Compensatory alterations in energy homeostasis characterized in uterine tumors from hereditary leiomyomatosis and renal cell cancer

Catherino, William H.; Mayers, C.; Mantzouris, Tammy; Armstrong, Alicia; Linehan, W. Marston; Segars, James H.

doi:10.1016/j.fertnstert.2006.11.198

Cited by 14 publications

(9 citation statements)

References 42 publications

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“…The evidence for the downstream effects of the HIF1 activation and pseudohypoxic drive have been obtained from expression arrays on HLRCC-tumors, siRNA and biochemical based inhibition of FH, tumor cell lines and a kidney specific Fh1 mutant mouse model [47,75,77,81,82]. Compared to sporadic tumors HLRCC leiomyomas have been shown to display increased expression of HIF1 targets, such as VEGF (vascular endothelial growth factor) and TSP1 (trombospondin 1) [83].…”

Section: Molecular Mechanisms Of the Hlrcc Tumorigenesismentioning

confidence: 99%

“…Thus, if a mutation negative patient's phenotype or family history is strongly suggestive of HLRCC, additional methods, such as MLPA, should be used to reveal possible copy-number changes in the FH gene. FH IHC has been used in some publications to study associated tumors, but sensitivity and specificity of the method has not been evaluated, or whether it could be applied to identification of FH mutation carriers [26,81].…”

Section: Management Of the Diseasementioning

confidence: 99%

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Hereditary leiomyomatosis and renal cell cancer: update on clinical and molecular characteristics

2011

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Hereditary leiomyomatosis and renal cell cancer (HLRCC, also known as multiple cutaneous and uterine leiomyomatosis, MCUL) is a highly penetrant autosomal dominant tumor predisposition syndrome characterized by benign leiomyomas of the skin and the uterus. Renal cell carcinomas, occurring in a subset of the HLRCC families, are exceptionally aggressive. Therefore careful, frequent surveillance strategies are recommended. Association of malignant smooth-muscle tumors, leiomyosarcomas, with HLRCC has been observed but the risk appears to be smaller than initially estimated. To date inactivating heterozygous mutations in the fumarate hydratase (FH, fumarase) gene, predisposing to HLRCC, have been found in approximately 180 families worldwide. The most extensively studied hypothesis on molecular mechanisms of HLRCC tumorigenesis is activation of the hypoxia pathway due to aberrant stabilization of the HIF1 transcription factor. HIF1 regulates transcription of genes relevant for vascularization, glucose transport and glycolysis, processes that facilitate tumor growth. However, additional mechanisms underlying tumor formation are likely to exist.

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Section: Molecular Mechanisms Of the Hlrcc Tumorigenesismentioning

confidence: 99%

Section: Management Of the Diseasementioning

confidence: 99%

Hereditary leiomyomatosis and renal cell cancer: update on clinical and molecular characteristics

2011

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“…Two isoenzymes, PGK1 and 2 have been identified. PGK has been shown to be upregulated in HER-2/neu-positive breast tumours , and in hereditary leiomyomatosis, renal cell cancer, and uterine tumours (Catherino et al 2007). Elevated serum levels of PGK1 correlates with poor outcome in lung cancer (Chen et al 2003).…”

Section: Glycolytic Modification In Cancer Cells: the Warburg Effectmentioning

confidence: 99%

“…Phosphoglycerate mutase (PGAM) and Enolase catalyse the next two steps in glycolysis and have been implicated in a variety of cancers (Hennipman et al 1987;Catherino et al 2007;Mikuriya et al 2007;Li et al 2006;Huang et al 2006), including human lung cancer (Li et al 2006;Huang et al 2006). …”

Section: Glycolytic Modification In Cancer Cells: the Warburg Effectmentioning

confidence: 99%

“…PK has been shown to be dysregulated in a number of tumours (Unwin et al 2003;Catherino et al 2007;Du et al 2007). Different isoforms of PK are expressed in a tissue-specific manner: pyruvate kinase type L (L-PK) is expressed in the liver and kidney; R-PK is expressed by erythrocytes; M1-PK is expressed in muscle and brain; and M2-PK is expressed in lung tissue, as well as cells with high rates of nucleic acid synthesis.…”

Section: Glycolytic Modification In Cancer Cells: the Warburg Effectmentioning

confidence: 99%

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Cancer’s craving for sugar: an opportunity for clinical exploitation

Yeluri

Madhok

Prasad

et al. 2009

J Cancer Res Clin Oncol

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More than 80 years ago, Otto Warburg described the phenomenon whereby cancer cells avidly take up glucose and produce lactic acid under aerobic conditions, a process subsequently referred to as the Warburg effect or aerobic glycolysis. The exact molecular mechanisms underlying cancers reliance on glycolysis remains unclear, but is likely a combination of an epigenetic response to the hypoxic tumour environment in combination with direct oncogenic stimulation. The aim of the current manuscript is to review the normal process of glycolysis and highlight the alterations that occur with malignant transformation, to consider the potential advantages of glycolytic respiration for cancer cell survival, and finally to explore areas where altered glucose metabolism can be exploited for clinical benefit.

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Trend analysis of metabonomics and systematic review of metabonomics-derived cancer marker metabolites

Pasikanti

Chan

2010

Metabolomics

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In this paper, trend analyses were performed to compare the different 'omic' technologies and the different analytical platforms and biological matrices exploited in metabonomic studies. While common and differential marker metabolites had been identified using various analytical platforms in metabonomics, little research was directed to review and consolidate marker metabolites in each disease state. A systematic review of metabonomicsderived marker metabolites in different cancers was performed to understand the significance of metabonomics in elucidating cancer biochemistry. The biological pathways associated with the cancer marker metabolites were further correlated to the pathology of cancers. Our trend analyses indicated that metabonomic publications increased exponentially in recent years, with nuclear magnetic resonance (NMR) spectroscopy and liquid chromatography/mass spectrometry (LC/MS) being the most popular analytical platforms while blood, urine and tissue are the most commonly profiled biological matrices. Based on the consolidated cancer marker metabolites, it is reinforced that different cancers possess some common and yet distinct metabolic phenotypes, exhibiting numerous perturbed biochemical pathways related to their needs to support cell growth and proliferation and facilitate cancer cell survival.

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Compensatory alterations in energy homeostasis characterized in uterine tumors from hereditary leiomyomatosis and renal cell cancer

Cited by 14 publications

References 42 publications

Hereditary leiomyomatosis and renal cell cancer: update on clinical and molecular characteristics

Hereditary leiomyomatosis and renal cell cancer: update on clinical and molecular characteristics

Cancer’s craving for sugar: an opportunity for clinical exploitation

Trend analysis of metabonomics and systematic review of metabonomics-derived cancer marker metabolites

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