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KRAS
Variants
VariantGeneTypeCOSMIC IDDNA Change (Coding Nucleotide)Exon
KRAS G12AKRASmissense2
KRAS G12VKRASmissense2
KRAS G12DKRASmissense2
KRAS G12CKRASmissense2
KRAS G12SKRASmissense2
KRAS G12RKRASmissense2
KRAS G13DKRASmissense2
KRAS G13CKRASmissense2
KRAS G13SKRASmissense2
KRAS G13RKRASmissense2
KRAS Q61HKRASmissense3
KRAS Q61LKRASmissense3
KRAS Q61KKRASmissense3
KRAS Q61RKRASmissense3
KRAS A146TKRASmissense4
KRAS A146VKRASmissense4
KRAS A146PKRASmissense4
KRAS A11VKRASmissense2
KRAS codon(s) 12, 13, 61, 117, 146 anyKRASany2, 2, 3, 4, 4
KRAS codon(s) 12 anyKRASany2
KRAS K117NKRASmissense4
KRAS codon(s) 117 anyKRASany4
KRAS Q22KKRASmissense64C>A2
KRAS V14IKRASmissense40G>A2
KRAS L19FKRASmissense57G>C2
KRAS copy number gainKRASCNV
KRAS copy number lossKRASCNV
KRAS any mutationKRASany

Interpretations

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Tier 2
KRAS
Variants
KRAS codon(s) 12, 13, 61, 117, 146 any
Primary Sites
Blood
Bone Marrow
Tumor Types
Acute Myeloid Leukemia
Chronic Myelomonocytic Leukemia
Myelodysplastic Syndrome
B Lymphoblastic Leukemia/Lymphoma
T Lymphoblastic Leukemia/Lymphoma
Acute Leukemia of Unspecified Cell Type
Anemia, Unspecified
Atypical Chronic Myeloid Leukemia
Chronic Myeloid Leukemia
Chronic Neutrophilic Leukemia
Cytopenia
Eosinophilia
Essential Thrombocythemia
Histiocytic and Dendritic Cell Neoplasms
Langerhans Cell Histiocytosis
Leukocytosis
Leukopenia
Mast Cell Neoplasm
MDS with Ring Sideroblasts
Monocytosis
Myelodysplastic/Myeloproliferative Neoplasm
Myeloproliferative Neoplasm
Myeloid Neoplasm
Other Acute Leukemia
Polycythemia Vera
Polycythemia
Primary Myelofibrosis
Thrombocytopenia, Unspecified
Thrombocytosis
Interpretation

KRAS is a well known proto-oncogene that belongs to the small GTPase family and functions as a central mediator of downstream growth factor receptor signaling, with a critical role for cell proliferation and survival. Pathogenic mutations in KRAS typically occur in codons 12-13 of exon 2 and codon 61 of exon 3; however, other, non-canonical, pathogenic mutations in KRAS have also been reported in acute myeoid leukemia. KRAS mutations have been described in approximately 3-15% of acute myeloid leukemia, 8-20% of chronic myelomonocytic leukemia, 14% of juvenile myelomonocytic leukemia, 8% of blastic plasmacytoid dendritic cell neoplasm 4% of patients with myelodysplastic syndrome, 2% of primary myelofibrosis, 12% of B cell acute lymphoblastic leukemia (often associated with MLL rearrangement) and 1-2% of T cell acute lymphoblastic leukemia. Investigation into the targetability of this pathway in leukemia has been attempted in some disease models.

Last updated: 2018-11-12 20:40:39 UTC
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Tier 1
KRAS
Variants
KRAS G12A
KRAS G12V
KRAS G12D
KRAS G12C
KRAS G12S
KRAS G12R
KRAS G13C
KRAS G13S
KRAS G13R
KRAS Q61H
KRAS Q61L
KRAS Q61K
KRAS Q61R
KRAS A146T
KRAS A146V
KRAS A146P
KRAS A11V
KRAS codon(s) 12, 13, 61, 117, 146 any
Primary Sites
Colon
Rectum
Tumor Types
Adenocarcinoma
Carcinoma
Interpretation

KRAS is a gene that encodes one of the several proteins in the epidermal growth factor receptor (EGFR) signaling pathway that is important in the development and progression of cancer. KRAS can harbor oncogenic mutations that yield a constitutively active protein. Such mutations are found in approximately 30% to 50% of metastatic colorectal tumors and are common in other tumor types. Mutations in the KRAS gene may indicate poor prognosis and poor drug response with therapies targeted to EGFR. The absence of a KRAS mutation predicts a greater likelihood of response to EGFR-targeted therapies and improved survival with such treatment. The relevant KRAS mutation is in one of five codons (12 13, 61, 117 or 146). The presence of KRAS mutations in codon 12, 13 or 61 is associated with a high likelihood of resistance to therapies targeting EGFR. In addition, mutations at codons 117 and 146 may also be associated with reduced response to EGFR-targeted therapies. Results should be interpreted in conjunction with other laboratory and clinical findings. Drug resistance: Panitumumab Cetuximab

Last updated: 2020-01-25 17:53:49 UTC
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Tier 2
KRAS
Variants
KRAS G12A
KRAS G12V
KRAS G12D
KRAS G12C
KRAS G12S
KRAS G12R
KRAS G13D
KRAS G13C
KRAS G13S
KRAS G13R
KRAS Q61H
KRAS Q61L
KRAS Q61K
KRAS Q61R
KRAS codon(s) 12, 13, 61, 117, 146 any
Primary Sites
Lung
Tumor Types
Squamous Cell Carcinoma
Interpretation

KRAS belongs to the RAS family of oncogenes. In lung, KRAS mutations are detected in approximately 20% to 25% of adenocarcinoma and less than 10% of squamous cell carcinoma which demonstrate a minor glandular component. KRAS mutations in NSCLC most often occur in codons 12 or 13 and with a lower frequency in codon 61. Mutations in KRAS are usually mutually exclusive with other oncogenic driver aberrations including EGFR, BRAF, HER2 mutations and ALK and ROS1 rearrangements. Contrary to most other oncogenic driver mutations, KRAS is more often found in smokers and is detected at lower frequency in East Asian patient cohorts. The prognostic as well as predictive role of KRAS mutations continues to be studied. Although various attempts inhibiting KRAS have been made, there is no established therapy specific for this large patient subpopulation. Recommend correlation with other clinical and lab findings.

Last updated: 2016-10-05 22:34:23 UTC
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Tier 2
KRAS
Variants
KRAS G12A
KRAS G12V
KRAS G12D
KRAS G12C
KRAS G12S
KRAS G12R
KRAS G13D
KRAS G13C
KRAS G13S
KRAS G13R
KRAS Q61H
KRAS Q61L
KRAS Q61K
KRAS Q61R
KRAS codon(s) 12, 13, 61, 117, 146 any
Primary Sites
Lung
Tumor Types
Adenocarcinoma
Pleomorphic Carcinoma
Carcinoma
Non-Small Cell Lung Carcinoma
Interpretation

KRAS belongs to the RAS family of oncogenes. KRAS mutations are detected in approximately 20% to 25% of lung adenocarcinoma. Contrary to most other oncogenic driver mutations, KRAS is more often found in smokers and is detected at lower frequency in East Asian patient cohorts. Mutations in KRAS are usually mutually exclusive with other oncogenic driver aberrations including EGFR, BRAF, HER2 mutations and ALK and ROS1 rearrangements. KRAS mutations in NSCLC most often occur in codons 12 or 13 and with a lower frequency in codon 61. The prognostic as well as predictive role of KRAS mutations continues to be studied. Although various attempts inhibiting KRAS have been made, there is no established therapy specific for this large patient subpopulation.

Last updated: 2021-12-30 20:04:08 UTC
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Tier 2
KRAS
Variants
KRAS G12A
KRAS G12V
KRAS G12D
KRAS G12C
KRAS G12S
KRAS G12R
KRAS G13D
KRAS G13C
KRAS G13S
KRAS G13R
KRAS Q61H
KRAS Q61L
KRAS Q61K
KRAS Q61R
KRAS A146T
KRAS A146V
KRAS A146P
KRAS A11V
KRAS codon(s) 12, 13, 61, 117, 146 any
Primary Sites
Pancreas
Tumor Types
Adenocarcinoma
Carcinoma
Interpretation

Pancreatic ductal adenocarcinoma (PDAC) is initiated by oncogenic mutant KRAS, which has been shown to drive pancreatic neoplasia. More than 90% of pancreatic ductal adenocarcinoma samples have a KRAS mutation which may have prognostic, and (with ongoing trials assessing the efficacy of novel KRAS inhibitors) possibly therapeutic implications. However, targeting KRAS directly has been difficult in these tumors.

Last updated: 2019-05-28 17:40:59 UTC
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Tier 2
KRAS
Variants
KRAS G12D
KRAS codon(s) 12 any
Primary Sites
Gall Bladder
Tumor Types
Adenocarcinoma
Interpretation

KRAS belongs to the RAS family of oncogenes. KRAS mutations have been described in approximately 3-40% gall bladder adenocarcinomas (more often in East Asia). The prognostic and therapeutic implications of KRAS mutations in gall bladder adenocarcinomas continue to be explored.

Last updated: 2020-07-24 14:52:02 UTC
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Tier 2
KRAS
Variants
KRAS Q22K
Primary Sites
Lung
Tumor Types
Adenocarcinoma
Interpretation

KRAS belongs to the RAS family of oncogenes. KRAS mutations are detected in approximately 20% to 25% of lung adenocarcinoma. Contrary to most other oncogenic driver mutations, KRAS is more often found in smokers and is detected at lower frequency in East Asian patient cohorts. Mutations in KRAS are usually mutually exclusive with other oncogenic driver aberrations including EGFR, BRAF, HER2 mutations and ALK and ROS1 rearrangements. KRAS mutations in NSCLC most often occur in codons 12 or 13 and with a lower frequency in codon 61. KRAS Q22K mutation consists of a C to A transversion substituting lysine for glutamine. This KRAS variant, at codon 22, is exceedingly rare in lung cancers, and also only rarely been described in very few other cancers. Mutations at this site have also been reported as germline mutations in Noonan syndrome. The preclinical studies have shown that cell lines expressing the KRAS Q22K mutation possess high in vivo oncogenic potential, higher than that of wild-type KRAS. The prognostic as well as predictive role of this and other KRAS mutations continues to be studied. Although various attempts inhibiting KRAS have been made, there is no established therapy specific for this large patient subpopulation.

Last updated: 2016-02-11 22:26:32 UTC
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Tier 2
KRAS
Variants
KRAS codon(s) 12, 13, 61, 117, 146 any
Primary Sites
Thyroid
Tumor Types
Papillary Carcinoma
Follicular Carcinoma
Interpretation

RAS mutations (HRAS, NRAS and KRAS) are found in all epithelial thyroid malignancies. The frequency of KRAS mutations in thyroid carcinomas is 2-3%. Overall, RAS mutations are identified in 10--20% of papillary carcinomas (follicular variant), 40--50% of follicular carcinomas and 20--40% of poorly differentiated and anaplastic carcinomas. Of note, RAS point mutations are mutually exclusive with other thyroid mutations such as BRAF, RET/PTC, or TRK rearrangements in papillary thyroid cancers. In follicular carcinomas, RAS mutations are mutually exclusive with PAX8-PPARG rearrangements. RAS mutations have also been associated with more aggressive disease and distant metastasis. The therapeutic implications of RAS mutations in thyroid cancer are unknown at this time.

Last updated: 2019-01-22 19:27:00 UTC
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Tier 2
KRAS
Variants
KRAS G12A
KRAS G12V
KRAS G12D
KRAS G12S
KRAS G12R
Primary Sites
Ovary
Tumor Types
Adenocarcinoma
Interpretation

KRAS mutations have been reported to be present in 16 to 41% of cases of low grade serous carcinoma of the ovary. The prognostic significance of KRAS mutations in ovarian tumors is uncertain; some reports suggest that patients with KRAS G12V may have shorter overall survival than patients without mutation, while other reports suggest that KRAS mutations in some low grade carcinomas of the ovary may be associated with slightly improved prognosis. In-vitro studies showed that cell lines with KRAS G12V mutation are more sensitive to selumetinib (MEK inhibitor) compared to cells with KRAS G12D. The clinical response to MEK inhibitors in patients with these tumors and mutations remains to be elucidated.

Last updated: 2016-02-12 21:08:04 UTC
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Tier 2
KRAS
Variants
KRAS codon(s) 12, 13, 61, 117, 146 any
Primary Sites
Appendix
Tumor Types
Adenocarcinoma
Interpretation

KRAS is a gene that encodes one of the several proteins in the epidermal growth factor receptor (EGFR) signaling pathway that is important in the development and progression of cancer. KRAS can harbor oncogenic mutations that yield a constitutively active protein. KRAS mutations are frequent in low-grade mucinous tumors of appendiceal origin and pseudomyxoma peritonei (43-100%) where mutations commonly occur in codon 12 or 13, with G12D and G12V being the most common. However, appendiceal adenocarcinoma cases with goblet cell features usually lack KRAS mutations. Mutations in the KRAS gene may indicate poor prognosis and drug response with therapies targeted to EGFR in some settings. However, this should be interpreted in conjunction with other laboratory and clinical findings.

Last updated: 2018-03-06 17:57:05 UTC
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Tier 2
KRAS
Variants
Primary Sites
Ampulla (Pancreaticobiliary Duct)
Pancreas
Tumor Types
Interpretation

KRAS is a gene that encodes one of the several proteins in the epidermal growth factor receptor (EGFR) signaling pathway that is important in the development and progression of cancer. KRAS can harbor oncogenic mutations that yield a constitutively active protein. The frequency of the KRAS gene mutations in intraductal papillary mucinous neoplasms (IPMNs) varies from 38.2% to 100%. There appears to be no significant difference among the incidence of KRAS mutation in the various grades of dysplasia: 87% in low-grade, 90.2% in intermediate grade and 70.7% in high-grade dysplasia. This mutation is considered to be an early event in the neoplastic transformation of IPMNs. KRAS mutations have the highest frequency in the pancreatobiliary subtype (100%) and the lowest frequency in the intestinal subtype (46.2%). Studies demonstrate that KRAS mutations in different tumors may have various biological, prognostic, and possibly therapeutic implications in some settings.

Last updated: 2016-03-18 21:03:01 UTC
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Tier 2
KRAS
Variants
Primary Sites
Bladder
Tumor Types
Urothelial Carcinoma
Interpretation

KRAS is a gene that encodes one of the several proteins in the growth factor signaling pathway(s) and is important in the development and progression of a variety of cancers. KRAS can harbor oncogenic mutations that yield a constitutively active protein. The frequency of the KRAS gene mutations in urothelial carcinoma of urinary bladder is very low (3% to 7%), and these mutations occur in all stages and grades. In the context of bladder tumors, mutations in the KRAS gene do not appear to be predictors for recurrence-free, progression-free and disease-specific survival according to some studies.

Last updated: 2016-03-29 19:28:17 UTC
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Tier 2
KRAS
Variants
KRAS codon(s) 12, 13, 61, 117, 146 any
Primary Sites
Ampulla (Pancreaticobiliary Duct)
Liver
Tumor Types
Adenocarcinoma
Cholangiocarcinoma
Interpretation

KRAS is a gene that encodes one of the several proteins in the epidermal growth factor receptor (EGFR) signaling pathway that is important in the development and progression of cancer. KRAS can harbor oncogenic mutations that yield a constitutively active protein. KRAS mutations are common in both extrahepatic (40-49%) and intrahepatic (24-27%) cholangiocarcinomas. Mutations in the KRAS gene may indicate poor prognosis and drug response with therapies targeted to EGFR in some settings. Of note, RAS mutations sensitize tumors to MEK inhibitors. However, this should be interpreted in conjunction with other laboratory and clinical findings.

Last updated: 2018-06-13 18:58:46 UTC
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Tier 2
KRAS
Variants
Primary Sites
Endometrium
Tumor Types
Adenocarcinoma
Interpretation

KRAS belongs to the RAS family of oncogenes. KRAS mutations are detected in approximately 10-30% of endometrial tumors, predominantly within codons 12 or 13. KRAS mutations are also identified in endometrial hyperplasias, although at a lower frequency than in carcinomas. According to some studies, the gain of the KRAS function may represent an early event in endometrioid-type tumorigenesis. It has been shown that endometrioid carcinomas with significant mucinous component are more likely to have such mutations. KRAS gene amplification and protein overexpression but not mutation may be associated with aggressive and metastatic endometrial cancer according to some studies.

Last updated: 2016-06-01 13:43:34 UTC
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Tier 2
KRAS
Variants
Primary Sites
Prostate
Tumor Types
Adenocarcinoma
Interpretation

KRAS belongs to the RAS family of oncogenes. KRAS mutations in codons 12 and 13 were found in 6-7% of prostatic adenocarcinomas. KRAS gene rearrangement has been reported in 3% of metastatic prostate cancer. Prognostic and predictive implications of KRAS gene alterations in prostate cancer need to be fully elucidated.

Last updated: 2016-08-01 19:23:22 UTC
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Tier 2
KRAS
Variants
Primary Sites
Esophagus
Gastroesophageal Junction
Tumor Types
Adenocarcinoma
Carcinoma
Interpretation

KRAS is a gene that encodes one of the several proteins in the epidermal growth factor receptor (EGFR) signaling pathway that is important in the development and progression of cancer. KRAS can harbor oncogenic mutations that yield a constitutively active protein. KRAS mutations are found in approximately 2-3% of esophageal cancers. In colorectal cancers, mutations in the KRAS gene may indicate poor prognosis and poor drug responses against anti-EGFR therapies. However, prognostic and predictive implications of KRAS mutations in esophageal cancers need to be fully elucidated. Results should be interpreted in conjunction with other laboratory and clinical findings.

Last updated: 2016-10-11 21:50:35 UTC
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Tier 2
KRAS
Variants
KRAS V14I
Primary Sites
Colon
Tumor Types
Adenocarcinoma
Interpretation

KRAS belongs to a family of small GTPases and gain-of-function mutations in the gene yield a constitutively active protein. Such mutations are found in approximately 30% to 50% of metastatic colorectal cancers and are common in other tumor types. The most frequent KRAS mutations occur at codons 12, 13, and 61. Mutations at codons 117 and 146 are less common. Mutations at codon 14 have been detected in adenocarcinomas of the small intestine and colon as well as AML. Germline V14I mutations have been identified in patients with Noonan syndrome. In vitro studies have shown that V14I mutations lead to moderately enhanced MEK1/2 and ERK1/2 phosphorylation suggesting increased downstream signaling, but with slightly less transforming capacity than G12D mutation. Mutations in the KRAS gene may indicate poor prognosis and poor drug response to EGFR-targeted therapies. Results should be interpreted in conjunction with other laboratory and clinical findings.

Last updated: 2016-10-11 21:38:34 UTC
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Tier 2
KRAS
Variants
Primary Sites
Kidney
Ureter
Tumor Types
Urothelial Carcinoma
Interpretation

KRAS belongs to the RAS family of oncogenes and is important in the development and progression of a variety of cancers. KRAS can harbor oncogenic mutations that yield a constitutively active protein. The frequency of KRAS gene mutations in upper tract urothelial carcinoma is low (5%). In the context of urothelial carcinoma of the bladder, mutations in the KRAS gene do not appear to be predictors for recurrence-free, progression-free and disease-specific survival according to some studies. The prognostic and predictive role of KRAS mutations in upper tract urothelial carcinoma needs to be further elucidated.

Last updated: 2016-11-04 00:36:09 UTC
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Tier 2
KRAS
Variants
KRAS G12V
KRAS G12D
KRAS G12C
KRAS G12S
KRAS G12R
KRAS G13D
KRAS G13C
KRAS G13S
KRAS G13R
KRAS G12A
Primary Sites
Stomach
Tumor Types
Adenocarcinoma
Interpretation

KRAS mutations are infrequent in gastric carcinomas and have been reported in approximately 6% of cases. Studies have shown no statistically significant difference in survival between KRAS-mutated and KRAS-non-mutated gastric carcinomas. However, one study showed a trend that the presence of a KRAS mutation was associated with better overall survival in gastric carcinoma patients. There is an increased frequency of KRAS mutations in gastric carcinomas with microsatellite instability. In gastric cancer, the predictive ability of KRAS has not been extensively studied, but a small study did not demonstrate an effect on survival in patients treated with an EGFR inhibitor.

Last updated: 2019-05-28 17:41:21 UTC
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Tier 2
KRAS
Variants
KRAS L19F
Primary Sites
Colon
Tumor Types
Adenocarcinoma
Interpretation

KRAS is a gene that encodes one of the several proteins in the epidermal growth factor receptor (EGFR) signaling pathway that is important in the development and progression of cancer. KRAS can harbor oncogenic mutations that yield a constitutively active protein. Such mutations are found in approximately 30% to 50% of metastatic colorectal tumors and are common in other tumor types. KRAS L19F has been previously reported in colorectal cancers, but its oncogenic and transforming potential was reported to be significantly lower compared to codons 12 or 13 KRAS mutants. The predictive and prognostic significance of this specific mutation in KRAS needs further elucidation. Results should be interpreted in conjunction with other laboratory and clinical findings.

Last updated: 2017-01-30 21:47:53 UTC
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Tier 1
KRAS
Variants
KRAS G13D
Primary Sites
Colon
Rectum
Tumor Types
Adenocarcinoma
Interpretation

KRAS is a gene that encodes one of the several proteins in the epidermal growth factor receptor (EGFR) signaling pathway that is important in the development and progression of cancer. KRAS can harbor oncogenic mutations that yield a constitutively active protein. Such mutations are found in approximately 30% to 50% of metastatic colorectal tumors and are common in other tumor types. Mutations in the KRAS gene may indicate poor prognosis and poor drug response with therapies targeted to EGFR. The absence of a KRAS mutation predicts a greater likelihood of response to EGFR-targeted therapies and improved survival with such treatment. The relevant KRAS mutation is in one of five codons (12 13, 61, 117 or 146). The presence of KRAS mutations in codon 12, 13 or 61 is associated with a high likelihood of resistance to therapies targeting EGFR. However, preclinical studies have shown that G13D mutant cell lines have intermediate sensitivity to cetuximab and panitumumab. Results should be interpreted in conjunction with other laboratory and clinical findings.

Last updated: 2017-03-24 18:09:45 UTC
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Tier 2
KRAS
Variants
Primary Sites
Brain
Tumor Types
Ganglioglioma
Interpretation

KRAS is a gene that encodes one of the several proteins in the epidermal growth factor receptor (EGFR) signaling pathway that is important in the development and progression of cancer. KRAS can harbor oncogenic mutations that yield a constitutively active protein. KRAS mutations have been reported in up to 1.6% of low-grade gliomas and in 1% of glioblastomas. KRAS mutations have not previously reported in ganglioglioma. The predictive and prognostic significance of KRAS mutations in ganglioglioma is unclear and needs to be further studied. Correlation with other clinical and laboratory findings is recommended.

Last updated: 2017-04-17 23:02:55 UTC
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Tier 2
KRAS
Variants
KRAS copy number gain
KRAS copy number loss
Primary Sites
Adrenal Gland
Anus
Ampulla (Pancreaticobiliary Duct)
Appendix
Bladder
Blood
Bone
Bone Marrow
Brain
Breast
Spinal Cord
Cervix
Chest Wall
Colon
Endometrium
Esophagus
Eye
Fallopian Tube
Fibroadipose Tissue
Gall Bladder
Kidney
Larynx
Liver
Lung
Lymph Node
Nasal Cavity
Oral Cavity
Ovary
Pancreas
Parathyroid
Penis
Peripheral Nervous System
Peritoneum
Pharynx
Pituitary
Placenta
Pleura
Prostate
Retroperitoneum
Salivary Gland
Seminal Vesicle
Skeletal Muscle
Skin
Small Intestine
Soft Tissue
Spleen
Stomach
Testis
Thymus
Thyroid
Tonsil
Unknown
Ureter
Uterus
Vagina
Rectum
Cartilage
Blood Vessel
Buccal Swab
Heart
Trachea
Salivary Duct
Spermatic Cord
Vulva
Brain, Infratentorial
Brain, Supratentorial
Gastroesophageal Junction
Sellar
Suprasellar
Peritoneal fluid
Pleural Fluid
Tongue
Tumor Types
Acinar Cell Carcinoma
Acinic Cell Carcinoma
Adenocarcinoma
Adenoid Cystic Carcinoma
Adenosarcoma
Ameloblastic Tumor
Anaplastic Large Cell Lymphoma
Angioimmunoblastic T-Cell Lymphoma
Angiomatoid Fibrous Histiocytoma
Angiomatosis
Angiomyolipoma
Angiosarcoma
Astrocytoma, Anaplastic
Basal Cell Carcinoma
Burkitt Lymphoma
Carcinoid Tumor
Carcinoma
Carcinosarcoma
Cholangiocarcinoma
Chondrosarcoma
Chordoma
Choriocarcinoma
Chromophobe Renal Cell Carcinoma
Chronic Lymphocytic Leukemia
Classical Hodgkin Lymphoma
Clear Cell Carcinoma
Clear Cell Renal Cell Carcinoma
Craniopharyngioma
Dermatofibrosarcoma
Desmoplastic Small Round Cell Tumor
Diffuse Large B Cell Lymphoma
Ductal Carcinoma
Ependymoma
Ewing Sarcoma
Fibromatosis
Follicular Carcinoma
Follicular Lymphoma
Gastrointestinal Stromal Tumor
Germ Cell Tumor
Giant Cell Tumor
Glioblastoma
Glomus Tumor
Granular Cell Tumor
Hairy Cell Leukemia
Hemangioendothelioma
Hepatocellular Carcinoma
Invasive Ductal Carcinoma
Kaposi Sarcoma
Leiomyoma
Leiomyosarcoma
Lipoma
Liposarcoma
Lobular Carcinoma
Lymphoplasmacytic Lymphoma
Malignant Mullerian Mixed Tumor
Mantle Cell Lymphoma
Marginal Zone B Cell Lymphoma
Medullary Carcinoma
Medulloblastoma
Melanoma
Meningioma
Merkel Cell Carcinoma
Mesothelioma
Mucinous Adenocarcinoma
Mucinous Tumors of Ovary
Mucoepidermoid Carcinoma
Myxofibrosarcoma
Nasopharyngeal Carcinoma
Neuroblastoma
Neuroendocrine Carcinoma
Neuroendocrine Neoplasm
NK Cell Lymphoproliferative Disorder
NLPHL
Non-Small Cell Lung Carcinoma
Oligodendroglioma
Osteosarcoma
Papillary Carcinoma
Papillary Renal Cell Carcinoma
Peripheral T Cell Lymphoma
Pheochromocytoma
Plasma Cell Disorder
Post-Transplant Lymphoproliferative Disorder
Primitive Neuroectodermal Tumor
Renal Cell Carcinoma
Reninoma
Retinoblastoma
Rhabdomyosarcoma
Sarcoma
Schwannoma
Serous Carcinoma
Sex Cord Stromal Tumor
Small Cell Carcinoma
Solid Pseudopapillary Tumor of Pancreas
Spindle Cell Neoplasm
Squamous Cell Carcinoma
T Cell Lymphoproliferative Disorder
T-Cell LGL Leukemia
Thymic Carcinoma
Thymoma
Urothelial Carcinoma
Tumors of Peripheral Nerves
Unknown
Wilms Tumor
Ependymoma, Anaplastic
Astrocytoma, Pilocytic
Ganglioglioma
Neuroepithelial Neoplasm, NOS
Pleomorphic Carcinoma
Solitary Fibrous Tumor
Neuroepithelial neoplasm, high grade
Astrocytoma, NOS
Astrocytoma, Diffusely Infiltrating
Diffuse Midline Glioma
Infiltrating Glioma, NOS
Intraductal Papillary Mucinous Neoplasm (IPMN)
Lymphadenopathy
Lymphocytosis, Symptomatic
Monoclonal Gammopathy
Mucinous or Serous Cystic Neoplasms of Pancreas
Mycosis Fungoides, Unspecified Site
Oligodendroglioma, Anaplastic
Pleomorphic Xanthoastrocytoma
Rash and Other Nonspecific Skin Eruption
Hurthle Cell Carcinoma
High Grade Glioma
Undifferentiated Sarcoma
Glioma
Interpretation

This gene is a known cancer gene.

Last updated: 2019-08-28 14:53:57 UTC
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Tier 2
KRAS
Variants
KRAS any mutation
Primary Sites
Adrenal Gland
Anus
Ampulla (Pancreaticobiliary Duct)
Appendix
Bladder
Blood
Bone
Bone Marrow
Brain
Breast
Spinal Cord
Cervix
Chest Wall
Colon
Endometrium
Esophagus
Eye
Fallopian Tube
Fibroadipose Tissue
Gall Bladder
Kidney
Larynx
Liver
Lung
Lymph Node
Nasal Cavity
Oral Cavity
Ovary
Pancreas
Parathyroid
Penis
Peripheral Nervous System
Peritoneum
Pharynx
Pituitary
Placenta
Pleura
Prostate
Retroperitoneum
Salivary Gland
Seminal Vesicle
Skeletal Muscle
Skin
Small Intestine
Soft Tissue
Spleen
Stomach
Testis
Thymus
Thyroid
Tonsil
Unknown
Ureter
Uterus
Vagina
Rectum
Cartilage
Blood Vessel
Buccal Swab
Heart
Trachea
Salivary Duct
Spermatic Cord
Vulva
Brain, Infratentorial
Brain, Supratentorial
Gastroesophageal Junction
Sellar
Suprasellar
Peritoneal fluid
Pleural Fluid
Tongue
Tumor Types
Acinar Cell Carcinoma
Acinic Cell Carcinoma
Adenocarcinoma
Adenoid Cystic Carcinoma
Adenosarcoma
Ameloblastic Tumor
Anaplastic Large Cell Lymphoma
Angioimmunoblastic T-Cell Lymphoma
Angiomatoid Fibrous Histiocytoma
Angiomatosis
Angiomyolipoma
Angiosarcoma
Astrocytoma, Anaplastic
Basal Cell Carcinoma
Burkitt Lymphoma
Carcinoid Tumor
Carcinoma
Carcinosarcoma
Cholangiocarcinoma
Chondrosarcoma
Chordoma
Choriocarcinoma
Chromophobe Renal Cell Carcinoma
Chronic Lymphocytic Leukemia
Classical Hodgkin Lymphoma
Clear Cell Carcinoma
Clear Cell Renal Cell Carcinoma
Craniopharyngioma
Dermatofibrosarcoma
Desmoplastic Small Round Cell Tumor
Diffuse Large B Cell Lymphoma
Ductal Carcinoma
Ependymoma
Ewing Sarcoma
Fibromatosis
Follicular Carcinoma
Follicular Lymphoma
Gastrointestinal Stromal Tumor
Germ Cell Tumor
Giant Cell Tumor
Glioblastoma
Glomus Tumor
Granular Cell Tumor
Hairy Cell Leukemia
Hemangioendothelioma
Hepatocellular Carcinoma
Invasive Ductal Carcinoma
Kaposi Sarcoma
Leiomyoma
Leiomyosarcoma
Lipoma
Liposarcoma
Lobular Carcinoma
Lymphoplasmacytic Lymphoma
Malignant Mullerian Mixed Tumor
Mantle Cell Lymphoma
Marginal Zone B Cell Lymphoma
Medullary Carcinoma
Medulloblastoma
Melanoma
Meningioma
Merkel Cell Carcinoma
Mesothelioma
Mucinous Adenocarcinoma
Mucinous Tumors of Ovary
Mucoepidermoid Carcinoma
Myxofibrosarcoma
Nasopharyngeal Carcinoma
Neuroblastoma
Neuroendocrine Carcinoma
Neuroendocrine Neoplasm
NK Cell Lymphoproliferative Disorder
NLPHL
Non-Small Cell Lung Carcinoma
Oligodendroglioma
Osteosarcoma
Papillary Carcinoma
Papillary Renal Cell Carcinoma
Peripheral T Cell Lymphoma
Pheochromocytoma
Plasma Cell Disorder
Post-Transplant Lymphoproliferative Disorder
Primitive Neuroectodermal Tumor
Renal Cell Carcinoma
Reninoma
Retinoblastoma
Rhabdomyosarcoma
Sarcoma
Schwannoma
Serous Carcinoma
Sex Cord Stromal Tumor
Small Cell Carcinoma
Solid Pseudopapillary Tumor of Pancreas
Spindle Cell Neoplasm
Squamous Cell Carcinoma
T Cell Lymphoproliferative Disorder
T-Cell LGL Leukemia
Thymic Carcinoma
Thymoma
Urothelial Carcinoma
Tumors of Peripheral Nerves
Unknown
Wilms Tumor
Ependymoma, Anaplastic
Astrocytoma, Pilocytic
Ganglioglioma
Neuroepithelial Neoplasm, NOS
Pleomorphic Carcinoma
Solitary Fibrous Tumor
Neuroepithelial neoplasm, high grade
Astrocytoma, NOS
Astrocytoma, Diffusely Infiltrating
Diffuse Midline Glioma
Infiltrating Glioma, NOS
Intraductal Papillary Mucinous Neoplasm (IPMN)
Lymphadenopathy
Lymphocytosis, Symptomatic
Monoclonal Gammopathy
Mucinous or Serous Cystic Neoplasms of Pancreas
Mycosis Fungoides, Unspecified Site
Oligodendroglioma, Anaplastic
Pleomorphic Xanthoastrocytoma
Rash and Other Nonspecific Skin Eruption
Hurthle Cell Carcinoma
High Grade Glioma
Undifferentiated Sarcoma
Glioma
Interpretation

This gene is a known cancer gene.

Last updated: 2019-08-28 14:53:59 UTC
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Tier 1
KRAS
Variants
KRAS codon(s) 12, 13, 61, 117, 146 any
Primary Sites
Small Intestine
Tumor Types
Adenocarcinoma
Interpretation

KRAS is a gene that encodes one of the several proteins in the epidermal growth factor receptor (EGFR) signaling pathway that is important in the development and progression of cancer. KRAS can harbor oncogenic mutations that yield a constitutively active protein. Such mutations are found in approximately 30% to 60% of small intestine adenocarcinomas and are common in other tumor types. The relevant KRAS mutation is in one of five codons (12 13, 61, 117 or 146). KRAS mutations in small intestine tumors are associated with higher pT classification and more frequent pancreatic invasion. The effect of KRAS mutations on drug therapy has not been well established in the literature, however it has been extensively studied in colorectal adenocarcinoma. Mutations in the KRAS gene may indicate poor prognosis and poor drug response with therapies targeted to EGFR in colon cancer, and the absence of a KRAS mutation predicts a greater likelihood of response to EGFR-targeted therapies and improved survival with such treatment. The presence of KRAS mutations in codon 12, 13 or 61 is associated with a high likelihood of resistance to therapies targeting EGFR in colon cancer. In addition, mutations at codons 117 and 146 may also be associated with reduced response to EGFR-targeted therapies in colon cancer. Results should be interpreted in conjunction with other laboratory and clinical findings.

Last updated: 2018-04-25 15:39:54 UTC
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Tier 2
KRAS
Variants
KRAS G12D
Primary Sites
Ampulla (Pancreaticobiliary Duct)
Tumor Types
Adenocarcinoma
Interpretation

KRAS, member of the RAS family of small GTPases which functions as an upstream regulator of the MAPK and PI3K pathways, is frequently mutated in a diverse range of cancers including pancreatic, colorectal and lung cancers. More than 90% of pancreatic ductal adenocarcinoma samples have a KRAS mutation which may have prognostic, and (with ongoing trials assessing the efficacy of novel KRAS inhibitors) possibly therapeutic implications. However, targeting KRAS directly has been difficult in these tumors. KRAS mutations are infrequent in gastric carcinomas and have been reported in approximately 6% of cases. The gain of function KRAS G12D mutation is known to be oncogenic.

Last updated: 2019-01-22 18:41:07 UTC
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PMKB Bot
  • Genes
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  • Interpretations
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  • Primary Sites
  • Activity

Disclaimer: You assume full responsibility for all risks associated with using this PMKB website. The Englander Institute for Precision Medicine at Weill Cornell Medicine makes no guarantee of the comprehensiveness, reliability or accuracy of the information on this website and assumes no responsibility for errors in the information associated with this web site. Healthcare providers and patients must integrate all clinical and laboratory findings as well as information from a variety of sources before deciding on appropriate clinical care options.


When using PMKB, please cite: Huang et al., JAMIA 2017


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