Quantitative microsatellite analysis to delineate the commonly deleted region 1p22.3 in mantle cell lymphomas

Balakrishnan, Asha; Neuhoff, Nils von; Rudolph, Cornelia; Kamphues, Kathrin; Schraders, Margit; Groenen, Patricia J.T.A.; Krieken, J. Han J.M. van; Callet‐Bauchu, Evelyne; Schlegelberger, Brigitte; Steinemann, Doris

doi:10.1002/gcc.20352

Cited by 18 publications

(15 citation statements)

References 32 publications

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“…About 89.7% of Bif-1 -/-mice developed spontaneous tumors at 12 months of age, compared to 14.3% of wild-type mice [13]. Moreover, reduced Bif-1 expression was observed in gastric carcinomas [57], invasive urinary bladder and gallbladder cancers [58], and a homozygous deletion of the Bif-1 gene was identified in mantle cell lymphomas [59]. Taken together, these findings suggest that two of the positive regulators of Beclin 1, UVRAG and Bif-1, function as potential tumor-suppressor genes.…”

Section: Beclin 1 and Its Regulatorsmentioning

confidence: 94%

The paradox of autophagy and its implication in cancer etiology and therapy

2009

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Autophagy is a cellular self-catabolic process in which cytoplasmic constituents are sequestered in double membrane vesicles that fuse with lysosomes where they are degraded. As this catabolic activity generates energy, autophagy is often induced under nutrient limiting conditions providing a mechanism to maintain cell viability and may be exploited by cancer cells for survival under metabolic stress. However, progressive autophagy can be cytotoxic and autophagy can under certain settings substitute for apoptosis in induction of cell death. Moreover, loss of autophagy is correlated with tumorigenesis and several inducers of autophagy are tumor-suppressor genes. Thus, the relation of autophagy to cancer development is complex and depends on the genetic composition of the cell as well as on the extra-cellular stresses a cell is exposed to. In this review we describe the intricate nature of autophagy and its regulators, particularly those that have been linked to cancer. We discuss the multifaceted relation of autophagy to tumorigenesis and highlight studies supporting a role for autophagy in both tumor-suppression and tumor-progression. Finally, various autophagy-targeting therapeutic strategies for cancer treatment are presented.

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Section: Beclin 1 and Its Regulatorsmentioning

confidence: 94%

The paradox of autophagy and its implication in cancer etiology and therapy

2009

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“…In accordance with these results showing endophilin B1 downregulation, the chromosomal region harboring the endophilin B1 gene suffers from loss of heterozygosity in a wide variety of tumor types. ( [113]; see also references provided in [112]). Recently, Lim and colleagues quantified protein expression in four different cell lines with increasing metastatic potential in a mouse model [114].…”

Section: Cancermentioning

confidence: 94%

The Structure and Function of Endophilin Proteins

Kjærulff

Brodin²,

Jung

2010

Cell Biochem Biophys

102

116

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Members of the BAR domain protein superfamily are essential elements of cellular traffic. Endophilins are among the best studied BAR domain proteins. They have a prominent function in synaptic vesicle endocytosis (SVE), receptor trafficking and apoptosis, and in other processes that require remodeling of the membrane structure. Here, we discuss the role of endophilins in these processes and summarize novel insights into the molecular aspects of endophilin function. Also, we discuss phosphorylation of endophilins and how this and other mechanisms may contribute to disease.

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“…Decreased hCLCA2 expression is also observed in breast cancer specimens, and this decrease appears to be due to DNA methylation (50). Recent work also shows that the hCLCA2 gene may be deleted in mantle cell lymphoma specimens (51). These studies highlight the possible role of hCLCA2 as a tumor suppressor, and set the stage for studies of hCLCA1 in inflammatory airway disease.…”

Section: Models Of Inflammatory Airway Diseasementioning

confidence: 99%

The Role of CLCA Proteins in Inflammatory Airway Disease

Patel

Brett

Holtzman

2009

Annu. Rev. Physiol.

165

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Inflammatory airway diseases such as asthma and chronic obstructive pulmonary disease (COPD) exhibit stereotyped traits that are variably expressed in each person. In experimental mouse models of chronic lung disease, these individual disease traits can be genetically segregated and thereby linked to distinct determinants. Functional genomic analysis indicates that at least one of these traits, mucous cell metaplasia, depends on members of the calcium-activated chloride channel (CLCA) gene family. Here we review advances in the biochemistry of the CLCA family and the evidence of a role for CLCA family members in the development of mucous cell metaplasia and possibly airway hyperreactivity in experimental models and in humans. Based on this information, we develop the model that CLCA proteins are not integral membrane proteins with ion channel function, but instead are secreted signaling molecules that specifically regulate airway target cells in healthy and disease conditions.

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Quantitative microsatellite analysis to delineate the commonly deleted region 1p22.3 in mantle cell lymphomas

Cited by 18 publications

References 32 publications

The paradox of autophagy and its implication in cancer etiology and therapy

The paradox of autophagy and its implication in cancer etiology and therapy

The Structure and Function of Endophilin Proteins

The Role of CLCA Proteins in Inflammatory Airway Disease

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