HRAS是致癌基因，编码蛋白是膜相关的GTP酶，其作为几种促增殖和抗凋亡信号转导途径的上游介质起着重要作用，包括促分裂原活化蛋白激酶（MAPK）和PI3激酶（PI3K）途径。HRAS，NRAS和KRAS由Ras原癌基因家族组成，三者具有相似的结构和功能。 RAS癌基因的转化，功能获得突变倾向于破坏GTP酶活性并促进细胞增殖和血管生成。致癌HRAS的过表达还触发生长因子非依赖性细胞周期进展和涉及肿瘤生长的蛋白质的上调（例如，基质金属蛋白酶2和9）。HRAS突变最常见于甲状腺癌，唾液腺癌，膀胱泌尿道癌，子宫颈癌和前列腺癌。HRAS的胚系突变与遗传性疾病Costello综合征相关，这种患者年轻时可发展成各种恶性肿瘤，包括神经母细胞瘤，横纹肌肉瘤和膀胱移行细胞癌。已发现RAS突变（包括HRAS）在RET阴性甲状腺髓样癌中存在显著的比例。

HRAS (Harvey Ras) is a membrane-associated GTPase. It plays an important role as an upstream mediator of several pro-proliferative and anti-apoptotic signal transduction pathways, including the mitogen activated protein kinase (MAPK) and PI3 kinase (PI3K) pathways. HRAS, NRAS and KRAS comprise the Ras proto-oncogene family, and all three have a similar structure and function. Transforming, gain-of-function mutations of RAS oncogenes tend to disrupt GTPase activity and promote cell proliferation and angiogenesis. Overexpression of oncogenic HRAS also triggers growth factor–independent cell cycle progression and upregulation of proteins implicated in tumor growth (e.g., matrix metalloproteinases 2 and 9). HRAS mutations are found most commonly in cancers of the thyroid, salivary glands, bladder urinary tract, cervix and prostate.Patients with Costello syndrome, a hereditary disorder with germline alterations in HRAS, can develop various malignancies at a young age, including neuroblastoma, rhabdomyosarcoma and transitional cell carcinoma of the bladder. RAS mutations (including HRAS) have been found in a significant proportion of RET negative medullary thyroid cancer.

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