bluuebunny/crossref_metadata_2025_split huggingface dataset:
Disparity between prostate tumor interior versus peripheral vasculature in response to verteporfin‐mediated vascular‐targeting therapy
Authors: Chen Bin , Crane Curtis , He Chong , Gondek David , Agharkar Priyanka , Savellano Mark D. , Hoopes P. Jack , Pogue Brian W. 
Published: May 2008

AbstractPhotodynamic therapy (PDT) is a light‐based cancer treatment modality. Here we employed both in vivo and ex vivo fluorescence imaging to visualize vascular response and tumor cell survival after verteporfin‐mediated PDT designed to target tumor vasculature. EGFP‐MatLyLu prostate tumor cells, transduced with EGFP using lentivirus vectors, were implanted in athymic nude mice. Immediately after PDT with different doses of verteporfin, tumor‐bearing animals were injected with a fluorochrome‐labeled albumin. The extravasation of fluorescent albumin along with tumor EGFP fluorescence was monitored noninvasively with a whole‐body fluorescence imaging system. Ex vivo fluorescence microscopy was performed on frozen sections of tumor tissues taken at different times after treatment. Both in vivo and ex vivo imaging demonstrated that vascular‐targeting PDT with verteporfin significantly increased the extravasation of fluorochrome‐labeled albumin in the tumor tissue, especially in the tumor periphery. Although PDT induced substantial vascular shutdown in interior blood vessels, some peripheral tumor vessels were able to maintain perfusion function up to 24 hr after treatment. As a result, viable tumor cells were typically detected in the tumor periphery in spite of extensive tumor cell death. Our results demonstrate that vascular‐targeting PDT with verteporfin causes a dose‐ and time‐dependent increase in vascular permeability and decrease in blood perfusion. However, compared to the interior blood vessels, peripheral tumor blood vessels were found less sensitive to PDT‐induced vascular shutdown, which was associated with subsequent tumor recurrence in the tumor periphery. © 2008 Wiley‐Liss, Inc.
Pathway based analysis of SNPs with relevance to 5‐FU therapy: Relation to intratumoral mRNA expression and survival
Authors: Nordgard Silje H. , Alnæs Grethe I.G. , Hihn Björn , Lingjærde Ole Christian , Liestøl Knut , Tsalenko Anya , Sørlie Therese , Lønning Per Eystein , Børresen‐Dale Anne‐Lise , Kristensen Vessela N. 
Published: May 2008

AbstractGenetic factors are thought to play a role in resistance towards chemotherapeutic agents such as 5‐fluorouracil (5‐FU). Approximately 30 genes are directly or indirectly involved in 5‐FU metabolism, and genetic variation in any of these may contribute to anti‐tumor response. Polymorphisms in these genes were analyzed in relation to tumoral mRNA levels of 5‐FU metabolizing genes, response to chemotherapy and survival. A total of 21 genetic variants were studied in 35 breast cancer patients treated with 5‐FluoroUracil, mitomycin (FUMI) and in a similar cohort of 90 doxorubicin treated breast cancer patients. Genotype distributions were compared using 109 healthy controls. No significant association was found between any polymorphisms and response to chemotherapy as measured by shrinkage of tumor. However, carriers of 3 copies of the TYMS 5′UTR repeat had shorter survival than noncarriers (p = .048) in the FUMI treatment group, but not in the doxorubicin treated group. Carriers of 3 copies of the repeat were also more frequently observed in both patients groups than in healthy controls (p = .034). Several highly significant associations were observed between genotypes and expression levels of 5‐FU metabolizing genes. A SNP in codon 72 of TP53 was revealed to be a key regulator of 5‐FU metabolizing genes such as DHFR and MTHFR, constituting 50% of all significant associations observed after FUMI therapy. These data suggest that 3 copies of the TYMS 5′UTR repeat may give a treatment specific reduced survival in breast cancer patients, and that TP53 may have a direct, allele specific, role in 5‐FU mediated response. © 2008 Wiley‐Liss, Inc.
Favorable outcome in clinically stage II melanoma patients is associated with the presence of activated tumor infiltrating T‐lymphocytes and preserved MHC class I antigen expression
Authors: van Houdt Inge S. , Sluijter Berbel J.R. , Moesbergen Laura M. , Vos Wim M. , de Gruijl Tanja D. , Molenkamp Barbara G. , van den Eertwegh Alfons J.M. , Hooijberg Erik , van Leeuwen Paul A.M. , Meijer Chris J.L.M. , Oudejans Joost J. 
Published: May 2008

AbstractIn this study we investigated whether the presence of specific populations of tumor infiltrating lymphocytes (TILs) in diagnostic primary melanoma biopsies are related to outcome in clinically stage II melanoma patients. Moreover, we investigated whether the presence of TILs correlates with expression of MHC class I antigen and MHC class II antigen on tumor cells and/or tumor infiltrating antigen presenting cells. Diagnostic primary melanoma samples of 15 patients with an unfavorable outcome were compared with 20 patients with favorable outcome. Patients were matched for age, gender and Breslow thickness. Biopsies were examined for the presence of granzyme B+, CD8+, CD4+ and CD56+ TILs and for expression of MHC class I antigen and MHC class II antigen on tumor and/or tumor infiltrating cells. A favorable clinical outcome was strongly associated with the presence of GrB+ and CD4+ TILs, with expression of MHC class I antigen on tumor cells and with expression of MHC class II antigen on intratumoral antigen presenting cells. These data strongly support the notion that in melanoma patients the cellular immune response is a major factor in preventing melanoma cell dissemination. © 2008 Wiley‐Liss, Inc.
Reduced local immunity in HPV‐related VIN: Expression of chemokines and involvement of immunocompetent cells
Authors: Santegoets Lindy A.M. , van Seters Manon , Heijmans‐Antonissen Claudia , KleinJan Alex , van Beurden Marc , Ewing Patricia C. , Kühne Liesbeth C.M. , Beckmann Ilse , Burger Curt W. , Helmerhorst Theo J.M. , Blok Leen J. 
Published: May 2008

AbstractUsual type VIN is a premalignant disorder caused by persistent HPV infection. High prevalence of VIN in immuno‐suppressed women suggests that a good innate and adaptive immune response is important for defense against HPV. Here, we explored expression levels of chemokines and related these to the presence or absence of immuno‐competent cells (dendritic and T‐cells) in affected (HPV‐positive VIN) and non‐affected (HPV‐negative) vulvar tissues from the same patients. Combining microarray data with quantitative real‐time RT‐PCR, it was observed that several important chemokines were differentially expressed between VIN and control samples (up‐regulation of IL8, CXCL10, CCL20 and CCL22 and down‐regulation of CXCL12, CCL21 and CCL14). Furthermore, an increased number of mature dendritic cells (CD208+) seemed to be bottled up in the dermis, and although a T‐cell response (increased CD4+ and CD8+ cells) was observed in VIN, a much larger response is required to clear the infection. In summary, it seems that most mature dendritic cells do not receive the proper chemokine signal for migration and will stay in the dermis, not able to present viral antigen to naive T‐cells in the lymph node. Consequently the adaptive immune response diminishes, resulting in a persistent HPV infection with increased risk for neoplasia. © 2008 Wiley‐Liss, Inc.
Aberrant expression of Cks1 and Cks2 contributes to prostate tumorigenesis by promoting proliferation and inhibiting programmed cell death
Authors: Lan Yongsheng , Zhang Yongyou , Wang Jianghua , Lin Chunhong , Ittmann Michael M. , Wang Fen 
Published: May 2008

AbstractThe mammalian Cks family consists of 2 well‐conserved small proteins, Cks1 and Cks2. Cks1 has been shown to promote cell‐cycle progression by triggering degradation of p27kip1. The function of Cks2 in somatic mammalian cells is not well understood although it is required for the first metaphase/anaphase transition during the meiosis. Emerging evidence shows that elevated expression of Cks1 and Cks2 is often found in a variety of tumors, and is correlated with poor survival rate of the patients. Here we demonstrated that expression of Cks1 and Cks2 were elevated in prostate tumors of human and animal models, as well as prostatic cancer cell lines. Forced expression of Cks1 and Cks2 in benign prostate tumor epithelial cells promoted cell population growth. Knockdown of Cks1 expression in malignant prostate tumor cells inhibited proliferation, anchorage‐independent growth, and migration activities, whereas knockdown of Cks2 expression induced programmed cell death and inhibited the tumorigenicity. Collectively, the data suggest that elevated expression of Cks1 contributes to the tumorigenicity of prostate tumor cells by promoting cell growth and elevated expression of Cks2 protects the cells from apoptosis. Thus, the finding suggests a novel therapeutic strategy for prostatic cancer based on inhibiting Cks1 and Cks2 activity. © 2008 Wiley‐Liss, Inc.
αvβ3 Integrin‐targeting radionuclide therapy and imaging with monomeric RGD peptide
Authors: Yoshimoto Mitsuyoshi , Ogawa Kazuma , Washiyama Kohshin , Shikano Naoto , Mori Hirofumi , Amano Ryohei , Kawai Keiichi 
Published: May 2008

AbstractThe αvβ3 integrin plays a pivotal role in angiogenesis and tumor metastasis. Angiogenic blood vessels overexpress αvβ3 integrin, as in tumor neovascularization, and αvβ3 integrin expression in other microvascular beds and organs is limited. Therefore, αvβ3 integrin is a suitable receptor for tumor‐targeting imaging and therapy. Recently, tetrameric and dimeric RGD peptides have been developed to enhance specificity to αvβ3 integrin. In comparison to the corresponding monomeric peptide, however, these peptides show high levels of accumulation in kidney and liver. The purpose of this study is to evaluate tumor‐targeting properties and the therapeutic potential of 111In‐ and 90Y‐labeled monomeric RGD peptides in BALB/c nude mice with SKOV‐3 human ovarian carcinoma tumors. DOTA‐c(RGDfK) was labeled with 111In or 90Y and purified by HPLC. A biodistribution study and scintigraphic images revealed the specific uptake to αvβ3 integrin and the rapid clearance from normal tissues. These peptides were renally excreted. At 10 min after injection of tracers, 111In‐DOTA‐c(RGDfK) and 90Y‐DOTA‐c(RGDfK) showed high uptake in tumors (7.3 ± 0.6% ID/g and 4.6 ± 0.8% ID/g, respectively) and gradually decreased over time (2.3 ± 0.4% ID/g and 1.5 ± 0.5% ID/g at 24 hr, respectively). High tumor‐to‐blood and ‐muscle ratios were obtained from these peptides. In radionuclide therapeutic study, multiple‐dose administration of 90Y‐DOTA‐c(RGDfK) (3 × 11.1 MBq) suppressed tumor growth in comparison to the control group and a single‐dose administration (11.1 MBq). Monomeric RGD peptides, 111In‐DOTA‐c(RGDfK) and 90Y‐DOTA‐c(RGDfK), could be promising tracers for αvβ3 integrin‐targeting imaging and radiotherapy. © 2008 Wiley‐Liss, Inc.
Multiple B‐vitamin inadequacy amplifies alterations induced by folate depletion in p53 expression and its downstream effector MDM2
Authors: Liu Zhenhua , Choi Sang‐Woon , Crott Jimmy W. , Smith Donald E. , Mason Joel B. 
Published: May 2008

AbstractFolate is required for biological methylation and nucleotide synthesis, aberrations of which are thought to be the mechanisms that enhance colorectal carcinogenesis produced by folate inadequacy. These functions of folate also depend on the availability of other B‐vitamins that participate in “one‐carbon metabolism,” including B2, B6 and B12. Our study therefore investigated whether combined dietary restriction of these vitamins amplifies aberrations in the epigenetic and genetic integrity of the p53 gene that is induced by folate depletion alone. Ninety‐six mice were group pair‐fed diets with different combinations of B‐vitamin depletion over 10 weeks. DNA and RNA were extracted from epithelial cells isolated from the colon. Within the hypermutable region of p53 (exons 5–8), DNA strand breaks were induced within exons 6 and 8 by folate combined with B2, B6 and B12 restriction (p < 0.05); such effects were not significantly induced by mild folate depletion alone. Similarly, a minor degree of hypomethylation of exon 6 produced by isolated folate depletion was significantly amplified (p ≤ 0.05) by simultaneous depletion of all 4 B‐vitamins. Furthermore, the expression of p53 and MDM2 were significantly decreased (p ≤ 0.05) by the combined depletion state but not by folate depletion alone. These data indicate that inadequacies of other 1‐carbon vitamins may amplify aberrations of the p53 gene induced by folate depletion alone, implying that concurrent inadequacies in several of these vitamins may have added tumorigenic potential beyond that observed with isolated folate depletion. © 2008 Wiley‐Liss, Inc.
FRAT1 overexpression leads to aberrant activation of β‐catenin/TCF pathway in esophageal squamous cell carcinoma
Authors: Wang Yihua , Liu Shuang , Zhu Hongxia , Zhang Wei , Zhang Guo , Zhou Xiaobo , Zhou Cuiqi , Quan Lanping , Bai Jinfeng , Xue Liyan , Lu Ning , Xu Ningzhi 
Published: May 2008

AbstractEsophageal squamous cell carcinoma (ESCC) is an aggressive tumor with a poor prognosis. Although aberrant activation of β‐catenin/T‐cell factor (TCF) pathway has been observed in ESCC, mechanisms underlying this phenomenon remain unknown. Frequently rearranged in advanced T‐cell lymphomas‐1 (FRAT1), overexpressed in some ESCC lines, is a positive regulator of β‐catenin/TCF pathway. However, little is known about the molecular relationship between FRAT1 and β‐catenin/TCF in ESCC. In this study, we analyzed freshly resected ESCC specimens and demonstrated that FRAT1 was overexpressed in approximately 74% of tumor samples compared with matched normal tissue. Overexpression of FRAT1 significantly promoted esophageal cancer cells growth, whereas suppression of FRAT1 level by RNAi markedly inhibited their growth. In addition, FRAT1 overexpression induced the nuclear accumulation of β‐catenin and promoted the transcriptional activity of β‐catenin/TCF. These effects were reversed by coexpression of GSK 3β or ΔN TCF4. Furthermore, accumulation of β‐catenin was correlated with FRAT1 overexpression in ESCC and the basal layer of normal esophageal epithelium. Finally, continued expression of c‐Myc is necessary and sufficient for maintenance of the growth state in cells expressing FRAT1. Taken together, these results support the novel hypothesis that aberrant activation of β‐catenin/TCF pathway in esophageal cancer appears to be due to upstream events such as FRAT1 overexpression, and c‐Myc may be an important element in oncogenesis of human ESCC induced by FRAT1. © 2008 Wiley‐Liss, Inc.
The many histories of community psychology: analyses of current trends and future prospects
Authors: Fowler Patrick J. , Toro Paul A. 
Published: May 2008

AbstractForty years since the seminal Swampscott Conference, the principles of community psychology transcend multiple areas of action and research, as well as international boundaries. The extensive development of community psychology offers an opportunity to examine from where the field has come and where it is going. Yet, a systematic approach to creating a history of community psychology is required to avoid distorting or excluding the voices of its diverse members. This special issue provides eight articles that highlight the importance of a pluralistic approach to historical analysis of the field. Of particular importance is the recognition of often‐underemphasized members of community psychology, including the important role of women, ethnic minorities, applied community psychologists, and international influences on the field. © 2008 Wiley Periodicals, Inc.
Some questions about “The history of community psychology”
Authors: Fryer David 
Published: May 2008

AbstractMost histories of the discipline of community psychology attribute its beginning to the Swampscott Conference that occurred in the mid‐20th century. The author argues that recognition of the community perspective on human behavior and on its positive as well as pathological characteristics arose far earlier and is reflected in the work of European social scientists. Work in central Europe in the 1930s by Marie Jahoda and her colleagues, for example, should be appreciated as an earlier manifestation of community psychology. The author also argues that the very project of trying to locate the historical origin for community psychology is by its very nature problematic! He views this effort as evidence of the intellectual colonizing of diverse indigenous community psychologies around the world by a culturally specific, largely acritical, United States–based community psychology. The author proposes that, rather than focusing on the origin of the discipline, scholars share his commitment to uncovering diverse historical community psychologies with their specific pasts and the construction of diverse community psychology futures, including most importantly of all, critical community psychologies. © 2008 Wiley Periodicals, Inc.
An insider's look at the development and current state of community psychology in Latin America
Authors: Montero Maritza 
Published: May 2008

AbstractThis article presents the rich history of community psychology in Latin America, describing how the field was systematically built during the second half of the 20th century. Discussed are social and political influences such as the critique of individualistic emphasis dominant at that moment, Paulo Freire's popular education, critical sociology (Fals Borda), and the need to intervene to transform unequal societies. Also described are early characteristics of Latin American community psychology, its rapid development during the 1980 s, marked by the emphasis on social transformation, participation, power and empowerment in communities, and a critical orientation. The construction of a paradigm during the 1990 s, as well as two models used in community psychology projects coexisting in Latin America societies, are presented. Current trends in community psychology in Latin America are summarized. © 2008 Wiley Periodicals, Inc.
Personal lineages and the development of community psychology: 1965 to 2005
Authors: Fowler Patrick J. , Toro Paul A. 
Published: May 2008

AbstractThe purpose of this study was twofold: (a) to examine and document the role of personal influence in the history of community psychology, and (b) to measure the field's inclusion of traditionally marginalized populations. In addition to presenting visually the genealogy of community psychology, results suggest that people have mattered in the development of the field independently from intellectual influence. Furthermore, community psychology has become more inclusive of ethnic minorities and women in positions of authority. Yet, representation of real‐world community psychologists appears to have stalled. Implications of findings on interventions to increase representation are discussed. © 2008 Wiley Periodicals, Inc.
Reflections on “Real‐World” community psychology
Authors: Wolff Tom , Swift Carolyn 
Published: May 2008

AbstractReflections on the history of real‐world (applied) community psychologists trace their participation in the field's official guild, the Society for Community Research and Action (SCRA), beginning with the Swampscott Conference in 1965 through the current date. Four benchmarks are examined. The issues these real‐world psychologists bring to the field include academic and community legitimacy, community psychology as an interdisciplinary field, and politics and advocacy. Challenges these issues create among community psychologists—real‐world and academic—are briefly addressed. These reflections end with a vision of the future of community psychology that includes a strong recommitment to social change and social justice. © 2008 Wiley Periodicals, Inc.
Women in community psychology: the trailblazer story
Authors: Ayala‐Alcantar Christina , Dello Stritto Mary Ellen , Guzmán Bianca L. 
Published: May 2008

AbstractThis article is an archival document which chronicles a herstory project organized and directed by the Society for Community Research and Action (Division 27 of the American Psychological Association) Women's Committee. The experiences of 55 trailblazing women in the field of community psychology are examined, and the authors' journey in collecting, documenting, and presenting the information is also included. © 2008 Wiley Periodicals, Inc. © 2008 Wiley Periodicals, Inc.
Influence of vanadate on migrating fibroblast orientation within a fibrin matrix
Authors: Lee Michael Y. , Ehrlich H. Paul 
Published: May 2008

AbstractTreating rats with vanadate, a nonspecific inhibitor of protein tyrosine phosphatases, optimizes the uniform packing of collagen fiber bundles in wound granulation tissue and doubles wound breaking strength in rat incisional wounds. The speculation is vanadate optimizes the packing of collagen fiber bundles through the orientation of newly arrived wound fibroblasts in the fibrin clot filling the defect. Segments of 14 day chick embryo tendons were placed on fibrin clots and maintained in organ culture with and without 30 µM vanadate. On day 7 explants were examined histologically and biochemically. Tendon fibroblast outgrowth from untreated explants migrated in a random fashion, while fibroblasts from vanadate‐treated explants migrated out in linear arrays. Fibroblasts were elongated by 20% form vanadate treated explant compared to controls. Myosin ATPase, required for optimal cell motility, is optimized by the phosphorylation of its myosin light chain (MLC). Western blot analysis of lysates from the fibroblasts that migrated into the fibrin showed vanadate increased MLC‐P levles. These findings support the notion that vanadate promotes the deposition of regular, parallel collagen fiber bundles by advancing the orientation of fibroblasts in parallel linear arrays early in the wound repair process. J. Cell. Physiol. 217: 72–76, 2008. © 2008 Wiley‐Liss, Inc.
Expression of secreted frizzled related protein 1, a Wnt antagonist, in brain, kidney, and skeleton is dispensable for normal embryonic development
Authors: Trevant Brune , Gaur Tripti , Hussain Sadiq , Symons John , Komm Barry S. , Bodine Peter V.N. , Stein Gary S. , Lian Jane B. 
Published: May 2008

AbstractSecreted frizzled related protein‐1 (sFRP1), an antagonist of Wnt signaling, regulates cell proliferation, differentiation and apoptosis and negatively regulates bone formation. The spatial and temporal pattern of endogenous sFRP1 expression and loss‐of‐function were examined in the sFRP1‐LacZ knock‐in mouse (sFRP1−/−) during embryonic development and post‐natal growth. β‐gal activity representing sFRP1 expression is robust in brain, skeleton, kidney, eye, spleen, abdomen, heart and somites in early embryos, but sFRP1 gene inactivation in these tissues did not compromise normal embryonic and post‐natal development. Kidney histology revealed increased numbers of glomeruli in KO mice, observed after 5 years of breeding. In the skeleton, we show sFRP1 expression is found in relation to the mineralizing front of bone tissue during skeletal development from E15.5 to birth. Trabecular bone volume and bone mineral density in the sFRP1−/− mouse compared to WT was slightly increased during post‐natal growth. Calvarial osteoblasts from newborn sFRP1−/− mice exhibited a 20% increase in cell proliferation and differentiation at the early stages of osteoblast maturation. sFRP1 expression was observed in osteoclasts, but this did not affect osteoclast number or activity. These findings have identified functions for sFRP1 in kidney and bone that are not redundant with other sFRPs. In summary, the absence of major organ abnormalities, the enhanced bone formation and a normal life span with no detection of spontaneous tumors suggests that targeting sFRP1 can be used as a therapeutic strategy for increasing bone mass in metabolic bone disorders or promoting fracture healing by modulating Wnt signaling. J. Cell. Physiol. 217: 113–126, 2008. © 2008 Wiley‐Liss, Inc.