the various PC346 lines. The common alterations include gain of chromosomes 1, 7 and 8q and loss of 13q, which are frequently found in prostate cancer. In conclusion, by in vitro hormone manipulations of a unique androgen‐dependent cell line expressing wtAR, we successfully reproduced common AR modifications observed in hormone‐refractory prostate cancer: downregulation, overexpression and mutation. © 2005 Wiley‐Liss, Inc.
Omega‐3 polyunsaturated fatty acids attenuate breast cancer growth through activation of a neutral sphingomyelinase‐mediated pathway
Authors: Wu Min , Harvey Kevin A. , Ruzmetov Nargiz , Welch Zachary R. , Sech Laura , Jackson Kim , Stillwell William , Zaloga Gary P. , Siddiqui Rafat A. 
Published: May 2005

AbstractThe effect of fish oils and their active omega‐3 fatty acid constituents, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), were investigated on breast cancer growth. In in vivo experiments, mice were fed diets that were rich in either omega‐3 (fish oil) or omega‐6 (corn oil) fatty acids. Three weeks after implantation of MDA‐MB‐231 breast cancer cells, the tumor volume and weight were significantly lower (p < 0.05) for mice fed the omega‐3 diets compared to those fed the omega‐6 diets. Dietary fish oil also caused a 40% (p < 0.05) increase in neutral sphingomyelinase (N‐SMYase) activity in the tumors. The tumor tissues from fish oil‐fed animals expressed elevated p21 (waf1/cip1) mRNA, whereas tumor tissues from corn oil‐fed animals exhibited undetectable levels of p21 expression. In in vitro experiments, at concentrations as low as 25 μM, DHA and EPA inhibited the growth of cultured MDA‐MB‐231 cells in a dose‐dependent manner by 20–25% (p < 0.05). N‐SMYase activity was also increased by 30–40% (p < 0.05) in the DHA‐ or EPA‐treated cells in which an increase in ceramide formation was observed. DHA and EPA were both observed to enhance membrane bleb formation and also to induce the expression of p21. Omega‐3 fatty acids‐induced bleb formation and p21 expression were inhibited by the N‐SMYase inhibitor GW4869, which also inhibited apoptosis by approximately 40% (p < 0.05). The results suggest that inhibition of breast cancer growth in nude mice by dietary fish oil and inhibition of breast cancer cell growth in culture by treatment with DHA and EPA is mediated by activation of N‐SMYase. © 2005 Wiley‐Liss, Inc.
Using dialogues with customers as sources of knowledge
Authors: Groen Martin 
Published: May 2005

AbstractEvery day organizations have numerous dialogues with (potential) customers. The representatives of the organization see themselves presented with the daunting task of how to identify and use the most relevant information that the customer communicated. Equally vexing for these dialogue participants is how to ensure that what is intended with a certain utterance in a dialogue is understood in the way the speaker intended. It is therefore not surprising that not all dialogues lead to satisfactory results for the participants. Customers tell organizations in dialogues (via media like e‐mail, telephone, letters or ‘physical’ visits) what they expect that the organization needs to know to be able to serve them in a satisfactory way. Equally, organizations would like to know whether the message they are communicating is understood in the way the organization intended and if the products or services they are providing matches any persistent (latent) need of a selected (group of) customer(s). This research is aimed at developing a computational instrument to come to terms with these issues. The seminal theory of Clark (1996) might assist us in this endeavour. In particular, the concepts of common ground and larger purpose present possibilities that could support us in our attempts to gain more knowledge from dialogues with customers. Copyright © 2005 John Wiley & Sons, Ltd.