Mouse Model for  ‐Induced Leukemogenesis

Parikh, Chaitali; Ren, Ruibao

doi:10.1016/s0076-6879(07)00402-8

Cited by 5 publications

(5 citation statements)

References 16 publications

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“…Activating point mutation in codons 12 and 13 in RAS gene is well established as a marker for molecular changes of normal or benign cells toward malignancy [12,13]. Mutant RAS oncoproteins have decreased GTPase activity, making them into an ''activated state'', and GTP-bound RAS transmits downstream signals that can change normal cellular functions [14].…”

Section: Discussionmentioning

confidence: 99%

RAS status in Korean patients with stage III and IV colorectal cancer

Lee

Baek

et al. 2015

Clin Transl Oncol

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Section: Discussionmentioning

confidence: 99%

RAS status in Korean patients with stage III and IV colorectal cancer

Lee

Baek

et al. 2015

Clin Transl Oncol

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“…Mutational activation of RAS via a point mutation at codon 12, 13 or 61 is well characterized as a marker for progression of normal or benign cells toward malignancy 41, 42. Mutant RAS oncoproteins have decreased GTPase activity, essentially locking them into an activated state, and GTP-bound RAS transmits strong downstream signals that alter normal cellular functions 5.…”

Section: Discussionmentioning

confidence: 99%

NRAS Mutations Are Rare in Colorectal Cancer

Irahara

Baba

Nosho

et al. 2010

Diagnostic Molecular Pathology

162

116

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Activating mutations in members of the RAS oncogene family (KRAS, HRAS and NRAS) have been found in a variety of human malignancies, suggesting a dominant role in carcinogenesis. In colon cancers, KRAS mutations are common and clearly contribute to malignant progression. The frequency of NRAS mutations and their relationship to clinical, pathologic, and molecular features remains uncertain. We developed and validated a Pyroseqencing assay to detect NRAS mutations at codons 12, 13 and 61. Utilizing a collection of 225 colorectal cancers from two prospective cohort studies, we examined the relationship between NRAS mutations, clinical outcome, and other molecular features, including mutation of KRAS, BRAF, and PIK3CA, microsatellite instability (MSI), and the CpG island methylator phenotype (CIMP). Finally, we examined whether NRAS mutation was associated with patient survival or prognosis. NRAS mutations were detected in 5 (2.2%) of the 225 colorectal cancers and tended to occur in left-sided cancers arising in women, but did not appear to be associated with any of the molecular features that were examined.

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“…Of the RAS family, NRAS is most frequently mutated (70%) in hematologic diseases, 33 so we focused on Nras. To determine whether lack of Dnmt3a would interact with Nras mutation and lead to a phenotypic change, we transduced Dnmt3a-KO and WT HSCs with NrasG12D or empty retroviral vector and sorted them into methylcellulose media.…”

Section: Comutations That Correlate With Human Disease Counterpartsmentioning

confidence: 99%