Gene Detail

Gene Symbol HRAS
Synonyms C-BAS/HAS | C-H-RAS | C-HA-RAS1 | c-K-ras | c-Ki-ras | CTLO | H-RASIDX | HAMSV | HRAS1 | Ki-Ras | KRAS | KRAS2 | p21ras | RASH1 | RASK2
Gene Description HRAS, HRas proto-oncogene, GTPase, is a member of the small GTPase family that upon activation by growth factors stimulates multiple downstream pathways such as RAF and PI3K to promote cell proliferation and survival (PMID: 21779504). HRAS activating mutations are commonly found in tumors, including dermatological, head and neck, thyroid, kidney, and bladder cancers (PMID: 29524560).
Entrez Id 3265
Chromosome 11
Map Location 11p15.5
Canonical Transcript NM_001130442

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Variant Impact Protein Effect Variant Description Associated with drug Resistance
Q61P missense loss of function HRAS Q61P is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61P results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
Q61K missense loss of function HRAS Q61K is a hotspot mutation that lies within the GTP nucleotide binding region of the Hras protein (UniProt.org). Q61K results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
A134T missense unknown HRAS A134T does not lie within any known functional domains of the Hras protein (UniProt.org). A134T has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
G15S missense unknown HRAS G15S lies within a GTP-binding region of the Hras protein (UniProt.org). G15S has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Nov 2018).
Q61X missense loss of function - predicted HRAS Q61X indicates any HRAS missense mutation that results in the glutamine (Q) at amino acid 61 being replaced by a different amino acid. HRAS codon 61 mutations are "hotspot" mutations that often result in decreased Hras GTPase activity and transformation of cultured cells (PMID: 3510078, PMID: 26985062) and therefore, are predicted to result in a loss of Hras protein function.
Q61C missense loss of function HRAS Q61C is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61C results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
R73C missense unknown HRAS R73C does not lie within any known function domains of the Hras protein (UniProt.org). R73C has been identified in the scientific literature (PMID: 22185227), but has not been biochemically characterized and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
Q61T missense loss of function HRAS Q61T is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61T results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
G48R missense no effect - predicted HRAS G48R does not lie within any known functional domains of the Hras protein (UniProt.org). G48R demonstrates GTP affinity and GTP hydrolysis activity similar to wild-type Hras, but enhances effector recruitment of HRAS G12V in culture (PMID: 26274561).
Q61W missense loss of function HRAS Q61W is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61W results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
A146T missense gain of function HRAS A146T lies within the SAK motif of the Hras protein (PMID: 24224811). A146T does not affect Hras intrinsic GTPase activity, but results in increased nucleotide exchange rates, which leads to increase GTP-bound Hras, activation of downstream signaling, and senescence of cultured cells (PMID: 24224811, PMID: 21850009).
G13R missense loss of function HRAS G13R is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G13R confers a loss of function on Hras protein as indicated by activation of Mapk and Pi3k signaling, increased cell proliferation in culture (PMID: 22683711).
Q61I missense loss of function HRAS Q61I is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61I results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
act mut unknown gain of function HRAS act mut indicates that this variant results in a gain of function in the Hras protein. However, the specific amino acid change has not been identified.
G12N missense loss of function - predicted HRAS G12N is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12N has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
inact mut unknown loss of function HRAS inact mut indicates that this variant results in a loss of function of the HRAS protein. However, the specific amino acid change has not been identified.
P174S missense unknown HRAS P174S lies within the hypervariable region of the Hras protein (UniProt.org). P174S has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
Q61M missense loss of function HRAS Q61M is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61M results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
A66T missense unknown HRAS A66T does not lie within any known functional domains of the Hras protein (UniProt.org). A66T has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
E162K missense unknown HRAS E162K does not lie within any known functional domains of the Hras protein (UniProt.org). E162K has been identified in the scientific literature (PMID: 22932669), but has not been biochemically characterized and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
E62G missense unknown HRAS E62G lies within the GTP binding domain of the Hras protein (PMID: 21779495). E62G has been identified in the scientific literature (PMID: 19628422), but has not been biochemically characterized, and therefore its effect on Hras protein function is unknown (PubMed, Oct 2018).
G13T missense loss of function HRAS G13T is hotspot mutation that lies within the GTP-binding domain of the Hras protein (UniProt.org). G13T results in increased Hras GTPase activity, but loss of response to GTPase-activating proteins, leading to transformation in Xenopus oocytes (PMID: 8430333).
G12A missense loss of function HRAS G12A is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12A results in decreased Hras GTPase activity, loss of sensitivity to GTPase-activating proteins, leading to transformation of cells in culture (PMID: 24224811, PMID: 6092966).
G151E missense unknown HRAS G151E does not lie within any known functional domains of the Hras protein (UniProt.org). G151E has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
L133R missense unknown HRAS L133R does not lie within any known functional domains of the Hras protein (UniProt.org). L133R has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
D47E missense unknown HRAS D47E does not lie within any known functional domains of the Hras protein (UniProt.org). D47E has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
D33N missense loss of function HRAS D33N lies within the effector region of the Hras protein (UniProt.org). D33N demonstrates decreased binding affinity for effector protein Raf compared to wild-type Hras, and is not transforming in cell culture (PMID: 28686159, PMID: 8035810).
G13D missense loss of function HRAS G13D is hotspot mutation that lies within the GTP nucleotide binding region of the Hras protein (UniProt.org). G13D results in decreased Hras GTPase activity and loss of response to GTPase-activating proteins, leading to activation of downstream signaling and senescence in cell culture (PMID: 24224811, PMID: 21850009).
K117E missense loss of function HRAS K117E lies within the GTP binding domain of the Hras protein (UniProt.org). K117E confers a loss of function on Hras protein as indicated by increased GTP-bound Hras, activation of downstream signaling, and transformation of cultured cells (PMID: 12569357).
Q61G missense loss of function HRAS Q61G is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61G results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
G12T missense loss of function - predicted HRAS G12T is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12T has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
G13C missense loss of function HRAS G13C is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G13C results in decreased Hras GTPase activity and loss of response to GTPase-activating proteins, leading to activation of downstream signaling and cell senescence in culture (PMID: 24224811, PMID: 21850009).
Q61N missense loss of function HRAS Q61N is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61N results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
G12W missense loss of function - predicted HRAS G12W is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12W has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
K117N missense loss of function HRAS K117N lies within the GTP binding domain of the Hras protein (UniProt.org). K117N results in decreased nucleotide binding affinity and activation of Hras in culture (PMID: 24247240).
R73H missense unknown HRAS R73H does not lie within any known function domains of the Hras protein (UniProt.org). R73H has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
R128L missense unknown HRAS R128L does not lie within any known functional domains of the Hras protein (UniProt.org). R128L has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
A11S missense unknown HRAS A11S lies within a GTP binding region of the Hras protein (UniProt.org). A11S has been identified in the scientific literature (PMID: 22683711), but has not been biochemically characterized and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
Q61H missense loss of function HRAS Q61H is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61H results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
mutant unknown unknown HRAS mutant indicates an unspecified mutation in the HRAS gene.
E143K missense unknown HRAS E143K does not lie within any known functional domains of the Hras protein (UniProt.org). E143K has not been characterized in the scientific literature and therefore, its effect on Hras function is unknown (PubMed, Oct 2018).
G12D missense loss of function HRAS G12D is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12D results in decreased Hras GTPase activity, loss of sensitivity to GTPase-activating proteins, thus leads to transformation of cells in culture (PMID: 24224811, PMID: 6092966).
A59D missense unknown HRAS A59D lies within a GTP binding region of the Hras protein (UniProt.org). A59D has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
G12L missense loss of function - predicted HRAS G12L is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12L has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
V81M missense unknown HRAS V81M does not lie within any known functional domains of the Hras protein (UniProt.org). V81M has been identified in the scientific literature (PMID: 14616967), but has not been biochemically characterized and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
amp none no effect HRAS amplification indicates an increased number of copies of the HRAS gene. However, the mechanism causing the increase is unspecified.
G12H missense loss of function - predicted HRAS G12H is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12H has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
R123H missense unknown HRAS R123H does not lie within any known functional domains of the Hras protein (UniProt.org). R123H has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
R128W missense unknown HRAS R128W does not lie within any known functional domains of the Hras protein (UniProt.org). R128W has not been characterized and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
A59T missense gain of function HRAS A59T lies within the GTP binding domain of the Hras protein (UniProt.org). A59T does not affect Hras GTPase activity, but increases nucleotide exchange rate, resulting in increase GTP-bound Hras and transformation of cultured cells (PMID: 21779495, PMID: 3004741).
G12I missense loss of function - predicted HRAS G12I is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12I has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
R123C missense unknown HRAS R123C does not lie within any known functional domains of the Hras protein (UniProt.org). R123C has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
wild-type none no effect Wild-type HRAS indicates that no mutation has been detected within the HRAS gene.
Y32* nonsense loss of function - predicted HRAS Y32* results in the premature truncation of the Hras protein at amino acid 32 of 189 (UniProt.org). Due to the loss of the GTP binding domain of Hras (UniProt.org), Y32* is predicted to confer loss of function to the Hras protein.
K117R missense gain of function HRAS K117R lies within the GTP binding region of the Hras protein (UniProt.org). K117R does not affect Hras intrinsic GTPase activity, but increases nucleotide exchange rates, resulting in increased GTP-boud Hras, activation of downstream signaling, and cell senescence in culture (PMID: 24224811, PMID: 17979197, PMID: 21850009).
A59Rfs*32 frameshift loss of function - predicted HRAS A59Rfs*32 indicates a shift in the reading frame starting at amino acid 59 and terminating 32 residues downstream causing a premature truncation of the 189 amino acid Hras protein (UniProt.org). Due to the loss of the GTP binding domain (UniProt.org), A59Rfs*32 is predicted to confer loss of function on the Hras protein.
G12C missense loss of function HRAS G12C is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12C results in decreased Hras GTPase activity, loss of sensitivity to GTPase-activating proteins, thus leads to transformation of cells in culture (PMID: 24224811, PMID: 6092966).
G12F missense loss of function - predicted HRAS G12F is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12F has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
G13S missense loss of function HRAS G13S is hotspot mutation that lies within the GTP-binding domain of the Hras protein (UniProt.org). G13S results in increased Hras GTPase activity, but loss of response to GTPase-activating proteins, leading to transformation in Xenopus oocytes (PMID: 8430333).
G12K missense loss of function - predicted HRAS G12K is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12K has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
Q61Y missense loss of function HRAS Q61Y is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61Y results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
Q61R missense loss of function HRAS Q61R is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61R results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
A134S missense unknown HRAS A134S does not lie within any known functional domains of the Hras protein (UniProt.org). A134S has been identified in sequencing studies (PMID: 26870252), but has not been biochemically characterized and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
A11D missense unknown HRAS A11D lies within a GTP binding region of the Hras protein (UniProt.org). A11D has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
E162G missense unknown HRAS E162G does not lie within any known functional domains of the Hras protein (UniProt.org). E162G has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
Q61V missense loss of function HRAS Q61V is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61V results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
R149Gfs*23 frameshift unknown HRAS R149Gfs*23 indicates a shift in the reading frame starting at amino acid 149 and terminating 23 residues downstream causing a premature truncation of the 189 amino acid Hras protein (UniProt.org). R149Gfs*23 has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
G12M missense loss of function - predicted HRAS G12M is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12M has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
Q61E missense loss of function HRAS Q61E is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61E results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
G12S missense loss of function HRAS G12S is hotspot mutation that lies within a GTP nucleotide binding region of the Hras protein (UniProt.org). G12S results in decreased Hras GTPase activity, loss of response to GTPase-activating proteins, leading to activation of downstream signaling pathways and transformation of cultured cells (PMID: 24224811, PMID: 21850009, PMID: 6330729).
Q61A missense loss of function HRAS Q61A is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61A results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
G13I missense unknown HRAS G13I is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G13I has been identified in sequencing studies (PMID: 22817889) but has not been biochemically characterized and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
N26S missense unknown HRAS N26S does not lie within any known functional domains of the Hras protein (UniProt.org). N26S has been identified in the scientific literature (PMID: 28229982), but has not been biochemically characterized and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
Q61L missense loss of function HRAS Q61L is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61L results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 23487764, PMID: 3510078).
L120V missense unknown HRAS L120V does not lie within any known functional domains of the Hras protein (UniProt.org). L120V has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
A146V missense gain of function HRAS A146V lies within the SAK motif of the Hras protein (PMID: 24224811). A146V does not affect Hras intrinsic GTPase activity, but results in increased nucleotide exchange rates, which leads to increase GTP-bound Hras, activation of downstream signaling, and transformation of cultured cells (PMID: 24224811, PMID: 21850009, PMID: 3043178).
G12Y missense loss of function - predicted HRAS G12Y is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12Y has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
G12V missense loss of function HRAS G12V is hotspot mutation that lies within a GTP nucleotide binding region of the Hras protein (UniProt.org). G12V results in decreased Hras GTPase activity, loss of response to GTPase-activating proteins, leading to activation of downstream signaling pathways, and transformation of cultured cells (PMID: 24224811, PMID: 21850009, PMID: 6330729).
G13X missense loss of function - predicted HRAS G13X indicates any HRAS missense mutation that results in the glycine (G) at amino acid 13 being replaced by a different amino acid. HRAS codon 13 mutations are "hotspot" mutations that often result in decreased Hras GTPase activity and transformation of cultured cells (PMID: 8430333, PMID: 21850009, PMID: 24224811, PMID: 26985062) and therefore, are predicted to result in a loss of Hras protein function.
A130T missense unknown HRAS A130T does not lie within any known functional domains of the Hras protein (UniProt.org). A130T has been identified in the scientific literature (PMID: 30348504), but has not been biochemically characterized and therefore, its effect on Hras protein function is unknown (PubMed, Nov 2018).
G10S missense unknown HRAS G10S lies within the GTP binding region of the Hras protein (UniProt.org). G10S has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
G12R missense loss of function HRAS G12R is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12R results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3042780, PMID: 6092966).
E91K missense unknown HRAS E91K does not lie within any known functional domains of the Hras protein (UniProt.org). E91K has not been characterized in the scientific literature and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
F82L missense unknown HRAS F82L does not lie within any known functional domains of the Hras protein (UniProt.org). F82L has been identified in the scientific literature (PMID: 25360634), but has not been biochemically characterized and therefore, its effect on Hras protein function is unknown (PubMed, Oct 2018).
G12Q missense loss of function - predicted HRAS G12Q is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12Q has not been biochemically characterized, but demonstrates transforming ability in cultured cells (PMID: 6092966) and therefore, is predicted to result in a loss of Hras protein function.
T58I missense loss of function HRAS T58I does not lie within any known functional domains of the Hras protein (UniProt.org). T58I confers a loss of function on the Hras protein as indicated by decreased GTP hydrolysis and binding to GEF proteins, leading to constitutive activation of Hras signaling in culture (PMID: 26888048).
G12E missense loss of function HRAS G12E is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G12E results in decreased Hras GTPase activity and loss of response to GTPase-activating proteins, and is transforming in cultured (PMID: 24224811, PMID: 6092966).
G12X missense loss of function - predicted HRAS G12X indicates any HRAS missense mutation that results in the glycine (G) at amino acid 13 being replaced by a different amino acid. HRAS codon 12 mutations are "hotspot" mutations that often result in decreased Hras GTPase activity and transformation of cultured cells (PMID: 6092966, PMID: 24224811, PMID: 26985062) and therefore, are predicted to result in a loss of Hras protein function.
Q61F missense loss of function HRAS Q61F is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). Q61F results in decreased Hras GTPase activity and leads to transformation of cells in culture (PMID: 3510078).
G13V missense loss of function HRAS G13V is hotspot mutation that lies within the GTP binding domain of the Hras protein (UniProt.org). G13V does not affect Hras GTPase activity, but results in a loss of response to GTPase-activating proteins, leading to increased GTP-bound Hras in culture (PMID: 24224811).
Molecular Profile Protein Effect Treatment Approaches
HRAS Q61P loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS Q61K loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
BRAF G466E HRAS Q61K
HRAS A134T unknown
HRAS G15S unknown
HRAS Q61X loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS Q61C loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS R73C unknown
HRAS Q61T loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G48R no effect - predicted
HRAS Q61W loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS A146T gain of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G13R KRAS G12R SRC T341M
HRAS G13R loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS Q61I loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS act mut gain of function
HRAS G12N loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS inact mut loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS P174S unknown
HRAS Q61M loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS A66T unknown
HRAS E162K unknown
HRAS E62G unknown
HRAS G13T loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12A loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G151E unknown
HRAS L133R unknown
HRAS D47E unknown
HRAS D33N loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G13D loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS K117E loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS K117E FGFR3 K650E
FGFR3 K650E FGFR3 over exp HRAS K117E
HRAS Q61G loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12T loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G13C loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS Q61N loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12W loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS K117N loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS R73H unknown
HRAS R128L unknown
HRAS A11S unknown
HRAS Q61H loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS mutant unknown
HRAS E143K unknown
HRAS G12D loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS A59D unknown
HRAS G12L loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS V81M unknown
EML4-ALK HRAS amp
HRAS amp no effect
HRAS G12H loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS R123H unknown
HRAS R128W unknown
HRAS A59T gain of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12I loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS R123C unknown
HRAS wild-type no effect
HRAS Y32* loss of function - predicted
HRAS K117R gain of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS A59Rfs*32 loss of function - predicted
HRAS G12C loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12F loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G13S loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12K loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS Q61Y loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS Q61R loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS A134S unknown
HRAS A11D unknown
HRAS E162G unknown
HRAS Q61V loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS R149Gfs*23 unknown
HRAS G12M loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS Q61E loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12S loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS Q61A loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G13I unknown MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS N26S unknown
HRAS Q61L loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS L120V unknown
HRAS A146V gain of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12Y loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
FGFR3 wild-type FGFR3 dec exp HRAS G12V
HRAS G12V loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G13X loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS A130T unknown
HRAS G10S unknown
HRAS G12R loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12R KRAS G13R
HRAS E91K unknown
HRAS F82L unknown
HRAS G12Q loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS T58I loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12E loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G12X loss of function - predicted MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS Q61F loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
HRAS G13V loss of function MEK inhibitor (Pan) MEK1 Inhibitor MEK2 Inhibitor PI3K Inhibitor (Pan) PIK3CA inhibitor PIK3CB inhibitor PIK3CD inhibitor PIK3CG inhibitor RAS Inhibitor (Pan)
Molecular Profile Indication/Tumor Type Response Type Therapy Name Approval Status Evidence Type Efficacy Evidence References
BRAF G466E HRAS Q61K melanoma sensitive Trametinib Preclinical - Cell culture Actionable In a preclinical study, Mekinist (trametinib) reduced ERK signaling and inhibited proliferation of a melanoma cell line harboring BRAF G466E and HRAS Q61K in culture (PMID: 28783719). 28783719
HRAS G13R KRAS G12R SRC T341M thyroid cancer sensitive Dasatinib + Trametinib Preclinical - Cell line xenograft Actionable In a preclinical study, Sprycel (dasatinib) and Mekinist (trametinib) synergistically inhibited proliferation and induced apoptosis in thyroid cancer cell lines harboring KRAS G13R, HRAS G12R, and an acquired SRC T341M mutation in culture, and resulted in sustained tumor suppression and prolonged survival in cell line xenograft models (PMID: 27222538). 27222538
HRAS G13R KRAS G12R SRC T341M thyroid cancer sensitive Trametinib Preclinical - Cell line xenograft Actionable In a preclinical study, Mekinist (trametinib) inhibited growth of Sprycel (dasatinib)-resistant thyroid cancer cell lines harboring KRAS G13R, HRAS G12R, and an acquired SRC T341M in culture and in cell line xenograft models (PMID: 27222538). 27222538
HRAS G13R KRAS G12R SRC T341M thyroid cancer sensitive Selumetinib Preclinical - Cell culture Actionable In a preclinical study, Selumetinib (AZD6244) inhibited growth of Sprycel (dasatinib)-resistant thyroid cancer cell lines harboring KRAS G13R, HRAS G12R, and an acquired SRC T341M mutation in culture (PMID: 27222538). 27222538
HRAS G13R KRAS G12R SRC T341M thyroid cancer sensitive Dasatinib + Selumetinib Preclinical - Cell culture Actionable In a preclinical study, Sprycel (dasatinib) and Selumetinib (AZD6244) synergistically inhibited proliferation and induced apoptosis in thyroid cancer cell lines harboring KRAS G13R, HRAS G12R, and an acquired SRC T341M mutation in culture (PMID: 27222538). 27222538
HRAS G13R KRAS G12R SRC T341M thyroid cancer sensitive Dasatinib + SCH772984 Preclinical - Cell culture Actionable In a preclinical study, Sprycel (dasatinib) and SCH772984 synergistically inhibited proliferation and induced apoptosis in thyroid cancer cell lines harboring KRAS G13R, HRAS G12R, and an acquired SRC T341M mutation in culture (PMID: 27222538). 27222538
HRAS G13R KRAS G12R SRC T341M thyroid cancer resistant Dasatinib Preclinical - Cell line xenograft Actionable In a preclinical study, thyroid cancer cell lines harboring HRAS G13R and KRAS G12R with an acquired SRC T341M mutation demonstrated resistance to Sprycel (dasatinib) in culture and in cell line xenograft models (PMID: 27222538). 27222538
HRAS G13R thyroid cancer sensitive MK2206 Preclinical - Cell culture Actionable In a preclinical study, MK2206 inhibited AKT activation, proliferation, and growth of thyroid cancer cell lines with PI3K/AKT pathway alterations in culture, including an anaplastic thyroid cancer cell line harboring HRAS G13R (PMID: 21289267). 21289267
HRAS inact mut thyroid cancer sensitive BEZ235 Preclinical Actionable In a preclinical study, BEZ235 inhibited growth of thyroid cancer cells harboring an HRAS pathway activating mutation in cell culture (PMID: 21831957). 21831957
FGFR3 K650E FGFR3 over exp HRAS K117E myeloid neoplasm sensitive AZ8010 Preclinical Actionable In a preclinical study, AZ8010 inhibited Fgfr3 signaling and decreased proliferation of myeloma cells with HRAS K117E and overexpression of FGFR3 K650E in culture (PMID: 22869148). 22869148
FGFR3 K650E FGFR3 over exp HRAS K117E multiple myeloma sensitive PD173074 Preclinical Actionable In a preclinical study, PD173074 inhibited Fgfr3 signaling, induced cell-cycle arrest, and decreased proliferation of multiple myeloma cells harboring HRAS H117E and over expression of FGFR3 K650E in culture (PMID: 22869148). 22869148
HRAS mutant Advanced Solid Tumor predicted - sensitive Everolimus Preclinical - Cell culture Actionable In a preclinical study, human solid tumor cell lines harboring HRAS mutations demonstrated increased sensitivity to growth inhibition by Afinitor (everolimus) in culture compared to cell lines with wild-type HRAS (PMID: 26544513). 26544513
HRAS mutant ovarian cancer predicted - sensitive Alpelisib + Binimetinib Phase Ib/II Actionable In a Phase Ib study, Alpelisib (BYL719) in combination with Binimetinib (MEK162) demonstrated preliminary safety and efficacy in patients with RAS-mutant advanced solid tumors, including patients with ovarian cancer (J Clin Oncol 32:5s, 2014 (suppl; abstr 9051). detail...
HRAS mutant transitional cell carcinoma resistant Trametinib Preclinical Actionable In a preclinical study, human urinary transitional cell carcinoma cells harboring mutant HRAS were insensitive to Mekinist (trametinib) in culture (PMID: 26343583). 26343583
HRAS mutant urinary bladder cancer sensitive Metformin Preclinical Actionable In a preclinical study, mouse models of bladder cancer harboring an HRAS mutation were sensitive to Glucophage (metformin), resulting in tumor growth reduction and prevention of hyperplasia regression (PMID: 26921394). 26921394 26951660
HRAS mutant endometrial cancer sensitive Trametinib Preclinical Actionable In a preclinical study, Mekinist (trametinib) inhibited growth of human endometrial cancer cells harboring mutant HRAS in culture (PMID: 26343583). 26343583
HRAS mutant breast cancer decreased response PI-273 Preclinical - Cell culture Actionable In a preclinical study, breast cancer cell lines harboring RAS mutations, including HRAS-mutant cell lines, demonstrated decreased sensitivity to growth inhibition by PI-273, in culture (PMID: 28827373). 28827373
HRAS mutant Advanced Solid Tumor predicted - sensitive Selumetinib Preclinical - Cell culture Actionable In a preclinical study, human solid tumor cell lines harboring HRAS mutations demonstrated increased sensitivity to growth inhibition by Selumetinib (AZD6244) in culture compared to cell lines with wild-type HRAS (PMID: 26544513). 26544513
HRAS mutant Advanced Solid Tumor predicted - sensitive Binimetinib Preclinical - Cell culture Actionable In a preclinical study, Binimetinib (MEK162) inhibited growth and induced apoptosis in human solid tumor cell lines harboring HRAS mutations in culture (PMID: 26544513). 26544513
HRAS mutant thyroid medullary carcinoma sensitive Cabozantinib Phase III Actionable In a Phase III trial, Cometriq (cabozantinib) treatment resulted in improved progression free survival (47 vs 8 weeks) compared to placebo in thyroid medullary carcinoma patients harboring RAS mutations (PMID: 27525386). 27525386
EML4-ALK HRAS amp non-small cell lung carcinoma predicted - resistant Crizotinib Clinical Study Actionable In a clinical study, a non-small cell lung carcinoma patient harboring EML4-ALK treated with Xalkori (crizotinib) responded, but eventually progressed, and was subsequently found to harbor a presumed resistance alteration, HRAS amplification (PMID: 29636358). 29636358
HRAS wild-type cancer predicted - sensitive FTI-277 Preclinical Actionable In a preclinical study, the farnesyltransferase inhibitor FTI-277 sensitized Hras transformed rat fibroblasts to radiation therapy (PMID: 8620483). 8620483
HRAS wild-type melanoma sensitive E6201 Preclinical Actionable In a preclinical study, E6201 inhibited proliferation of several melanoma cell lines in culture and hypersensitivity was associated with wild-type HRAS (PMID: 23039341). 23039341
HRAS Q61R Advanced Solid Tumor sensitive Binimetinib Preclinical - Cell culture Actionable In a preclinical study, transformed cells expressing HRAS Q61R demonstrated sensitivity to growth inhibition by Binimetinib (MEK162) in culture (PMID: 26544513). 26544513
HRAS Q61R Advanced Solid Tumor sensitive Everolimus Preclinical - Cell culture Actionable In a preclinical study, transformed cells expressing HRAS Q61R demonstrated sensitivity to growth inhibition by Afinitor (everolimus) in culture (PMID: 26544513). 26544513
HRAS Q61L lung squamous cell carcinoma no benefit Buparlisib Preclinical - Cell culture Actionable In a preclinical study, BKM120 did not inhibit growth of a lung squamous cell carcinoma cell line harboring HRAS Q61L in culture (PMID: 26544513) 26544513
HRAS Q61L Advanced Solid Tumor sensitive Binimetinib Preclinical - Cell culture Actionable In a preclinical study, transformed cells expressing HRAS Q61L demonstrated sensitivity to growth inhibition by Binimetinib (MEK162) in culture (PMID: 26544513). 26544513
HRAS Q61L Advanced Solid Tumor sensitive Binimetinib + Everolimus Preclinical - Cell culture Actionable In a preclinical study, the combination of Binimetinib (MEK162) and Afinitor (everolimus) worked synergistically to inhibit growth of transformed cells expressing HRAS Q61L in culture (PMID: 26544513). 26544513
HRAS Q61L Advanced Solid Tumor sensitive Everolimus Preclinical - Cell culture Actionable In a preclinical study, transformed cells expressing HRAS Q61L demonstrated sensitivity to growth inhibition by Afinitor (everolimus) in culture (PMID: 26544513). 26544513
HRAS Q61L lung squamous cell carcinoma sensitive Selumetinib Preclinical - Cell line xenograft Actionable In a preclinical study, Selumetinib (AZD6244) inhibited growth of a lung squamous cell carcinoma cell line harboring HRAS Q61L in culture, and inhibited tumor growth in xenograft models (PMID: 26544513). 26544513
HRAS Q61L bladder carcinoma sensitive NS1 Preclinical - Cell culture Actionable In a preclinical study, bladder carcinoma cells expressing HRAS Q61L demonstrated sensitivity to NS1, resulting in inhibition of Mapk signaling and cell proliferation in culture (PMID: 27820802). 27820802
HRAS Q61L head and neck squamous cell carcinoma sensitive Sirolimus + Trametinib Preclinical - Cell line xenograft Actionable In a preclinical study, Rapamune (sirolimus) worked synergistically with Mekinist (trametinib) to inhibit proliferation of head and neck squamous carcinoma cell lines harboring HRAS Q61L in culture and to reduce tumor growth in cell line xenograft models (PMID: 26882569). 26882569
HRAS Q61L lung squamous cell carcinoma sensitive AZD8055 + Binimetinib Preclinical - Cell culture Actionable In a preclinical study, the combination of Binimetinib (MEK162) and AZD8055 reduced phosphorylation of ERK and S6 and worked synergistically to inhibit growth of a lung squamous cell carcinoma cell line harboring HRAS Q61L in culture (PMID: 26544513). 26544513
HRAS Q61L lung squamous cell carcinoma sensitive Everolimus + Selumetinib Preclinical - Cell line xenograft Actionable In a preclinical study, the combination of Selumetinib (AZD6244) and Afinitor (everolimus) inhibited growth of a lung squamous cell carcinoma cell line harboring HRAS Q61L in culture, and inhibited tumor growth in xenograft models, with increased efficacy compared to either agent alone (PMID: 26544513). 26544513
HRAS Q61L skin squamous cell carcinoma no benefit PLX7904 Preclinical - Cell line xenograft Actionable In a preclinical study, PLX7904 did not stimulate growth of Zelboraf (vemurafenib)-induced cutaneous squamous cell carcinoma cells harboring HRAS Q61L in culture or in cell line xenograft models (PMID: 26466569). 26466569
HRAS Q61L lung squamous cell carcinoma sensitive Binimetinib + Everolimus Preclinical - Cell culture Actionable In a preclinical study, the combination of Binimetinib (MEK162) and Afinitor (everolimus) reduced phosphorylation of ERK and S6 and worked synergistically to inhibit growth of a lung squamous cell carcinoma cell line harboring HRAS Q61L in culture (PMID: 26544513). 26544513
FGFR3 wild-type FGFR3 dec exp HRAS G12V transitional cell carcinoma decreased response AZ8010 Preclinical Actionable In a preclinical study, urothelial cancer cells with low expression of wild-type FGFR3 that harbored HRAS G12V demonstrated resistance to AZ8010 in culture (PMID: 22869148). 22869148
FGFR3 wild-type FGFR3 dec exp HRAS G12V transitional cell carcinoma resistant PD173074 Preclinical Actionable In a preclinical study, urothelial cancer cells with low expression of wild-type FGFR3 that harbored HRAS G12V demonstrated resistance to PD173074 in culture (PMID: 22869148). 22869148
FGFR3 wild-type FGFR3 dec exp HRAS G12V transitional cell carcinoma resistant AZD4547 Preclinical Actionable In a preclinical study, urothelial cancer cells with low expression of wild-type FGFR3 that harbored HRAS G12V demonstrated resistance to AZD4547 in culture (PMID: 22869148). 22869148
HRAS G12V Advanced Solid Tumor resistant Cetuximab Preclinical Actionable In a preclinical study, tumor cells expressing HRAS G12V demonstrated resistance to treatment with Erbitux (cetuximab) (PMID: 22797062). 22797062
HRAS G12V Advanced Solid Tumor sensitive Everolimus Preclinical - Cell culture Actionable In a preclinical study, transformed cells expressing HRAS G12V demonstrated sensitivity to growth inhibition by Afinitor (everolimus) in culture (PMID: 26544513). 26544513
HRAS G12V urinary bladder cancer sensitive Binimetinib + Everolimus Preclinical - Cell culture Actionable In a preclinical study, the combination of Binimetinib (MEK162) and Afinitor (everolimus) reduced phosphorylation of ERK and S6 and worked synergistically to inhibit growth of a bladder cell line harboring HRAS G12V in culture (PMID: 26544513). 26544513
HRAS G12V melanoma sensitive CI-1040 Preclinical Actionable In a preclinical study CI-1040 (PD-184352) inhibited melanoma progression in a transgenic zebrafish model of melanoma expressing HRAS G12V (PMID: 26267534). 26267534
HRAS G12V Advanced Solid Tumor resistant Panitumumab Preclinical Actionable In a preclinical study, tumor cells expressing HRAS G12V demonstrated resistance to treatment with Vectibix (panitumumab) (PMID: 22797062). 22797062
HRAS G12V urinary bladder cancer sensitive Everolimus + Selumetinib Preclinical - Cell culture Actionable In a preclinical study, the combination of Selumetinib (AZD6244) and Afinitor (everolimus) reduced phosphorylation of ERK and S6 and worked synergistically to inhibit growth of a bladder cancer cell line harboring HRAS G12V in culture (PMID: 26544513). 26544513
HRAS G12V Advanced Solid Tumor sensitive Pz-1 Preclinical - Cell line xenograft Actionable In a preclinical study, Pz-1 reduced tumor growth in xenograft models of transformed cells over expressing HRAS G12V in a dose-dependent manner (PMID: 26126987). 26126987
HRAS G12V Advanced Solid Tumor sensitive rigosertib Preclinical - Cell culture Actionable In a preclinical study, Estybon (rigosertib) inhibited oncogenic transformation in fibroblast cells over-expressing HRAS G12V in culture (PMID: 27104980). 27104980
HRAS G12V Advanced Solid Tumor predicted - sensitive SR9009 Preclinical - Cell culture Actionable In a preclinical study, SR9009 treatment resulted in apoptosis in HRAS G12V-induced senescent firbroblast cells in culture (PMID: 29320480). 29320480
HRAS G12V Advanced Solid Tumor sensitive Binimetinib Preclinical - Cell culture Actionable In a preclinical study, transformed cells expressing HRAS G12V demonstrated sensitivity to growth inhibition by Binimetinib (MEK162) in culture (PMID: 26544513). 26544513
HRAS G12V Advanced Solid Tumor sensitive Binimetinib + Everolimus Preclinical - Cell culture Actionable In a preclinical study, the combination of Binimetinib (MEK162) and Afinitor (everolimus) worked synergistically to inhibit growth of transformed cells expressing HRAS G12V in culture (PMID: 26544513). 26544513
HRAS G12V Advanced Solid Tumor predicted - sensitive SR9011 Preclinical - Cell culture Actionable In a preclinical study, SR9011 treatment resulted in apoptosis in HRAS G12V-induced senescent firbroblast cells in culture (PMID: 29320480). 29320480
HRAS G12V malignant glioma sensitive SF1126 Preclinical - Cell line xenograft Actionable In a preclinical study, SF1126 inhibited Akt activation, proliferation, and migration of transgenic mouse glioma cells expressing HRAS G12V in culture, and suppressed tumor growth in xenograft models (PMID: 25425962). 25425962
HRAS G12R KRAS G13R thyroid cancer sensitive Selumetinib Preclinical - Cell culture Actionable In a preclinical study, Selumetinib (AZD6244) inhibited growth of thyroid cancer cell lines harboring KRAS G13R and HRAS G12R in culture (PMID: 27222538). 27222538
HRAS G12R KRAS G13R thyroid cancer sensitive Trametinib Preclinical - Cell line xenograft Actionable In a preclinical study, Mekinist (trametinib) inhibited growth of thyroid cancer cell lines harboring KRAS G13R and HRAS G12R in culture and in cell line xenograft models (PMID: 27222538). 27222538
HRAS G12R KRAS G13R thyroid cancer sensitive Dasatinib + Selumetinib Preclinical - Cell culture Actionable In a preclinical study, Sprycel (dasatinib) and Selumetinib (AZD6244) synergistically inhibited proliferation and induced apoptosis in thyroid cancer cell lines harboring KRAS G13R and HRAS G12R in culture (PMID: 27222538). 27222538
HRAS G12R KRAS G13R thyroid cancer sensitive Dasatinib + Trametinib Preclinical - Cell culture Actionable In a preclinical study, Sprycel (dasatinib) and Mekinist (trametinib) synergistically inhibited proliferation and induced apoptosis in thyroid cancer cell lines harboring KRAS G13R and HRAS G12R in culture (PMID: 27222538). 27222538
HRAS G12R KRAS G13R thyroid cancer sensitive Dasatinib + SCH772984 Preclinical - Cell culture Actionable In a preclinical study, Sprycel (dasatinib) and SCH772984 synergistically inhibited proliferation and induced apoptosis in thyroid cancer cell lines harboring KRAS G13R and HRAS G12R in culture (PMID: 27222538). 27222538