Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to investigate the changes in expression pattern of the most important genes connected with apoptosis in proliferative apoptotic lesions (hyperplasia, adenoma), applying cDNA microarray technique, in order to promote the possible diagnostic or therapeutic utilisation of any difference in gene expression compared to the healthy (normal) parathyroid gland. Samples were taken from surgically removed 2 hyperplasias, 2 adenomas and 2 normal parathyroid glands. The Apoptosis Gene Array (Superarray) was used. This contains 112 genes, in tetraspot arrangement. The probes measured 250-600 base pairs. Streptavidin was bound to the array. CDP Star TM chemiluminescent substrate was used for detection. The samples deriving from hyperplasia or adenoma were compared to samples from normal parathyroid glands. The following genes were overexpressed in both hyperplasia and adenoma: CHEK1, ATM, BCL-XL, FAS, TNF, cIAP1, TRAIL, FADD, CASP 4,5,6,8, CD120b, CD137, LTA, TANK, TARF2, CAD, LIGHTR, DR3LG. CASP1,10, BFAR, BOD, BCL2L2, TRANCE were underexpressed in both hyperplasia and adenoma. Genes overexpressed only in hyperplasia were: MDM2, MCL1, BCL2A1, BLK, RIPK2, CD40LG, TRAF5, HUS1, BNIP3. Underexpressed only in hyperplasia: BOK, CIDEA, TRAF1, TRIP. Overexpressed only in adenoma: APOLLON, RIPK1, LTB, LTBR, CASP2,13, cIAP2, CIDEB. Underexpressed only in adenoma: TRAF4 and FASLG. Overexpresion or underexpression meant 1.5-fold difference from normal average values. As a result of this study, both pro-apoptotic and antiapoptotic genes were identified in hyperplasia and adenoma of the parathyroid gland. It seems that increased proliferation is connected also with increased apoptotic activity, but tumor cell candidates are able to survive, by activation of signal pathways resulting in overexpresion of anti-apoptotic genes.
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PMID:[Changes in gene expression in the course of proliferative processes in the parathyroid gland]. 1688 77

Cancer cells alter their metabolism for the production of precursors of macromolecules. However, the control mechanisms underlying this reprogramming are poorly understood. Here we show that metabolic reprogramming of colorectal cancer is caused chiefly by aberrant MYC expression. Multiomics-based analyses of paired normal and tumor tissues from 275 patients with colorectal cancer revealed that metabolic alterations occur at the adenoma stage of carcinogenesis, in a manner not associated with specific gene mutations involved in colorectal carcinogenesis. MYC expression induced at least 215 metabolic reactions by changing the expression levels of 121 metabolic genes and 39 transporter genes. Further, MYC negatively regulated the expression of genes involved in mitochondrial biogenesis and maintenance but positively regulated genes involved in DNA and histone methylation. Knockdown of MYC in colorectal cancer cells reset the altered metabolism and suppressed cell growth. Moreover, inhibition of MYC target pyrimidine synthesis genes such as CAD, UMPS, and CTPS blocked cell growth, and thus are potential targets for colorectal cancer therapy.
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PMID:Global metabolic reprogramming of colorectal cancer occurs at adenoma stage and is induced by MYC. 2884 64