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NRAS, G13D (c.38G>A)

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Expand Collapse No disease selected  - General Description
Mass General Hospital Cancer Center treats patients with many cancer types. To learn more about the different cancer types that can be treated at the Cancer Center, please visit the Cancer Center website at the following page: http://www.massgeneral.org/cancer/services/
Expand Collapse NRAS  - General Description NRAS is a gene that provides the code for making NRAS, a GTPase that converts GTP to GDP. This protein is part of the MAP kinase signaling cascade that relays chemical signals from the outside of the cell to the cell's nucleus, and is primarily involved in controlling cell division. When NRAS is attached (bound) to GDP, it is in its “off” position and can't send signals to the nucleus. But when a GTP molecule arrives and binds to NRAS, NRAS is activated and sends its signal, and then it converts the GTP into GDP and returns to the "off" position. HRAS and KRAS are other GTPases that are similar to NRAS. When mutated, however, NRAS can act as an oncogene, causing normal cells to become cancerous. The mutations can shift the NRAS protein into the "on" position all the time. These NRAS mutations are said to be somatic, because instead of coming from a parent and being present in every cell (hereditary), they are acquired during the course of a person's life and are found only in cells that become cancerous. Tumor mutation profiling performed clinically at the MGH Cancer Center has identified the highest incidence of NRAS mutations in melanoma (~30%), acute myeloid leukemia (~15%) and thyroid carcinoma (5-10%). Source: Genetics Home ReferenceNRAS (neuroblastoma RAS viral oncogene homolog) is a member of the closely related RAS gene family that also includes KRAS and HRAS. These RAS members are small GTPases that mediate extracellular signals to the downstream effectors RAF, PI3K and RALGDS. RAS members are involved in regulating diverse cellular processes including survival, proliferation and differentiation. While activating mutations in the RAS genes lead to sustained GTPase activation that contributes to oncogenesis, each oncogene exerts clear differences. Mutational hotspots in NRAS reside primarily in amino acid residues 12, 13 or 61 and function to suppress apoptosis. Clinical tumor genotyping performed at the MGH Cancer Center has identified the highest incidence of NRAS mutations in melanoma (~30%), acute myeloid leukemia (~15%) and thyroid carcinoma (5-10%). Source: Genetics Home Reference
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NRAS is a gene that provides the code for making NRAS, a GTPase that converts GTP to GDP. This protein is part of the MAP kinase signaling cascade that relays chemical signals from the outside of the cell to the cell's nucleus, and is primarily involved in controlling cell division. When NRAS is attached (bound) to GDP, it is in its “off” position and can't send signals to the nucleus. But when a GTP molecule arrives and binds to NRAS, NRAS is activated and sends its signal, and then it converts the GTP into GDP and returns to the "off" position. HRAS and KRAS are other GTPases that are similar to NRAS.

When mutated, however, NRAS can act as an oncogene, causing normal cells to become cancerous. The mutations can shift the NRAS protein into the "on" position all the time. These NRAS mutations are said to be somatic, because instead of coming from a parent and being present in every cell (hereditary), they are acquired during the course of a person's life and are found only in cells that become cancerous.

Tumor mutation profiling performed clinically at the MGH Cancer Center has identified the highest incidence of NRAS mutations in melanoma (~30%), acute myeloid leukemia (~15%) and thyroid carcinoma (5-10%).

Source: Genetics Home Reference
NRAS (neuroblastoma RAS viral oncogene homolog) is a member of the closely related RAS gene family that also includes KRAS and HRAS. These RAS members are small GTPases that mediate extracellular signals to the downstream effectors RAF, PI3K and RALGDS. RAS members are involved in regulating diverse cellular processes including survival, proliferation and differentiation. While activating mutations in the RAS genes lead to sustained GTPase activation that contributes to oncogenesis, each oncogene exerts clear differences. Mutational hotspots in NRAS reside primarily in amino acid residues 12, 13 or 61 and function to suppress apoptosis.

Clinical tumor genotyping performed at the MGH Cancer Center has identified the highest incidence of NRAS mutations in melanoma (~30%), acute myeloid leukemia (~15%) and thyroid carcinoma (5-10%).

Source: Genetics Home Reference
PubMed ID's
18372904, 21779495
Expand Collapse G13D (c.38G>A)  in NRAS
The NRAS G13D mutation arises from a single nucleotide change (c.38G>A) and results in an amino acid substitution of the glycine (G) at position 13 by an aspartic acid (D).
The NRAS G13D mutation arises from a single nucleotide change (c.38G>A) and results in an amino acid substitution of the glycine (G) at position 13 by an aspartic acid (D).

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Your Matched Clinical Trials

Trial Matches: (G) - Gene, (M) - Mutation
Trial Status: Showing all 2 results Per Page:
Protocol # Title Location Status Match
NCT02327169 A Phase 1B Study of MLN2480 in Combination With MLN0128 or Alisertib, or Paclitaxel, or Cetuximab, or Irinotecan in Adult Patients With Advanced Nonhematologic Malignancies A Phase 1B Study of MLN2480 in Combination With MLN0128 or Alisertib, or Paclitaxel, or Cetuximab, or Irinotecan in Adult Patients With Advanced Nonhematologic Malignancies MGH Open GM
NCT02296112 Trametinib in Treating Patients With Advanced Melanoma With BRAF Non-V600 Mutations Trametinib in Treating Patients With Advanced Melanoma With BRAF Non-V600 Mutations MGH Open GM
MGH has many open clinical trials for other cancers not shown on the Targeted Cancer Care website. They can be found on the MassGeneral.org clinical trials search page.

Additional clinical trials may be applicable to your search criteria, but they may not be available at MGH. These clinical trials can typically be found by searching the clinicaltrials.gov website.
Trial Status: Showing all 2 results Per Page:

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