GAVRETO (pralsetinib)
RET FUSION-POSITIVE METASTATIC NON-SMALL CELL LUNG CANCER·+1
BLUEPRINT MEDICINES
Indication
RET fusion-positive thyroid cancer
RET fusion-positive thyroid cancer refers to a molecularly defined malignancy of the endocrine system—predominantly differentiated thyroid carcinomas such as papillary thyroid cancer—characterized by oncogenic genomic rearrangements involving the *RET* proto-oncogene. Read more about RET fusion-positive thyroid cancer
2 drugs 2 manufacturers
Drugs that treat it
Common RET fusion-positive thyroid cancer therapies.
GAVRETO (pralsetinib)
ANTINEOPLASTIC - PROTEIN-TYROSINE KINASE INHIBITORS·RET FUSION-POSITIVE METASTATIC NON-SMALL CELL LUNG CANCER·+1
RIGEL PHARMACEU
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News & literature
Coming soonRelated codes
Coming soonRelated conditions & guidelines
Coming soonRET fusion-positive thyroid cancer refers to a molecularly defined malignancy of the endocrine system—predominantly differentiated thyroid carcinomas such as papillary thyroid cancer—characterized by oncogenic genomic rearrangements involving the *RET* proto-oncogene.
These chromosomal fusions join the kinase domain of *RET* to partner genes, such as *CCDC6* or *NCOA4*, causing ligand-independent dimerization and continuous activation of downstream MAPK and PI3K/AKT proliferation pathways.
Pathophysiologically, this driver alteration fosters tumor growth, invasiveness, and, in advanced or metastatic settings, resistance to conventional radioactive iodine therapy.
- nih.gov
RET fusion-positive thyroid cancer refers to a molecularly defined malignancy of the endocrine system—predominantly differentiated thyroid carcinomas such as papillary thyroid cancer—characterized by oncogenic genomic rearrangements involving the *RET* proto-oncogene
- retpositive.org
RET fusion-positive thyroid cancer refers to a molecularly defined malignancy of the endocrine system—predominantly differentiated thyroid carcinomas such as papillary thyroid cancer—characterized by oncogenic genomic rearrangements involving the *RET* proto-oncogene These chromosomal fusions join the kinase domain of *RET* to partner genes, such as *CCDC6* or *NCOA4*, causing ligand-independent dimerization and continuous activation of downstream MAPK and PI3K/AKT proliferation pathways
- oncokb.org
These chromosomal fusions join the kinase domain of *RET* to partner genes, such as *CCDC6* or *NCOA4*, causing ligand-independent dimerization and continuous activation of downstream MAPK and PI3K/AKT proliferation pathways
- onclive.com
These chromosomal fusions join the kinase domain of *RET* to partner genes, such as *CCDC6* or *NCOA4*, causing ligand-independent dimerization and continuous activation of downstream MAPK and PI3K/AKT proliferation pathways
- fda.gov
Pathophysiologically, this driver alteration fosters tumor growth, invasiveness, and, in advanced or metastatic settings, resistance to conventional radioactive iodine therapy
- gavreto-hcp.com
Pathophysiologically, this driver alteration fosters tumor growth, invasiveness, and, in advanced or metastatic settings, resistance to conventional radioactive iodine therapy
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