bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluating requirements for spatial resolution of fMRI for neurosurgical planning
Authors: Yoo Seung‐Schik , Talos Ion‐Florin , Golby Alexandra J. , Black Peter McL. , Panych Lawrence P. 
Published: December 2003

AbstractThe unambiguous localization of eloquent functional areas is necessary to decrease the neurological morbidity of neurosurgical procedures. We explored the minimum spatial resolution requirements for functional magnetic resonance imaging (fMRI) data acquisition when brain mapping is used in neurosurgical planning and navigation. Using a 1.5 Tesla clinical MRI scanner, eight patients with brain tumors underwent fMRI scans using spatial resolution of approximately 4 × 4 × 4 mm3 to map the eloquent motor and language areas during the performance of cognitive/sensorimotor tasks. The fMRI results were then used intra‐operatively in an open MRI system to delineate eloquent areas. Retrospectively, activation patterns were visually inspected by a neurosurgeon to determine qualitatively whether ambiguity with respect to the activation boundaries, due to low spatial resolution, could be of potential significance for surgical guidance. A significant degree of ambiguity in both the extent and shape of activation was judged to be present in data from six of the eight patients. Analysis of fMRI data at multiple resolutionsom sixl aia frogfica ger showed that at 3 mm isotropic resolution, eloquent areas were better localized within the gray matter although there was still some potential for ambiguity caused by activations appearing to cross a sulcus. The data acquired with 2‐mm isotropic voxels significantly enhanced the spatial localization of activation to within the gray matter. Thus, isotropic spatial resolution on the order of 2 × 2 × 2 mm3, which is much higher than the resolutionsoused in typical fMRI examinations, may be needed for the unambiguous identification of cortical activation with respect to tumors and important anatomical landmarks. Hum. Brain Mapp. 21:34–43, 2004. © 2003 Wiley‐Liss, Inc.
Feature uncertainty activates anterior cingulate cortex
Authors: Kéri Szabolcs , Decety Jean , Roland Per E. , Gulyás Balázs 
Published: December 2003

AbstractIn visual discrimination tasks, the relevant feature to discriminate is defined before stimulus presentation. In feature uncertainty tasks, a cue about the relevant feature is provided after stimulus offset. We used 15O‐butanol positron emission tomography (PET) in order to investigate brain activation during a feature uncertainty task. There was greater activity during the feature uncertainty task, compared with stimulus detection and discrimination of orientation and spatial frequency, in the lateral and medial prefrontal cortex, the cuneus, superior temporal and inferior parietal cortex, cortical motor areas, and the cerebellum. The most robust and consistent activation was observed in the dorsal anterior cingulate cortex (Brodmann area 32; x = 0 y = 16, z = 40). The insula, located near the claustrum (x = −38, y = 8, z = 4), was activated during the discrimination tasks compared with the feature uncertainty condition. These results suggest that the dorsal anterior cingulate cortex is important in feature uncertainty conditions, which include divided attention, expectancy under uncertainty, and cognitive monitoring. Hum. Brain Mapp. 21:26–33, 2004. © 2003 Wiley‐Liss, Inc.
p75 neurotrophin receptor functions as a survival receptor in brain‐metastatic melanoma cells
Authors: Marchetti Dario , Aucoin Rebecca , Blust Jason , Murry Brian , Greiter‐Wilke Andrea 
Published: December 2003

AbstractThe p75 neurotrophin receptor (p75NTR), a common receptor for members of the neurotrophins (NT) family, was previously identified as a molecular determinant of brain metastasis. We have also reported that NT treatment of murine and human brain‐metastatic melanoma cells affects their invasive capacities and increases the production of heparanase, an important and unique extracellular matrix (ECM) degradative enzyme. Neurotrophism can be a survival‐support mechanism for brain‐metastatic cells and a survival assay was devised to mimic the growth limiting conditions of rapidly expanding metastatic tumors prior to neoangiogenesis. We report that p75NTR promoted the survival of brain‐metastatic melanoma cells but not melanocytes in stress cultures conditions. Secondly, melanoma cells fluorescently sorted for high p75NTR expression (p75NTR‐H cells) had an up to a 15‐fold greater survival than those sorted for low p75NTR expression (p75NTR‐L cells). Thirdly, cells overexpressing p75NTR associated with the growth fraction and provided these cells with an inherent growth advantage. Finally, we observed an increased survival of sorted p75NTR‐L cells, dependent upon treatment of NT members whose functional receptors are present on these cells. Together, these results delineate that p75NTR‐mediated trophic support profoundly affects competitive melanoma‐cell survival when the tumor cell microenvironment becomes growth limiting. © 2003 Wiley‐Liss, Inc.
Galectins and urological cancer
Authors: Oka Natsuo , Takenaka Yukinori , Raz Avraham 
Published: December 2003

AbstractGalectins are a family of proteins defined by their affinity for β‐galactoside and by their conserved sequence. Each galectins exhibits a specific expression pattern in various tissues and their expression is regulated during development. Their expression is altered in many types of cancers and non‐cancerous disorders. They interact with glycoproteins in both extracellular and intracellular milieu and regulate various biological phenomenon including cell growth, cell differentiation, cell adhesion, and apoptosis. A series of experimental and clinical evidences have been reported to support correlation between galectin expressions and neoplastic transformation. The recent findings show that expressions of galectins are elevated with neoplastic progression in certain malignancies, and therefore, galectins are expected to serve as reliable tumor markers. In this review, we describe the expression and role of galectins in urological cancers and their clinical applications for diagnostic and therapeutic use. © 2003 Wiley‐Liss, Inc.
Emerging views of integrin signaling: Implications for prostate cancer
Authors: Slack‐Davis Jill K. , Parsons J. Thomas 
Published: December 2003

AbstractIntegrins are heterodimeric transmembrane cellular receptors that link the cell to its underlying substratum. Alterations in integrin expression and signaling have been implicated in many aspects of tumorigenesis and metastasis including cell survival, migration, and invasion. In prostate cancer, the progression from normal to metastatic cells is accompanied by changes in the repertoire of integrins expressed and up‐regulation of key adhesion‐dependent signaling pathways. Recent work from several laboratories indicates the emergence of new mechanisms for the regulation of growth and migratory pathways by integrin engagement. These pathways are likely to provide novel sites of therapeutic intervention for the treatment of prostate cancer. © 2003 Wiley‐Liss, Inc.
Integrin clipping: A novel adhesion switch?
Authors: Demetriou Manolis C. , Cress Anne E. 
Published: December 2003

AbstractDuring human prostate cancer progression, the majority of normally expressed integrins are suppressed with the exception of the α6, α3, and β1 integrins. We have shown that in prostate cancer, the α6 integrin is found paired with the β1 integrin and that a novel form of the α6 integrin that lacks a large portion of the extracellular domain (α6p) exists. The α6pβ1 integrin is found in human prostate cancer tissue specimens as well as tissue culture cell lines and is formed on the cell surface. This review discusses the mechanism of α6pβ1 production and the potential functions of this integrin variant. Our current working model predicts that the α6pβ1 integrin maintains the intracellular cytoskeletal connections associated with the heterodimer while allowing for an alteration in cell adhesion. The mechanism provides a selective advantage for cancer cell metastasis. © 2003 Wiley‐Liss, Inc.
Bone morphogenetic protein signaling in prostate cancer cell lines
Authors: Brubaker K.D. , Corey E. , Brown L.G. , Vessella R.L. 
Published: December 2003

AbstractProstate cancer is the most commonly diagnosed malignancy in men and is often associated with bone metastases. Prostate cancer bone lesions can be lytic or schlerotic, with the latter predominating. Bone morphogenetic proteins (BMPs) are a family of growth factors, which may play a role in the formation of prostate cancer osteoblastic bone metastases. This study evaluated the effects of BMPs on prostate cancer cell lines. We observed growth inhibitory effects of BMP‐2 and ‐4 on LNCaP, while PC‐3 was unaffected. Flow cytometric analysis determined that LNCaP cell growth was arrested in G1 after bone morphogenetic protein‐2 treatment. Treatment of LNCaP and PC‐3 with BMP‐2 and ‐4 activated downstream signaling pathways involving SMAD‐1, up‐regulation of p21CIP1/WAF1 and changes in retinoblastoma (Rb) phosphorylation. Interestingly, bone morphogenetic protein‐2 treatment stimulated a 2.7‐fold increase in osteoprotegerin (OPG), a molecule, which inhibits osteoclastogenesis, production in PC‐3. © 2003 Wiley‐Liss, Inc.
Ras signaling in prostate cancer progression
Authors: Weber Michael J. , Gioeli Daniel 
Published: December 2003

AbstractWhen prostate cancer is first detected it generally is dependent on the presence of androgens for growth, and responds to androgen ablation therapies. However, the disease often recurs in a disseminated and apparently androgen independent (AI) form, and in this state is almost invariably fatal. Considerable evidence indicates that the Androgen receptor (AR) continues to be required even in androgen independent (AI) disease. Thus, a key to understanding hormone independent prostate cancer is to determine the mechanism(s) by which the AR can function even in the absence of physiologic levels of androgen. In this article, we argue that growth factors and receptors that utilize Ras family members drive prostate cancer progression to a state of androgen hypersensitivity; and that post‐translational modifications (e.g., phosphorylations) of transcriptional cofactors might be responsible for modulating the function of the AR so that it is active even at low concentrations of androgen. © 2003 Wiley‐Liss, Inc.
Role of the extracellular matrix in prostate carcinogenesis
Authors: Nagle Ray B. 
Published: December 2003

AbstractThis review summarizes the current state of knowledge regarding the proteins composing the extracellular matrix in the human prostate. The normal expression as well as the changes which occur in PIN and carcinoma are described for the lamins, collagens, and glycosaminoglycans. © 2003 Wiley‐Liss, Inc.
Death receptor‐induced cell death in prostate cancer
Authors: Guseva Natalya V. , Taghiyev Agshin F. , Rokhlin Oskar W. , Cohen Michael B. 
Published: December 2003

AbstractProstate cancer mortality results from metastasis and is often coupled with progression from androgen‐dependent to androgen‐independent growth. Unfortunately, no effective treatment for metastatic prostate cancer increasing patient survival is available. The absence of effective therapies reflects in part a lack of knowledge about the molecular mechanisms involved in the development and progression of this disease. Apoptosis, or programmed cell death, is a cell suicide mechanism that enables multicellular organisms to regulate cell number in tissues. Inhibition of apoptosis appears to be a critical pathophysiological factor contributing to the development and progression of prostate cancer. Understanding the mechanism(s) of apoptosis inhibition may be the basis for developing more effective therapeutic approaches. Our understanding of apoptosis in prostate cancer is relatively limited when compared to other malignancies, in particular, hematopoietic tumors. Thus, a clear need for a better understanding of apoptosis in this malignancy remains. In this review we have focused on what is known about apoptosis in prostate cancer and, more specifically, the receptor/ligand‐mediated pathways of apoptosis as potential therapeutic targets. © 2003 Wiley‐Liss, Inc.
Fatty acid synthase: A metabolic oncogene in prostate cancer?
Authors: Baron Antonella , Migita Toshiro , Tang Dan , Loda Massimo 
Published: December 2003

AbstractIn 1920, Warburg suggested that tumors consistently rely on anaerobic pathways to convert glucose to ATP even in the presence of abundant oxygen [Warberg, 1956] despite the fact that it is less efficient for energy supply than aerobic glycolysis. The reasons for this remain obscure to date. More often than not, the microenvironment of solid tumors contains regions of poor oxygenation and high acidity. In this context hypoxia can act in an epigenetic fashion, inducing changes in gene expression and in metabolism for survival. It is reasonable to assume that only the tumor cells capable of developing an unusual tolerance to limiting oxygen availability and to the acidosis resulting from excessive lactate production, can survive. In addition to the striking changes that occur in glucose metabolism, studies in human cancer patients suggest that there is often also an increase in free fatty acid turnover, oxidation and clearance [Legaspi et al., 1987; Hyltander et al., 1991]. For instance, a lipid mobilizing factor produced by tumor cells appears to be responsible for the increase in whole body fatty acid oxidation [Russell and Tisdale, 2002]. Fatty acids synthesis in tumor tissues also occurs at very high rates, as first demonstrated more than half a century ago [Medes et al., 1953]. Importantly, 14C glucose studies have shown that in tumor cells almost all fatty acids derive from de novo synthesis despite adequate nutritional supply [Sabine and Abraham, 1967; Ookhtens et al., 1984; Weiss et al., 1986]. In addition, tumors overexpressing fatty acid synthase (FAS), the enzyme responsible for de novo synthesis of fatty acids, display aggressive biologic behavior compared to those tumors with normal FAS levels, suggesting that FAS overexpression confers a selective growth advantage. Here, we will review the roles that FAS plays in important cellular processes such as apoptosis and proliferation. In addition, speculations on the putative role of FAS in the altered metabolic pathways of prostate cancer cells will be explored. Because of the frequent overexpression of this enzyme prostate cancer, FAS constitutes a therapeutic target in this disease. © 2003 Wiley‐Liss, Inc.
NF‐κB activation in human prostate cancer: Important mediator or epiphenomenon?
Authors: Suh Junghan , Rabson Arnold B. 
Published: December 2003

AbstractThe NF‐κB family of transcription factors has been shown to be constitutively activated in various human malignancies, including leukemias, lymphomas, and a number of solid tumors. NF‐κB is hypothesized to contribute to development and/or progression of malignancy by regulating the expression of genes involved in cell growth and proliferation, anti‐apoptosis, angiogenesis, and metastasis. Prostate cancer cells have been reported to have constitutive NF‐κB activity due to increased activity of the IκB kinase complex. Furthermore, an inverse correlation between androgen receptor (AR) status and NF‐κB activity was observed in prostate cancer cell lines. NF‐κB may promote cell growth and proliferation in prostate cancer cells by regulating expression of genes such as c‐myc, cyclin D1, and IL‐6. NF‐κB may also inhibit apoptosis in prostate cancer cells through activation of expression of anti‐apoptotic genes, such as Bcl‐2, although pro‐apoptotic activity of NF‐κB has also been reported. NF‐κB‐mediated expression of genes involved in angiogenesis (IL‐8, VEGF), and invasion and metastasis (MMP9, uPA, uPA receptor) may further contribute to the progression of prostate cancer. Constitutive NF‐κB activity has also been demonstrated in primary prostate cancer tissue samples and suggested to have prognostic importance for a subset of primary tumors. The limited number of samples analyzed in those studies and the relative lack of NF‐κB target genes identified in RNA expression microarray analyses of prostate cancer cells suggest that further studies will be required in order to determine if NF‐κB actually plays a role in human prostate cancer development, and/or progression, and to characterize its potential as a therapeutic target. © 2003 Wiley‐Liss, Inc.
Molecular aspects of diagnostic nucleolar and nuclear envelope changes in prostate cancer
Authors: Fischer Andrew H. , Bardarov Svetoslav , Jiang Zhong 
Published: December 2003

AbstractProstate cancer is still diagnosed by pathologists based on subjective assessment of altered cell and tissue structure. The cellular‐level structural changes diagnostic of some forms of cancer are known to be induced by cancer genes, but the relation between specific cellular‐level structural features and cancer genes has not been explored in the prostate. Two important cell structural changes in prostate cancer—nucleolar enlargement and nuclear envelope (NE) irregularity—are discussed from the perspective that they should also relate to the function of the genes active in prostate cancer. Enlargement of the nucleolus is the key diagnostic feature of high‐grade prostatic intraepithelial neoplasia (PIN), an early stage that appears to be the precursor to the majority of invasive prostate cancers. Nucleolar enlargement classically is associated with increased ribosome production, and production of new ribosomes appears essential for cell‐cycle progression. Several cancer genes implicated in PIN are known (in other cell types) to augment ribosome production, including c‐Myc, p27, retinoblastoma, p53, and growth factors that impact on ERK signaling. However, critical review of the available information suggests that increased ribosome production per se may be insufficient to explain nucleolar enlargement in PIN, and other newer functions of nucleoli may therefore need to be invoked. NE irregularity develops later in the clonal evolution of some prostate cancers, and it has adverse prognostic significance. Nuclear irregularity has recently been shown to develop dynamically during interphase following oncogene expression, without a requirement for post‐mitotic NE reassembly. NE irregularity characteristic of some aggressive prostate cancers could reflect cytoskeletal forces exerted on the NE during active cell locomotion. NE irregularity could also promote chromosomal instability because it leads to chromosomal asymmetry in metaphase. Finally, NE irregularity could impact replication competence, transcriptional programming and nuclear pore function. © 2003 Wiley‐Liss, Inc.
Fingerprinting the diseased prostate: Associations between BPH and prostate cancer
Authors: Shah Uzma S. , Getzenberg Robert H. 
Published: December 2003

AbstractTwo of the most common diseases which occur in ageing men relate to their prostate. BPH and prostate cancer are prevalent diseases which have an impact on most men as they age. The advent of gene expression analysis has provided an opportunity to examine these diseases in a novel fashion. These analyses, to date, have revealed associations between these two diseases which have not been previously identified. These commonalities include global genetic changes which occur throughout the prostates in individuals with these diseases. Understanding the fingerprints of these diseases is providing novel markers and treatment strategies for both BPH and prostate cancer. © 2003 Wiley‐Liss, Inc.
Molecular basis for the antiandrogen withdrawal syndrome
Authors: Miyamoto Hiroshi , Rahman Mujib M. , Chang Chawnshang 
Published: December 2003

AbstractIn patients with prostate cancer who manifest disease progression during combined androgen blockade therapy, discontinuation of antiandrogen treatment might result in prostate‐specific antigen decline, often associated with clinical improvement. The response called antiandrogen withdrawal syndrome is thus acknowledged as a general phenomenon. However, molecular mechanisms responsible for this syndrome are not completely understood. This article outlines the proposed mechanisms, including alterations of androgen receptor gene and its coregulatory proteins and activation of the signal transduction pathway, and the potential therapeutic approaches based on the specific mechanisms. © 2003 Wiley‐Liss, Inc.
In vitro culturing and characteristics of transit amplifying epithelial cells from human prostate tissue
Authors: Uzgare Aarti R. , Xu Yi , Isaacs John T. 
Published: December 2003

AbstractThe prostatic epithelium is functionally organized in stem cell units. This unit consists of a slow turn over stem cell within the basal epithelial layer which can replenish itself and provide progeny which differentiate down either a neuroendocrine or exocrine pathway. The maturation along the exocrine pathway initially involves transit amplifying cells within the basal layer proliferating and subsequently the progeny maturing into intermediate cells. These intermediate cells migrate into the luminal layer where they terminally differentiate into non‐proliferative secretory luminal cells which express prostate specific differentiation markers, like PSA. A growing body of experimental evidence has identified the proliferating transit amplifying/intermediate cells as the cells of origin for the common prostatic adenocarcinomas. Using a series of growth characteristics, and mRNA and protein markers, we have validated that primary cultures can be established in serum free defined media from surgically resected human prostates which are composed of essentially pure population of transit amplifying cells. At each serial passage, the subsequent cultures undergo enhanced maturation into intermediate cells and by the 7–10th passage these cells eventually lose their proliferative ability. This study validates that these cells are a useful and relevant system for the determination of molecular events involved in prostatic carcinogenesis. © 2003 Wiley‐Liss, Inc.
Angiogenesis and prostate cancer tumor growth
Authors: Nicholson Brian , Theodorescu Dan 
Published: December 2003

AbstractThe initiation of new blood vessels through angiogenesis is critical to tumor growth. Tumor cells release soluble angiogenic factors that induce neovascularization, without which nutrients and oxygen would not be available to allow tumors to grow more than 2–3 mm in diameter. This “angiogenic switch” or angiogenic phenotype requires an imbalance between proangiogenic and antiangiogenic factors since the formation of new blood vessels is highly regulated. This review discusses angiogenesis mediators, and the potential for manipulation of angiogenic factors as a practical cancer therapy, particularly in prostate cancer. © 2003 Wiley‐Liss, Inc.