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HRAS, G12V (c.35G>T)

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Expand Collapse No disease selected  - General Description
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Expand Collapse HRAS  - General Description HRAS is a gene that provides the code for making an enzyme called HRAS that converts a molecule called GTP into GDP. This enzyme is part of a signaling pathway (MAP kinase signaling cascade) that relays chemical signals from the outside of the cell to the cell's nucleus, telling the cell when to grow and divide. When it is in its off position, HRAS is attached (bound) to GDP and cannot send signals to the nucleus. But when a GTP molecule arrives and binds to HRAS, HRAS is activated and sends its signal. It then immediately changes the GTP into GDP and returns to the off position. When mutated, HRAS can act as an oncogene, causing normal cells to become cancerous. The mutations can shift HRAS into the on position all the time, resulting in signaling that tells the cell to grow and divide abnormally. Some mutations that can lead to cancer are inherited, but that's not the case with these HRAS mutations. They're known as somatic mutations 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. Somatic HRAS mutations have been associated with some cases of bladder, thyroid and kidney cancers. Source: Genetics Home ReferenceHRAS (v-Ha-ras Harvey rat sarcoma viral oncogene homolog) is a member of the closely related RAS gene family that also includes KRAS and NRAS. 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 HRAS reside primarily in amino acid residues 12, 13 or 61. Source: Genetics Home Reference
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HRAS is a gene that provides the code for making an enzyme called HRAS that converts a molecule called GTP into GDP. This enzyme is part of a signaling pathway (MAP kinase signaling cascade) that relays chemical signals from the outside of the cell to the cell's nucleus, telling the cell when to grow and divide. When it is in its off position, HRAS is attached (bound) to GDP and cannot send signals to the nucleus. But when a GTP molecule arrives and binds to HRAS, HRAS is activated and sends its signal. It then immediately changes the GTP into GDP and returns to the off position.

When mutated, HRAS can act as an oncogene, causing normal cells to become cancerous. The mutations can shift HRAS into the on position all the time, resulting in signaling that tells the cell to grow and divide abnormally. Some mutations that can lead to cancer are inherited, but that's not the case with these HRAS mutations. They're known as somatic mutations 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. Somatic HRAS mutations have been associated with some cases of bladder, thyroid and kidney cancers.

Source: Genetics Home Reference
HRAS (v-Ha-ras Harvey rat sarcoma viral oncogene homolog) is a member of the closely related RAS gene family that also includes KRAS and NRAS. 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 HRAS reside primarily in amino acid residues 12, 13 or 61.

Source: Genetics Home Reference
PubMed ID's
21779495
Expand Collapse G12V (c.35G>T)  in HRAS
The HRAS G12V mutation arises from a single nucleotide change (c.35G>T) and results in an amino acid substitution of glycine (G) at position 12 by a valine (V).
The HRAS G12V mutation arises from a single nucleotide change (c.35G>T) and results in an amino acid substitution of glycine (G) at position 12 by a valine (V).

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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
NCT02857270 A Study of LY3214996 Administered Alone or in Combination With Other Agents in Participants With Advanced/Metastatic Cancer A Study of LY3214996 Administered Alone or in Combination With Other Agents in Participants With Advanced/Metastatic Cancer MGH Open G
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.
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