bluuebunny/crossref_metadata_2025_split huggingface dataset:
Alpha‐6 integrin is necessary for the tumourigenicity of a stem cell‐like subpopulation within the MCF7 breast cancer cell line
Authors: Cariati Massimiliano , Naderi Ali , Brown John P. , Smalley Matthew J. , Pinder Sarah E. , Caldas Carlos , Purushotham Anand D. 
Published: October 2007

AbstractThe identification of mammary epithelial stem cells raises the hypothesis that these cells may be crucial in the pathogenesis of breast cancer. To further support this, a highly tumourigenic sub‐population of cancer cells has recently been identified in primary and metastatic breast cancer samples. In this study, a sub‐population of cells displaying features normally attributed to stem cells was identified within the breast cancer cell line MCF‐7. This sub‐population is capable of growth in anchorage‐independent conditions as spherical organoids, displays resistance to proapoptotic agents and significantly greater tumourigenicity than its parental line, with as few as 1,000 cells able to form tumours in immunodeficient mice. Cells within this sub‐population can be enriched by serial passages in anchorage‐independence, and are characterized by over‐expression of the adhesion molecule α6‐integrin. Alpha‐6 integrin proves to be required for the growth and survival of these cells, as the knockdown of ITGA6 causes mammosphere‐derived cells to lose their ability to grow as mammospheres and abrogates their tumourigenicity in mice. These findings support the existence of a highly tumourigenic sub‐population in breast cancer cells. Furthermore, it shows α6‐integrin as a potential therapeutic target aimed at tumour‐generating subsets of breast cancer cells. © 2007 Wiley‐Liss, Inc.
Exogenous expression of Esophagin/SPRR3 attenuates the tumorigenicity of esophageal squamous cell carcinoma cells via promoting apoptosis
Authors: Zhang Yu , Feng Yan‐Bin , Shen Xiao‐Ming , Chen Bao‐Sheng , Du Xiao‐Li , Luo Man‐Li , Cai Yan , Han Ya‐Ling , Xu Xin , Zhan Qi‐Min , Wang Ming‐Rong 
Published: October 2007

AbstractEsophagin/SPRR3 is one of the cornified‐envelope structural precursor proteins, which is expressed during epithelia cell differentiation. In 1996, another research group discovered, and our own laboratory subsequently confirmed, frequent and dramatic decreased Esophagin/SPRR3 expression in esophageal squamous cell carcinoma (ESCC). However, the role of Esophagin/SPRR3 in tumorigenesis of esophageal epithelium remains undetermined. In this study, we demonstrate that expression of Esophagin/SPRR3 is frequently downregulated in ESCC. In contrast, no correlations between downregulation of Esophagin/SPRR3 expression and clinicopathologic characteristics were observed. Diminished Esophagin/SPRR3 expression was present in dysplastic epithelia, suggesting that Esophagin/SPRR3 alteration could represent an early event in squamous carcinogenesis of the esophagus. Exogenous expression of Esophagin/SPRR3 significantly suppressed the ability of ESCC cells to form colonies in plastic and soft agar, as well as tumor formation in vivo. Terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end label assay and immunofluorescence analysis of the active form of Caspase 3 indicated that dysregulated apoptosis might contribute to reduced tumorigenicity. In particular, upregulation of CDK11p46 protein was observed in ESCC cells expressing Esophagin/SPRR3, but not in control cells, indicating that Esophagin/SPRR3‐induced apoptosis may be due, at least in part, to increased expression of CDK11p46 protein. These findings suggest that Esophagin/SPRR3 may play a role in the maintenance of normal esophageal epithelial homeostasis, and that aberrant expression of Esophagin/SPRR3 may contribute to the tumorigenesis of ESCC. © 2007 Wiley‐Liss, Inc.
Gankyrin oncoprotein overexpression as a critical factor for tumor growth in human esophageal squamous cell carcinoma and its clinical significance
Authors: Ortiz Cristian M. , Ito Tetsuo , Tanaka Eiji , Tsunoda Shigeru , Nagayama Satoshi , Sakai Yoshiharu , Higashitsuji Hiroaki , Fujita Jun , Shimada Yutaka 
Published: October 2007

AbstractTo elucidate the possible involvement of gankyrin in ESCC progression and the effect of its down‐regulation in ESCC, we investigated the expression of gankyrin in ESCC tissues comparing it with the corresponding normal esophageal epithelia and tested a short‐hairpin RNA (shRNA) expression vector for gankyrin in ESCC cell lines. Gankyrin protein expression in 11 ESCC cell lines (KYSE series) was examined by RT‐PCR and western blot. The expression of gankyrin mRNA in 30 ESCC tissues was compared with the corresponding normal epithelia by Real‐time PCR. Expression of gankyrin protein was immunohistochemically analyzed in the ESCC of 103 patients. A gankyrin‐shRNA vector was stably transfected into KYSE 170 cells to assess the role of gankyrin in cell motility, invasion and proliferation in vitro and tumor formation in vivo. Gankyrin expression increased in all 11 ESCC cell lines. Real‐time PCR revealed that gankyrin expression was higher in the cancerous tissue for all 30 patients. In immunohistochemistry, gankyrin overexpression was correlated with lower survival rate (p = 0.0001), extent of the primary tumor, lymph node metastasis, distant lymph node metastasis and stage (p = 0.0072, p = 0.0004, p = 0.0172 and p = 0.0002, respectively). A shRNA vector against gankyrin repressed growth, cell motility, invasiveness in vitro and tumor formation in vivo. Gankyrin overexpression is associated with poor prognosis. It may play an important role in ESCC tumor progression and could be a potentially important therapeutic gene target in ESCC. © 2007 Wiley‐Liss, Inc.
Retracted: Immunotherapy of metastatic breast cancer patients with vitamin D‐binding protein‐derived macrophage activating factor (GcMAF)
Authors: Yamamoto Nobuto , Suyama Hirofumi , Yamamoto Nobuyuki , Ushijima Naofumi 
Published: October 2007

AbstractThe above article from the International Journal of Cancer, published online on 12 October 2007 in Wiley Online Library and in Volume 122, Issue 2, pp 461–467, has been retracted by agreement between the journal Editor‐in‐Chief Peter Lichter and Wiley Periodicals, Inc. due to irregularities in the documentation for institutional review board approval.
Cutaneous human papillomavirus 88: Remarkable differences in viral load
Authors: Kullander Johanna , Handisurya Alessandra , Forslund Ola , Geusau Alexandra , Kirnbauer Reinhard , Dillner Joakim 
Published: October 2007

AbstractA human papillomavirus (HPV) was cloned from a patient with multiple squamous cell carcinomas (SCCs) and identified as HPV88, recently categorized into a new species within the genus Gamma. The HPV88 viral load in an SCC of the index patient exceeded 1 million copies/cell. By contrast, a survey of 447 skin lesions (79 actinic keratoses, 73 seborrhoeic keratoses, 169 basal cell carcinomas and 126 SCCs) and 362 healthy skin biopsies found detectable HPV88 DNA in only 7 specimens. All these had very low viral loads (<1 copy/103 cells) implying extreme biological variability in viral load. © 2007 Wiley‐Liss, Inc.
Passive smoking and lung cancer in Japanese non‐smoking women: A prospective study
Authors: Kurahashi Norie , Inoue Manami , Liu Ying , Iwasaki Motoki , Sasazuki Shizuka , Sobue Tomotaka , Tsugane Shoichiro ,   for the JPHC Study Group
Published: October 2007

AbstractAlthough smoking is a major cause of lung cancer, the proportion of lung cancer cases among Japanese women who never smoked is high. As the prevalence of smoking in Japan is relatively high in men but low in women, the development of lung cancer in non‐smoking Japanese women may be significantly impacted by passive smoking. We conducted a population‐based prospective study established in 1990 for Cohort I and in 1993 for Cohort II. The study population was defined as all residents aged 40–69 years at the baseline survey. 28,414 lifelong non‐smoking women provided baseline information on exposure to tobacco smoke from their husband, at the workplace and during childhood. Over 13 years of follow‐up, 109 women were newly diagnosed with lung cancer, of whom 82 developed adenocarcinoma. Compared with women married to never smokers, hazard ratio (HR) [95% confidence interval (CI)] for all lung cancer incidence in women who lived with a smoking husband was 1.34 (95% CI 0.81–2.21). An association was clearly identified for adenocarcinoma (HR 2.03, 95% CI 1.07–3.86), for which dose‐response relationships were seen for both the intensity (p for trend = 0.02) and amount (p for trend = 0.03) of the husband's smoking. Passive smoking at the workplace also increased the risk of lung cancer (HR 1.32, 95% CI 0.85–2.04). Moreover, a higher risk of adenocarcinoma was seen for combined husband and workplace exposure (HR 1.93, 95% CI 0.88–4.23). These findings confirm that passive smoking is a risk factor for lung cancer, especially for adenocarcinoma among Japanese women. © 2007 Wiley‐Liss, Inc.
2‐Methoxyestradiol modulates β‐catenin in prostate cancer cells: A possible mediator of 2‐methoxyestradiol‐induced inhibition of cell growth
Authors: Van Veldhuizen Peter J. , Ray Gibanananda , Banerjee Snigdha , Dhar Gopal , Kambhampati Suman , Dhar Animesh , Banerjee Sushanta K. 
Published: October 2007

Abstract2‐Methoxyestradiol (2‐ME2) is a novel anticancer agent because of its ability to potentiate apoptotic cell death and inhibit cancer cell growth and angiogenesis. The modes of action of this agent, however, have not yet been fully elucidated. In our study, we have investigated whether 2‐ME2 is able to modulate β‐catenin signaling in prostate cancer cells, which is one of the major players in cell–cell adhesion, proliferation, apoptosis and carcinogenesis. We found that β‐catenin levels were significantly upregulated by 2‐ME2 in a dose‐dependent manner in androgen dependent and independent prostate cancer total cellular extracts. We further show that β‐catenin levels were significantly increased in the membrane fraction, while nuclear fractions of β‐catenin were downregulated in the 2‐ME2‐treated cells. Accumulation of dephospho‐β‐catenin (nondegraded form) parallel with Bcl‐2 and Cyclin D1 downregulation was also achieved after 2‐ME2 treatment. Moreover, we demonstrate that the β‐catenin production by 2‐ME2 is mediated through the MEK/ERK‐2 signaling pathway. Collectively, these results suggest that the cytostatic effect of 2‐ME2 may be mediated through the prevention of the translocation of β‐catenin to the nucleus parallel with an increase in cell–cell adhesion by increasing membrane β‐catenin production, eventually preventing cell migration. Moreover, dephospho‐β‐catenin accumulation by 2ME2 in the cytoplasm may contribute to the induction of apoptosis of these cells. Finally, studies testing the efficacy of 2‐ME2 in human prostate cancer are warranted to determine whether the inhibition of the expected loss of membranous β‐catenin and the upregulation of nuclear β‐catenin can prevent prostate cancer development and progression. © 2007 Wiley‐Liss, Inc.
Cost‐effectiveness of primary cytology and HPV DNA cervical screening
Authors: Bistoletti Peter , Sennfält Karin , Dillner Joakim 
Published: October 2007

AbstractBecause cost‐effectiveness of different cervical cytology screening strategies with and without human papillomavirus (HPV) DNA testing is unclear, we used a Markov model to estimate life expectancy and health care cost per woman during the remaining lifetime for 4 screening strategies: (i) cervical cytology screening at age 32, 35, 38, 41, 44, 47, 50, 55 and 60, (ii) same strategy with addition of testing for HPV DNA persistence at age 32, (iii) screening with combined cytology and testing for HPV DNA persistence at age 32, 41 and 50, iv) no screening. Input data were derived from population‐based screening registries, health‐service costs and from a population‐based HPV screening trial. Impact of parameter uncertainty was addressed using probabilistic multivariate sensitivity analysis. Cytology screening between 32 and 60 years of age in 3–5 year intervals increased life expectancy and life‐time costs were reduced from 533 to 248 US Dollars per woman compared to no screening. Addition of HPV DNA testing, at age 32 increased costs from 248 to 284 US Dollars without benefit on life expectancy. Screening with both cytology and HPV DNA testing, at ages 32, 41 and 50 reduced costs from 248 to 210 US Dollars with slightly increased life expectancy. In conclusion, population‐based, organized cervical cytology screening between ages 32 to 60 is highly cost‐efficient for cervical cancer prevention. If screening intervals are increased to at least 9 years, combined cytology and HPV DNA screening appeared to be still more effective and less costly. © 2007 Wiley‐Liss, Inc.
Assessment of causes of death in a prostate cancer screening trial
Authors: Mäkinen Tuukka , Karhunen Pekka , Aro Jussi , Lahtela Jorma , Määttänen Liisa , Auvinen Anssi 
Published: October 2007

AbstractAccurate assessment of the causes of death is crucial for a conclusive evaluation of the ongoing prostate cancer screening trials. Here, we report the validity of the official causes of death as compared with an independent expert review in the Finnish prostate cancer screening trial. Because nearly 80,000 men were involved, death‐cause evaluation was restricted to men diagnosed for prostate cancer. Medical charts were retrieved and the cause of death was assigned by an expert review panel for all deaths among men with prostate cancer during the study period, 1996–2003. The panel decision was compared with both death certificates and the official causes of death as assigned by Statistics Finland. Of a total of 315 deaths, the review panel attributed 127 (41%) to prostate cancer and 184 (59%) to other causes, the corresponding figures in death certificates being 124 (40%) and 187 (60%). Four cases were excluded because of insufficient information. The death‐certificate data were in agreement with the panel's assessment in 305 out of 311 cases (overall agreement 97.7%, κ = 0.95). The overall agreement between the official causes of death and the panel's decision was 97.4% (304/311, κ = 0.95). The sensitivity of the certificates in identifying prostate cancer deaths was 96.1% (panel as golden standard). Correspondingly, specificity was 98.9%. The official causes of death thus provide an accurate means for evaluating disease‐specific mortality in a large population‐based prostate‐cancer screening trial in Finland. © 2007 Wiley‐Liss, Inc.
Haplotypes of the estrogen receptor beta gene and breast cancer risk
Authors:   Breast and Prostate Cancer Cohort Consortium
Published: October 2007

AbstractExposure to exogenous (oral contraceptives, postmenopausal hormone therapy) and endogenous (number of ovulatory cycles, adiposity) steroid hormones is associated with breast cancer risk. Breast cancer risk associated with these exposures could hypothetically be modified by genes in the steroid hormone synthesis, metabolism and signaling pathways. Estrogen receptors are the first step along the path of signaling cell growth and development upon stimulation with estrogens. The National Cancer Institute Breast and Prostate Cancer Cohort Consortium has systematically selected haplotype tagging SNPs in genes along the steroid hormone synthesis, metabolism and binding pathways, including the estrogen receptor beta (ESR2) gene. Four htSNPs tag the 6 major (>5% frequency) haplotypes of the ESR2 gene. These polymorphisms have been genotyped in 5,789 breast cancer cases and 7,761 controls nested within the American Cancer Society Cancer Prevention Study II, European Prospective Investigation into Cancer and Nutrition, Multiethnic Cohort, Nurses' Health Study and Women's Health Study cohorts. None of the SNPs were independently associated with breast cancer risk. One haplotype of the ESR2 gene was associated with breast cancer risk before correction for multiple testing (OR 1.17, 95% CI 1.07–1.28, p = 0.0007). This haplotype remained associated with breast cancer risk after adjustment for multiple testing using a permutation procedure. There was no statistically significant heterogeneity in SNP or haplotype odds ratios across cohorts. These data suggest that inherited variants in ESR2 (while possibly conferring a small increased risk of breast cancer) are not associated with appreciable (OR > 1.2) changes in breast cancer risk among Caucasian women. © 2007 Wiley‐Liss, Inc.
Effects of two whole blood systems (DALI and Liposorber D) for LDL apheresis on lipids and cardiovascular risk markers in severe hypercholesterolemia
Authors: Otto Carsten , Berster Jutta , Otto Bärbel , Parhofer Klaus G. 
Published: October 2007

AbstractLDL apheresis is an extracorporal modality to lower the concentration of atherogenic lipoproteins, e.g., LDL cholesterol. We compared two recently introduced whole‐blood LDL apheresis systems inpatients with hypercholesterolemia in a randomized cross‐over trial with respect to their effects on lipoproteins as well as on other cardiovascular risk markers. Six patients (4 women, 2 men, median age 62.5 years, median BMI 25.9 kg/m2) on regular LDL apheresis were randomly assigned to receive six weekly treatments with either DALI (Fresenius) or Liposorber D (Kaneka). After 6 weeks, the patients were switched to the other device (again six weekly treatments). Blood was drawn before and immediately after LDL apheresis at three time points (last regular apheresis before the study; after six treatments with DALI and after six treatments with Liposorber D). LDL cholesterol concentration before the sixth apheresis (DALI 129 mg/dL, Liposorber D 132 mg/dL) as well as LDL cholesterol reduction during the sixth apheresis (DALI 68.3% and Liposorber D 68.4%) were similar with the two systems. CRP and fibrinogen concentrations were lower but interleukin‐6, myeloperoxidase, and resistin concentrations were higher after the last Liposorber treatment compared with DALI (P < 0.05, respectively). No differences were observed concerning adiponectin, ghrelin, and PYY levels. In conclusion, both devices were highly effective in eliminating atherogenic lipoproteins. CRP and fibrinogen were better eliminated with Liposorber D. However, following Liposorber D, interleukin‐6 levels were higher than after DALI possibly indicating an increased inflammatory activation. J. Clin. Apheresis, 2007. © 2007 Wiley‐Liss, Inc.
“Non‐heart‐beating,” or “cardiac death,” organ donation: Why we should care
Authors: Rady Mohamed Y. , Verheijde Joseph L. , McGregor Joan 
Published: October 2007

AbstractBACKGROUNDOrgan donation after cessation of cardiac pump activity is referred to as non‐heart‐beating organ donation (NHBOD). NHBOD donors can be neurologically intact; they do not fulfill the brain death criteria prior to cessation of cardiac pump activity. For hospitals to participate in NHBOD, they must comply with a newly introduced federal requirement for ICU patients whose deaths are considered imminent after withdrawal of life support. This report describes issues related to NHBOD.METHODSA nonstructured review of selected publications and Web sites was undertaken.RESULTSScientific evidence from autoresuscitation and extracorporeal perfusion suggests that verifying cardiorespiratory arrest lasting 2–5 minutes does not uniformly comply with the dead donor rule, so that the process of organ procurement can be the irreversible event defining death in organ donors. The interest of organ procurement organizations and affiliates in maximizing recovery of transplantable organs introduces self‐serving bias in gaining consent for organ donation and abandons the basic tenet of obtaining true informed consent. The impact of donor management and procurement protocols on end‐of‐life (EOL) care and the potential trade‐off are not disclosed, raising concern about whether potential donors and their families are fully informed before consenting to donation.CONCLUSIONSThe use of comprehensive quality indicators for EOL care can determine the impact of NHBOD on care offered to donors and the effects on families and health care providers. Detailed evaluation of NHBOD will enable the public to make informed decisions about participating in this type of organ donation. Journal of Hospital Medicine 2007;2:324–334. © 2007 Society of Hospital Medicine.
Barriers to mobility during hospitalization from the perspectives of older patients and their nurses and physicians
Authors: Brown Cynthia J. , Williams Beverly R. , Woodby Lesa L. , Davis Linda L. , Allman Richard M. 
Published: October 2007

AbstractBACKGROUNDLow mobility is common during hospitalization and is associated with adverse outcomes. Understanding barriers to the maintenance or improvement of mobility is important to the development of successful interventions.OBJECTIVESTo identify barriers to mobility during hospitalization from the perspectives of older patients and their primary nurses and physicians, to compare and contrast the perceived barriers among these groups, and to make a conceptual model.DESIGNQualitative interviews analyzed and interpreted using a grounded theory approach.SETTINGMedical wards of a university hospital.PARTICIPANTSTwenty‐nine participants—10 patients ≥ 75 years, 10 nurses, and 9 resident physicians.MEASUREMENTSParticipants were interviewed using a semistructured interview guide, with similar questions for patients and health care providers. Interviews were audiotaped, transcribed, and reviewed for common themes by independent reviewers. Perceived barriers to mobility were identified, and their nature and frequency were examined for each respondent group.RESULTSContent analysis identified 31 perceived barriers to increased mobility during hospitalization. Barriers most frequently described by all 3 groups were: having symptoms (97%), especially weakness (59%), pain (55%), and fatigue (34%); having an intravenous line (69%) or urinary catheter (59%); and being concerned about falls (79%). Lack of staff to assist with out‐of‐bed activity was mentioned by patients (20%), nurses (70%), and physicians (67%). Unlike patients, health care providers attributed low mobility among hospitalized older adults to lack of patient motivation and lack of ambulatory devices.CONCLUSIONSRecognizing and understanding perceived barriers to mobility during hospitalization of older patients is an important first step toward developing successful interventions to minimize low mobility. Journal of Hospital Medicine 2007;2:305–313. © 2007 Society of Hospital Medicine.
Promoting effective transitions of care at hospital discharge: A review of key issues for hospitalists
Authors: Kripalani Sunil , Jackson Amy T. , Schnipper Jeffrey L. , Coleman Eric A. 
Published: October 2007

AbstractThe period following discharge from the hospital is a vulnerable time for patients. About half of adults experience a medical error after hospital discharge, and 19%–23% suffer an adverse event, most commonly an adverse drug event. This article reviews several important challenges to providing high‐quality care as patients leave the hospital. These include the discontinuity between hospitalists and primary care physicians, changes to the medication regimen, new self‐care responsibilities that may stress available resources, and complex discharge instructions. We also discuss approaches to promoting more effective transitions of care, including improvements in communication between inpatient and outpatient physicians, effective reconciliation of prescribed medication regimens, adequate education of patients about medication use, closer medical follow‐up, engagement with social support systems, and greater clarity in physician–patient communication. By understanding the key challenges and adopting strategies to improve patient care in the transition from hospital to home, hospitalists could significantly reduce medical errors in the postdischarge period. Journal of Hospital Medicine 2007;2:314–323. © 2007 Society of Hospital Medicine.