kidney neoplasms/proline

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miR-23b targets proline oxidase, a novel tumor suppressor protein in renal cancer.

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Proline oxidase (POX) is a novel mitochondrial tumor suppressor that can suppress proliferation and induce apoptosis through the generation of reactive oxygen species (ROS) and decreasing hypoxia-inducible factor (HIF) signaling. Recent studies have shown the absence of expression of POX in human

Pathway analysis of kidney cancer using proteomics and metabolic profiling.

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BACKGROUND Renal cell carcinoma (RCC) is the sixth leading cause of cancer death and is responsible for 11,000 deaths per year in the US. Approximately one-third of patients present with disease which is already metastatic and for which there is currently no adequate treatment, and no biofluid

Fumarate hydratase deficiency in renal cancer induces glycolytic addiction and hypoxia-inducible transcription factor 1alpha stabilization by glucose-dependent generation of reactive oxygen species.

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Hereditary leiomyomatosis and renal cell cancer (HLRCC) is an inherited cancer syndrome linked to biallelic inactivation of the gene encoding the tricarboxylic acid cycle enzyme fumarate hydratase (FH). Individuals with HLRCC are at risk to develop cutaneous and uterine leiomyomas and an aggressive

Anticancer effect of lysine, proline, arginine, ascorbic acid and green tea extract on human renal adenocarcinoma line 786-0.

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Five-year survival is limited to 60% in renal cancer patients at diagnosis. Due to the cancer's resistance to conventional treatments and associated high morbidity, we investigated the antimetastatic effects of a specific nutrient mixture (NM) containing lysine, proline, arginine, ascorbic acid and

The von Hippel-Lindau tumor suppressor protein and Egl-9-Type proline hydroxylases regulate the large subunit of RNA polymerase II in response to oxidative stress.

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Human renal clear cell carcinoma (RCC) is frequently associated with loss of the von Hippel-Lindau (VHL) tumor suppressor (pVHL), which inhibits ubiquitylation and degradation of the alpha subunits of hypoxia-inducible transcription factor. pVHL also ubiquitylates the large subunit of RNA polymerase

Reprogramming of proline and glutamine metabolism contributes to the proliferative and metabolic responses regulated by oncogenic transcription factor c-MYC.

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In addition to glycolysis, the oncogenic transcription factor c-MYC (MYC) stimulates glutamine catabolism to fuel growth and proliferation of cancer cells through up-regulating glutaminase (GLS). Glutamine is converted to glutamate by GLS, entering the tricarboxylic acid cycle as an important energy

Tumour-specific proline vulnerability uncovered by differential ribosome codon reading.

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Tumour growth and metabolic adaptation may restrict the availability of certain amino acids for protein synthesis. It has recently been shown that certain types of cancer cells depend on glycine, glutamine, leucine and serine metabolism to proliferate and survive. In addition, successful therapies

A human novel gene DERPC on 16q22.1 inhibits prostate tumor cell growth and its expression is decreased in prostate and renal tumors.

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BACKGROUND Deletion of chromosome 16q is frequently associated with diverse tumors. Numerous studies strongly suggest the presence of one or more tumor suppressor genes on chromosome 16q22 to 16qter including the widely studied cadherin gene family. However, the specific tumor suppressor genes

ARPP protein is selectively expressed in renal oncocytoma, but rarely in renal cell carcinomas.

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We have recently isolated a gene, Ankyrin-repeated protein with a proline-rich region (ARPP), that is highly expressed in the skeletal and cardiac muscle. Our previous immunohistochemical analysis revealed that ARPP expression was augmented in rhabdomyosarcoma but scarcely detectable in

The WTX Tumor Suppressor Interacts with the Transcriptional Corepressor TRIM28.

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WTX encodes a tumor suppressor implicated in the pediatric kidney cancer Wilms tumor and in mesenchymal differentiation with potentially distinct functions in the cytoplasm, at the plasma membrane, and in the nucleus. Although modulating components of the WNT signaling pathway is a proposed function

[Four new cases with WT1 gene mutations in Chinese patients with Wilms' tumor].

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OBJECTIVE Wilms' tumor (WT) is the most common malignant renal tumor in childhood. The WT1 gene located at 11p13 was identified in 1990 as a tumor suppressor gene important in the development in WT. The WT1 gene consists of 10 exons, with exons 1 to 6 encoding an N-terminal proline- and

Effects of four bisphosphonates on bone resorption, lysosomal enzyme release, protein synthesis and mitotic activities in mouse calvarial bones in vitro.

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The effects of 3-amino-1-hydroxy-propylidene-1,1-bisphosphonate (AHPrBP), 1-hydroxyethylidene-1,1-bisphosphonate (HEBP), dichloromethylenebisphosphonate (Cl2MBP) and azacycloheptylidene-2,2-bisphosphonate (AHBP) on bone were examined in organ culture using newborn mice calvaria. AHPrBP, HEBP and

Further insights into chemical characterization through GC-MS and evaluation for anticancer potential of Dracaena draco leaf and fruit extracts.

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The present study reports for the first time the amino acid and fatty acid compositions and the antitumoral activity of aqueous extracts obtained from Dracaena draco L. leaf and fruit. Metabolite profiles were determined by gas chromatography-ion trap-mass spectrometry (GC-IT-MS), with several amino

Familial multiple cutaneous and uterine leiomyomas associated with papillary renal cell cancer.

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Multiple cutaneous and uterine leiomyomas is an autosomal dominant condition that results in benign smooth muscle tumours of the skin and, in females, uterine fibroids. This syndrome overlaps with hereditary leiomyomatosis and renal cell cancer syndrome in which affected individuals may develop the

MERTK mediated novel site Akt phosphorylation alleviates SAV1 suppression.

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Akt plays indispensable roles in cell proliferation, survival and metabolism. Mechanisms underlying posttranslational modification-mediated Akt activation have been extensively studied yet the Akt interactome is less understood. Here, we report that SAV1, a Hippo signaling component, inhibits Akt, a

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