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A genetic model for colorectal tumorigenesis
Tumorigenesis has long been thought to be a multistep process (Foulds, 1958); however, only recently has it become possible to identify the molecular events that underlie the initiation andExpand
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Genetic alterations during colorectal-tumor development.
Because most colorectal carcinomas appear to arise from adenomas, studies of different stages of colorectal neoplasia may shed light on the genetic alterations involved in tumor progression. WeExpand
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The SLUG zinc-finger protein represses E-cadherin in breast cancer.
Loss of expression of the E-cadherin cell-cell adhesion molecule is important in carcinoma development and progression. Because previous data suggest that loss of E-cadherin expression in breastExpand
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p53-Mediated Activation of miRNA34 Candidate Tumor-Suppressor Genes
BACKGROUND In response to varied cell stress signals, the p53 tumor-suppressor protein activates a multitude of genes encoding proteins with functions in cell-cycle control, DNA repair, senescence,Expand
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Molecular genetics of colorectal cancer.
  • E. Fearon
  • Medicine, Biology
  • Annual review of pathology
  • 24 January 2011
Over the past three decades, molecular genetic studies have revealed some critical mutations underlying the pathogenesis of the sporadic and inherited forms of colorectal cancer (CRC). A relativelyExpand
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Mitogenic Signaling Mediated by Oxidants in Ras-Transformed Fibroblasts
NIH 3T3 fibroblasts stably transformed with a constitutively active isoform of p21Ras, H-RasV12 (v-H-Ras or EJ-Ras), produced large amounts of the reactive oxygen species superoxide (·O2−). ·O2−Expand
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Identification of a chromosome 18q gene that is altered in colorectal cancers.
Allelic deletions involving chromosome 18q occur in more than 70 percent of colorectal cancers. Such deletions are thought to signal the existence of a tumor suppressor gene in the affected region,Expand
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Heterogeneity in Cancer: Cancer Stem Cells versus Clonal Evolution
The identification and characterization of cancer stem cells might lead to more effective treatments for some cancers by focusing therapy on the most malignant cells. To achieve this goal it will beExpand
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Suppression of human colorectal carcinoma cell growth by wild-type p53.
Mutations of the p53 gene occur commonly in colorectal carcinomas and the wild-type p53 allele is often concomitantly deleted. These findings suggest that the wild-type gene may act as a suppressorExpand
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Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth
Approximately 2% of colorectal cancer is linked to pre-existing inflammation known as colitis-associated cancer, but most develops in patients without underlying inflammatory bowel disease.Expand
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