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Validated All-in-One™ qPCR Primer for KRAS(NM_004985.4) Search again
Product ID:
HQP088420
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
'C-K-RAS, C-K-RAS, CFC2, K-RAS2A, K-RAS2B, K-RAS4A, K-RAS4B, K-Ras, K-Ras 2, KI-RAS, KRAS1, KRAS2, NS, NS3, OES, RALD, RASK2, c-Ki-ras, c-Ki-ras2
Gene Description:
KRAS proto-oncogene, GTPase
Target Gene Accession:
NM_004985.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene, a Kirsten ras oncogene homolog from the mammalian ras gene family, encodes a protein that is a member of the small GTPase superfamily. A single amino acid substitution is responsible for an activating mutation. The transforming protein that results is implicated in various malignancies, including lung adenocarcinoma, mucinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma. Alternative splicing leads to variants encoding two isoforms that differ in the C-terminal region.
Gene References into function
- It is proposed that lowering the affinity for GTP allows G12D Ras an escape from the oncogenic GTP-bound state, whereas GTP tightly bound to G12V mutant Ras generates a more persistent, potentially oncogenic, signal.
- Mutations were detected by using allele-specific amplification method.
- oncogenic levels of mitogen-activated protein kinase (MAPK) signaling of the dinucleotide KRAS2 mutations G12F and GG12-13VC
- valine-12 Ki-Ras mutants demonstrated a greater ability to invade Matrigel than cells expressing the aspartate-12 mutant or wild-type Ki-Ras proteins.
- KRAS2 mutations have been detected in laser-capture microdissected atypical endometrial hyperplasia specimens arising concurrently with endometrial carcinoma.
- Ras modulates the proliferative response of RSF to TNF-alpha and TGF-alpha
- mutations in K-ras have been detected in primary carcinoma of small intestine
- Coordinated traffic of Grb2 and Ras during epidermal growth factor receptor endocytosis
- K-ras mutations and RASSF1A promoter methylation in colorectal cancer
- Multiple K-RAS mutations are frequent both in PC with associated PanIN and in biliary cancers, and indicate that clonally distinct precursor lesions of PC might variably contribute to tumor development.
- Constitutive activation of NF-kappaB in Ki-ras-transformed prostate epithelial cells
- Mutations in APC, Kirsten-ras, and p53--alternative genetic pathways to colorectal cancer. The most common combination of mutations was p53 and APC (27.1%), whereas mutations in both p53 and K-ras were extremely rare.
- Uncommon mutation types of K-ras may contribute to long term patient survival in pancreatic adenocarcinoma.
- study performed to determine the status of K-ras-2 in liver angiosarcomas (LAS) from workers occupationally exposed to vinyl chloride
- Immunohistochemical staining of p21 appears to be of prognostic value in patients receiving systemic adjuvant chemotherapy for locally advanced bladder cancer.
- the constitutive activation of Ras might have induced the persistent expression of p21cip1 and p27kip1, and that this induction of p21cip1 and p27kip1 expression possibly caused the cell cycle arrest at the G1 phase.
- Review: Exploring environmental causes of altered ras effects: fragmentation plus integration?
- Specific T-cell immunity against Ki-ras peptides in patients with pancreatic and colorectal cancers.
- acute hyperglycemia-mediated mononuclear cell activation is dependent on activation of ras, p42/p44 mitogen-activated protein kinase phosphorylation, and subsequent NF-kappaB activation
- LOH of chromosome 12p was seen in about 50% of human lung adenocarcinomas & large cell carcinomas. Kras2 mutations were seen at codon 12 in about 40% of adenocarcinomas & large cell carcinomas. The wild-type Kras2 is a tumor suppressor of lung cancer.
- results demonstrate that the mutational status of BRAF and KRAS is distinctly different among histologic types of ovarian serous carcinoma, occurring most frequently in invasive micropapillary serous carcinomas and its precursors, serous borderline tumor
- Ki-ras mutations and HGF signaling cooperate to enhance tumor growth by increased duration of MAPK activation and decreased apoptosis in human carcinoma cells.
- results suggest that carcinogenesis in the biliary tract epithelium in anomalous pancreaticobiliary ductal union (APBDU) is accompanied by multistep genetic mutational events; K-ras gene mutation occurs early in epithelial hyperplasia or metaplasia
- The results suggest a potential role for Ca2+/calmodulin in the regulation of K-RasB function.
- No somatic mutations were identified in either TP53 or KRAS, indicating that disregulation of these genes is not required for leiomyomas development
- types of mutations in sinonasal NK/T cell lymphoma in northeast district of China
- codon 12 K-ras mutations in lung tumors or sputum samples from 102 lung cancer patients
- p21Ras activation is instrumental in FVIIa signal transduction and the FVIIa-dependent activation of p21Ras involves either PKC or Src-dependent mechanisms, depending on the cell type investigated.
- K-Ras4B polybasic domain or an alternatively prenylated CAAX renders Ras prenylation, Ras-induced Elk-1 activation, and anchorage-independent cell growth farnesyltransferase inhibitor-resistant.
- Point mutations in Ki-ras gene is associated with colorectal cancers in mexican patients
- signaling initiated by activated Ki-ras interferes with the IFN/STAT signaling pathway and modulates the responsiveness of cancer cells to interferons
- K-ras mutations may have an effect on proliferation in pancreatic ductal adenocarcinoma
- there is an inverse relationship between Kras2 activation and RASSF1A promoter methylation in the majority of human lung adenocarcinomas and large cell carcinomas
- BRAF mutations, which are present in a variety of other human cancers, do not seem to be involved in gastric cancer development
- KRAS2 mutations were seen in stomach neoplasms.
- findings indicate the wild-type KRAS allele is occasionally lost in lung cancer and the oncogenic activation of mutant KRAS is more frequently associated with overexpression of the mutant allele than with loss of the wild-type allele in NSCLC development
- The positive expression rates of p21 and p53 proteins were 75.0% and 57.3% respectively in pancreatic carcinoma, which were significantly different from those in the normal tissue (P<0.05). p21 and p53 proteins were positively correlated (P<0.05).
- Oncogene Protein p21(ras) accumulation was confined to the upper layer of esophageal squamous cell carcinoma.
- RAS or BRAF mutations are detected in about 32% of all Barrett's adenocarcinomas; the disruption of the Raf/MEK/ERK (MAPK) kinase pathway is a frequent but also early event in the development of Barrett's adenocarcinoma
- Detection of P21 may be used as the screening marker for diagnosis of polycyclic aromatic hydrocarbons (PAHs)-related lung cancer related lung cancer, and may supplement the diagnostic value of conventional cytology.
- Mutations in K-ras gene is associated with malignant melanomas
- These studies identify isoprenylcysteine carboxyl methyltransferase as a potential target for reducing the growth of K-Ras- and B-Raf-induced malignancies.
- Mutant-type [(12)Asp]K-ras4B can enhance the expression of estrogen receptor alpha and beta proteins and their transcriptional activity as a transcription factor in endometrial carcinoma HEC-1A cell line.
- p21Ras, hSOS1, and p120GAP are not involved in polycystic ovary disease
- k-ras has a role in cell death through the p38 MAP kinase pathway in human colonic cancer cells
- K-ras mutation may play a role in the malignant transformation of pancreatic ductal cell.
- ovarian serous cystadenomas do not contain mutations in either BRAF or KRAS genes
- K-ras mutations are frequently found in surgical margins in non-small-cell lung carcinoma patients.
- Results suggest that changes in telomerase activity and K-ras point mutation at codon 12 may be an early event of malignant progression in pancreatic cancer.
- k-Ras has a role in promoting butyrate-induced apoptosis by inhibiting gelsolin expression
- Sensitivity of PNA clamp PCR assay in identifying occult micrometastases in the sentinal lymph nodes of colorectal cancer patients by single-base mutation analysis.
- H-Ras mediates FucT-VII induction in Jurkat T cells via the activation of the Raf, PI3K, and a distinct, H-Ras-specific effector signaling pathway.
- K-Ras mutations were found in 80% of pancreatic adenocarcinoma cell lines and 100% of primary tumors. They were all missense mutations of Gly(12) to Val or Asp.
- Mutations of BRAF or KRAS oncogenes are early events in the serrated polyp neoplasia pathway. CpG island methylation plays a role in serrated polyp progression to colorectal carcinoma.
- Detection of K-ras mutations in normal colonic mucosa might serve as a high-specificity approach to colorectal cancer.
- c-Myc antagonized the induction of p21Cip1 mediated by oncogenic H-, K-, and N-Ras and by constitutively activated Raf and ERK2
- Co-mutation of p53 and K-ras gene has neither synergic carcinogenesis-promoting effect, nor prognostic effect on rectal cancer.
- ANCA selectively activates K-ras during induction of a respiratory burst via pathways involving multiple upstream kinases.
- Simultaneous measurement of K-ras and p16 mutations provides an additional tool in differential diagnosis of chronic pancreatitis and pancreatic adenocarcinoma.
- comparison with mouse data show a pattern of gene expression indicative of KRAS2 mutation and oncogenic activity
- K-ras mutations occur prominently in type 1 and type 2 gastric cancers.
- Mutations in either the EGFR TK domain or the KRAS gene can lead to lung cancer pathogenesis. EGFR TK domain mutations are the first molecular change known to occur specifically in never smokers.
- data suggest that mutations of epidermal growth factor receptor (EGFR) and K-RAS genes might separately, but not cooperatively, contribute to lung adenocarcinoma pathogenesis
- Activating KRAS2 mutations were found in 82% of lethal metastatic pancreatic neoplasms.
- The results obtained from the RASCAL studies suggest that Ki-ras mutations might have an effect on survival rate of colorectal cancer patients, and that the specific codon 12 glycine/valine mutation might play a role in the progression of this neoplasia.
- Specific TP53 mutations in L3 domain alone (only in DFS) or in combination with specific Ki-ras mutations at codon 13 are associated with a worse prognosis in sporadic colorectal cancer.
- The sequential accumulation of mutations in K-ras drives the transition from normal epithelium through increasing adenomatous dysplasia to colorectal cancer.
- Mutant human Kras(D12) suppresses IL-18 production in murine colorectal tumor cells, which may contribute to evasion of the local immune system during tumor development
- Clinical evidence that suggests a role for K-Ras in the formation of colorectal metastases. (review)
- controversial link of KRAS mutations in colorectal cancer with chromosomal instability and patient prognosis (review)
- MUC5AC and MUC2, TFF1 and TFF3, APC and p21 in subsets of colorectal polyps and cancers suggests a distinct pathway of pathogenesis of mucinous carcinoma of the colorectum
- Ras mutations do not play a significant role in the pathogenesis of multiple myeloma in the Spanish population
- hepatocyte growth factor signaling and Ki-ras oncogene activation have roles in colorectal cancer
- mechanistic insights are now possible into how K-Ras contributes to pancreatic ductal carcinogenesis (review)
- While most aberrant crypt foci do not have adenopolyposis coli mutations, a large proportion has KRAS mutations. (review)
- The results suggest that oncogenic K-Ras enhances the malignant phenotype and identify the mitogen-activated protein kinase p38 as a target to inhibit oncogenic K-Ras-induced pancreatic tumor cell migration.
- Allelic loss on 12p12-13 region would influence the KRAS2 expression by reducing the gene-dosage in colon carcinogenesis.
- Mutation and elevated expression of KRAS2 is associated with the development of testicular germ cell tumors
- KRAS has a role in villous growth in colorectal adenomas
- Polymorphisms in some insulin-related genes are associated with an increased risk of colon cancer with specific KRAS2 and TP53 mutations, implying a link between these genetic changes and specific mutational pathways in carcinogenesis.
- Mutations do not confer a growth advantage to somatic heterozygous clusters or maintenance turnover units.
- Cardio-facio-cutaneous (CFC) syndrome involves dysregulation of the RAS-RAF-ERK pathway.
- Germline KRAS mutations are a cause of human disease and infer that the constellation of developmental abnormalities seen in Noonan syndrome spectrum is due to hyperactive Ras.
- Mutations in transfect Ki-ras promote the formation of benign lung tumors and suggest potential targets for the development of novel chemotherapeutic and chemopreventive agents during the early stages of lung tumor progression.
- These findings suggest that endogenous Nore1B recruits active Ras to the APC-T cell interface and mediates the interaction between Ras and Carma1.
- Genomic instability may occur on 12p-12-13 of Kras2 gene in the development and progression of colon carcinoma. The high LOH of Kras2 gene may directly influence the transcription and translation of wild type Kras2 gene.
- K-ras mutations were detected in 70% of neoplastic tissue samples, but no mutated DNA resulted in circulating DNA samples in pancreatic cancers.
- In 239 Thai adult AML cases, 35 RAS mutations were found in 32 cases (13%) predominantly classified as M1/M2 (53%) followed by M4/M5 (38%). Ten cases were positive for NRAS codon 12, 11 for NRAS codon 61, 13 for NRAS codon 13, and one for KRAS codon 13.
- Rodent and human tumor cells containing constitutively activated Raf/Raf/MEK/ERK pathways were resistant to mda-5-induced killing.
- The role of K-ras codon 12 and codon 13 mutations in human papillomavirus virus-associated colon tumors.
- A nuclease hypersensitive polypurine-A polypyrimidine element within the promoter of the KRAS proto-oncogene regulates transcription.
- BRAF mutations are as uncommon as KRAS mutations in prostate adenocarcinoma
- the combination of an activating mutation of the TSH receptor (T620I) and a mutation of the Ki-RAS (G12C) genes may play an important role in both the hyperfunction of follicular thyroid carcinoma and the carcinogenetic process
- In 50 of the 66 primitive colorectal tumor cases at least one significant alteration was identified in Ki-Ras and/or TP53 and/or p16(INK4A) genes.
- ras may be involved in early stages of larynx carcinogenesis and may be activated by other mechanisms different from mutations, such as epigenetic events
- trichostatin A-induced cell death of Ki-Ras-transformed cells is enhanced by inhibition of NF-kappaB
- KRAS mutation occurred frequently (26.5%) in adenomas and particularly in adenomas with villous architecture.
- These data describe a functional association between K-Ras4B and nucleolin
- Ki-ras proto-oncogene mutation and p53 gene overexpression is associated with sporadic colorectal adenomas
- K-ras mutations are associated with colorectal cancers
- analysis of H-RAS, K-RAS and N-RAS expression in acute myeloid leukemia
- BRAF, K-ras and BAT26 are expressed in colorectal polyps and stool
- Concomitant KRAS and BRAF mutations increased along progression of MSS colorectal cancer, suggesting that activation of both genes is likely to harbour a synergistic effect
- Recurrent KRAS codon 146 mutations is associated with human colorectal cancer
- 6 haplotype blocks were identified across the KRAS locus in endometriosis patients. No germline variants or differences in SNPs or haplotypes were seen between cases and controls.
- KRAS and p53 gene mutations, which are rarely simultaneous and are associated with specific DI aneuploid values, do not represent a synergistic evolutionary pathway but may influence mechanisms of chromosomal instability.
- Phenotypic variability may be related, at least in part, to specific genotypes and possibly reflects the central role of K-Ras in a number of different signalling pathways.
- These findings suggest that continuous K-Ras activation accelerates cell growth and evokes a feedback system through IGFBP-4/2 to prevent excessive growth.
- Presence of an oncogenic KRAS allele results in a dynamic physical interaction between endogenous N-RAS and gelsolin that correlates with survival in colorectal cancer cell lines.
- K-RAS is uniquely oncogenic in the colonic epithelium, though the molecular aspects of its oncogenic contribution are not necessarily conserved across cell lines.
- data suggest that mutations of the k-ras oncogene may induce activation of ERK1/2 in colorectal carcinoma
- RASSF1A methylation was observed in a high frequency in endometrioid endometrial carcinoma whereas K-ras and B-raf mutations were observed in a low frequency
- Rna silencing of K-ras(V12) markedly decreased K-ras(V12) gene expression and inhibited cellular proliferation of lung cancer cells.
- High-resolution melting analysiswill enable screening of gene mutations, such as KRAS to allow appropriate therapeutic choices for patients and accelerate research aimed at identifying novel mutations in human cancer.
- Urine might be a better resource for detecting K-ras mutation in circulating DNA in patients with colorectal cancer.
- association between K-ras mutation and smoking in pancreatic cancer patients
- Taken together, the observations indicate that both H-Ras(G12V) and K-Ras4B(G12V) activates non-conventional and perhaps unique effector pathways to induce cytoplasmic vacuolation in glioblastoma cells.
- This pilot study suggests that low-level fractional allelic loss or K-ras mutation in the negative/atypical cytology samples of bile duct with malignant outcome is a representation of morphologically subtle molecular alterations.
- analysis of oxidative posttranslational modifications of cysteine thiols of p21ras associated with redox modulation
- One female patient exhibiting the distal phalangeal creases had a mutation in the KRAS gene.
- patients having juvenile myelomonocytic leukemia with NRAS or KRAS2 glycine to serine substitution received no chemotherapy, but hematologic improvement was observed during a 2- to 4-year follow up.
- K-Ras promotes growth transformation and invasion of immortalized human pancreatic cells by Raf and phosphatidylinositol 3-kinase signaling.
- The wild-type Kras2 gene effectively inhibits the growth of the colonic adenocarcinoma cell line Caco-2.
- findings show that RASSF1A hypermethylation and KRAS mutations and BRAF mutations are inversely correlated and play an important role in the development of cervical adenocarcinomas
- mutational analysis of KRAS, BRAF, and MAP2K1/2 in 56 patients with CFC syndrome; comparison of the genotype-phenotype correlation of CFC with that of Costello syndrome suggest a significant clinical overlap but not genotype overlap.
- data suggest that BRAF mutations might be present less frequently than KRAS mutations in Greek patients with colorectal carcinomas
- Mutations of K-ras and Dpc4 genes can accumulate already in non-malignant, inflammatory pancreatic tissue, suggesting its applicability in monitoring of further destruction of pancreatic tissue and progression into malignancy.
- KRAS mutations were present in 3 of 16 serrated compared with 14 of 33 non-serrated hyperplastic aberrant crypt foci
- Circulating KRAS mutations originate from tumors and are prognostically relevant in lung cancer.
- KRAS KRAS mutations were observed significantly frequently in bronchial-type tumors
- Genetically, the non-polypoid growth type of submucosal invasive colorectal carcinoma shows much less frequent K-ras mutation.
- c-kit expression is not alternative to BRAF and/or KRAS activation.
- it is suggested that atypical adenomatous hyperplasia (AAH) could develop by either KRAS or EGFR gene mutation, but AAH harbouring a KRAS gene mutation might not progress further to an invasive cancer
- Activated K-ras is associated with non-small cell lung cancer
- A KRAS mutation in a baby girl with an early clinical diagnosis of cardio-facio-cutaneous syndrome associated with a large ulcerating hemangioma, is reported.
- KRAS G34A mutation was relatively common to all classes of specimen, whereas TP53 gene C742T and G818C mutations were significantly more frequent in lichen sclerosus than normal genital skin.
- study of EGFR, HER2, TP53& KRAS mutations of p14arf expression of non-small cell lung cancers in relation to smoking
- study reveals there are differences in the frequencies & types of K-ras & p53 mutations found in pancreatic adenocarcinomas of patients in high-pollution & low-pollution regions in Egypt & suggests that environmental factors may explain these differences
- among adenocarcinomas, nonmucinous and mucinous bronchioloalveolar carcinoma components were significantly associated with EGFR and K-ras gene mutations, respectively
- In bronchioalveolar carcinoma/adenocarcinoma with bronchioalveolar features mucinous differentiation was significantly correlated with the absence of EGFR mutation and presence of KRAS mutation.
- In 2 cases of ovarian tumors the same mutations of KRAS occurred in both the atypical proliferative serous (borderline) tumor and the high-grade serous carcinoma component of the tumor, indicating a clonal relationship.
- EGFR and K-ras mutations may have a role in progression of resected non-small-cell lung cancer
- De novo germline HRAS (G12A) and KRAS (F156L) mutations in two siblings with short stature and neuro-cardio-facio-cutaneous features.
- NSCLC cases with wt- or mutant KRAS, downregulation of EGFR expression was a rare event although upregulation in bone metastases was observed more frequently in wt K-RAS cases.
- an important relationship between K-ras codon 12 mutations and overall survival in colorectal cancer patients
- tobacco does not play a major part in acquisition of K-ras mutations in the pancreatic epithelium; although both smoking & K-ras mutations have important roles in the etiopathogenesis of exocrine pancreatic cancer, the 2 processes may act independently
- Mutations in KRAS is associated with colon tumors
- oncogenic K-RAS/ERK in pancreatic adenocarcinoma facilitates TGFbeta-induced transcriptional down-regulation of the tumor suppressor PTEN in a SMAD4-independent manner
- Combined with screening of K-ras mutations and allelic losses of tumor suppressors p16 and DPC4 represents a very sensitive approach in screening for pancreatic malignancy.
- KLF6 and p53 mutations are involved in the development of nonpolypoid colorectal carcinoma, whereas K-ras and B-raf mutations are not
- Kras mutant lung cancer patients have a significantly worse prognosis than wild-type patients.
- The majority of colorectal and gastric cancer cells with KRAS mutations are homogeneous because they have the same KRAS mutation.
- 2 novel mutations (K5E, G12S) were identified in 7 patients withcardio-facio-cutaneous syndrome, Costello syndrome or Noonan syndrome.
- Report genetic alterations of K-ras in Korean colorectal cancer patients.
- tumor budding and podia formation were observed to be significantly higher in the 32 (34.7%) of colorectal tumors with K-ras gene mutations (29 mutations in codon 12, 3 in codon 13)
- data support the notion that K-ras-dependent inhibition of anoikis plays an important casual role in colorectal carcinoma progression
- KRAS is rarely mutated in pilocytic astrocytomas.
- The K-RAS gene was screened for mutations in Congenital cystic airway malformation/congenital pulmonary airway malformation...no mutations were present
- Wild type K-ras2 is related to the negative regulation of cell proliferation, metabolism and transcriptional control in colon carcinoma cells.
- experiments provide a rationale for targeting Ras and associated signaling pathways in mesothelioma and also suggest cap-dependent translation as one mechanism by which Ras induces proliferation in this disease.
- The regulation of p21WAF1/CIP1, independent of p53 or bcl-2 expression, appears to be associated with Kras mutations.
- Data suggest that the intrinsic k-Ras/Ras GTPase activity, the responsiveness of these proteins to GTPase-activating proteins, and guanine nucleotide dissociation all regulate developmental programs in vivo.
- Frequently mutated in high hyperdiploid childhood acute lymphoblastic leukemia.
- study of point mutations in RAS oncogenes in papillary thyroid carcinoma; 2 mutations found (GAA/CAA at codon 31 of K-RAS & CAA/CAC at codon 61 of N-RAS); data confirm previous studies, showing RAS mutations are more rare in PTC than follicular neoplasms
- 54% of childhood CBF-AML had RTKs and/or Ras mutations
- In conclusion, the data support a model whereby RbAp48 regulates cellular morphology and cytoskeletal organization by increasing K-Ras activity and signaling through MAPK.
- KRAS WT status is associated to survival benefit in cetuximab treated metastatic colorectal cancer.
- k-ras codon 12 mutation is associated with non-small cell lung carcinoma
- Smoking and diabetes were associated with pancreatic cancer patients positive for K-ras codon 12 mutations
- Quantification of mutant KRAS2 in pancreatic juice differentiates pancreatic adenocarcinoma from chronic pancreatitis, and may be a useful early detection tool for pancreatic cancer.
- KRAS2 c.34G > T somatic prescreening, followed by MUTYH hotspot mutation analysis when positive, can identify patients with (atypical) MUTYH-associated polyposis
- A worse clinical outcome was found for CIMP-high, microsatellite stable colorectal cancer with KRAS/BRAF mutation but not for those lacking KRAS/BRAF mutation.
- results confirm the high prognostic value of KRAS mutations on response to cetuximab and survival in metastatic colorectal cancer patients treated with cetuximab
- All cases were wild-type for HER2. Mutations of EGFR and K-ras genes represent an early event in lung adenocarcinomagenesis, and AAH convincingly seems to be a precursor lesion in a subset of cases of adenocarcinoma.
- genetic alterations of KRAS and PIK3CA may play equivalent roles in endometrial carcinogenesis
- Mutations in the K-ras is associated with colon cancers
- The data support that the frequencies and patterns of somatic mutation of the K-ras gene in colorectal cancer are variable among populations.
- while activated HrasV12 promotes differentiation and growth arrest in these endodermal progenitors, KrasV12 promotes their proliferation
- K-ras mutations have a limited role in development of sinonasal cancer
- KRAS polymorphisms were indicated to be involved in risk for the development of atypical adenomatous hyperplasia that progresses to lung adenocarcinoma.
- first direct comparison of survival of resected patients with either EGFR or KRAS mutant lung adenocarcinomas compared with those wild type for both genes; EGFR & KRAS mutations define distinct molecular subsets of resected lung adenocarcinoma
- KRAS status should be considered in selecting patients with mCRC as candidates for panitumumab monotherapy
- In patients with lung adenocarcinoma, mutation analyses of EGFR and KRAS show whether or not to apply treatments targeting against EGFR and the selection of dosage for such treatments.
- high frequency of mutations in the PIK3CA, HRAS and KRAS genes leads us to believe that dysregulation of the phosphatidylinositol 3-kinase or Ras pathway is significant for the development and progression of penile carcinoma.
- apart from K-ras codons 12/13 point mutations, overexpression of the ras family genes is important in the development of colorectal cancer but it appears not to be predictive of survival.
- The incidence of K-ras mutation may be associated with the hypersecretion of mucin in IPMN patients.
- KRAS mutation may occur at a very low frequency in Chinese NSCLC patients regardless of pathology, smoking status, or gender.
- Kras may uniquely contribute to the initiation of tumors in endodermally-derived tissues by expanding a stem/progenitor cell population
- Data show that germ cell single base substitution mutation frequencies are very similar to somatic tissue Kirsten-RAS mutation frequencies.
- Before panitumumad administration KRAS oncogene must be analysed to determine "continuous activation" or wild type gene is involved.
- K-ras mutation has been detected in the tumor tissue of 25 patients (33%). K-ras mutation hasn't been detected in the blood. tumors with K-ras mutation have a worse prognosis and often lead to disemination
- CpG island methylator phenotype in colorectal neoplasms may result from activating mutations in either BRAF or KRAS.
- The G-rich strand of a nuclease hypersensitive element, located in the human KRAS promoter, can fold into a dynamic intra-molecular G-quadruplex that can assume two distinct conformations.
- may be involved with imatinib resistance in chronic myeloid leukemia
- Provide a unique view of the tumor-initiating effects of oncogenic KRAS in a zebrafish model of pancreatic cancer.
- Increased frequency of K-ras mutations are associated with colorectal oncogenesis
- KRAS mutations are associated with cetuximab failure in EGFR FISH+ colorectal cancer.
- RAS signaling network is extensively dysregulated in colorectal carcinomas.
- Mutational activation of the K-ras gene, HPV infection and tobacco or alcohol abuse, can be considered independently or in combination as high risk factors for esophageal squamous cell carcinoma development.
- A variety of molecular assays have been devised to detect mutated KRAS in pancreatic cancer.
- analysis of a signaling mechanism for the regulation of the Ras/ERK pathway based on the eNOS-dependent differential activation of N-Ras and K-Ras at specific cell compartments
- K-RasG12D-induced T-cell lymphoblastic lymphoma/leukemias harbor Notch1 mutations
- This is the first report in colorectal carcinoma of humans of internal tandem duplication longer than 1 codon in th KRAS gene and first insertion detected in exon 2.
- KRAS mutations and PI3KCA/PTEN deregulation significantly correlate with resistance to cetuximab.
- both Kras and integrin alpha1beta1 cooperate to drive the growth of non-small cell lung cancer in vivo
- All of the KRAS-mutant Microsatellite instability (MSI)-H (high) tumors harbored sequence alterations MLH1, which implies that KRAS mutation more frequently and almost exclusively occurs in DNA mismatch repair gene-mutant MSI-H tumors.
- Mutation in KRAS is associated with childhood acute lymphoblastic leukemia
- KRAS and BRAF mutations can impair response to anti-EGFR therapy for colorectal neoplasms
- Bayesian network analysis of these and other datasets revealed that PTRF might be a potentially important component of the ERBB signaling network
- BRAF, KRAS and PIK3CA mutations occur prior to malignant transformation demonstrating that these oncogenic alterations are primary genetic events in colorectal carcinogenesis
- All K-ras positive patients revealed a poor survival prognosis and had a tumor relapse after resection.
- With at least 3 markers methylated, new CIMP-positive colorectal cancers were closely associated with proximal tumor location, low frequency of KRAS mutation, and high frequency of BRAF mutation.
- The LCS6 variant allele in a KRAS miRANA complementary site is significantly associated with increased risk for NSCLC among moderate smokers.
- Patients with a colorectal tumor bearing mutated K-ras did not benefit from cetuximab, whereas patients with a tumor bearing wild-type K-ras did benefit from cetuximab.
- Hereditary pancreatitis patients with PRSS1 mutations also had mutations in BRAF and KRAS2.
- KRAS mutation is related with a random CpG island methylation pattern which may lead to CpG island methylator phenotype in colorectal cancer .
- the presence of mutations in the KRAS oncogene can be used to predict which patients are unlikely to benefit from treatment with epidermal growth factor receptor-directed therapy.
- ovarian cancer patients with KRAS or BRAF mutations may benefit from CI-1040 treatment
- Mutations in the KRAS are associated with Noonan syndrome.
- The digital melt curve assay detected 16 (59%) of 27 advanced adenoma samples that contained KRAS mutations, compared with 7% with the Hemoccult, 15% with the HemoccultSensa, and 26% with the PreGenPlus assays.
- KRAS mutations in either primary or metastatic tumors from patients with colorectal cancer is concordant.
- The prevalence of mutant KRAS2 is similar in familial pancreatic adenocarcinoma as in sporadic pancreatic adenocarcinomas.
- KRAS, and CMET mutations are associated with advanced non-small cell lung cancer.
- KRAS mutations or TP53 mutations are associated with lung adenocarcinoma.
- p53 mutation is an initiating mutation in the majority of colitis-associated neoplasia, and K-RAS activation is an alternative gatekeeping mutation.
- oncogenic KRAS could cause the accumulation of phosphatidylinositides and modulate the cell shape and migration.
- Evidence from several randomized studies has established that advanced colorectal tumors harboring a mutation in the KRAS gene do not respond to epidermal growth factor receptor-directed monoclonal antibodies, such as cetuximab or panitumumab.
- miR-143 is significant in suppressing colorectal cancer cell growth through inhibition of KRAS translation.
- KRAS mutations were associated with lower response rate to cetuximab plus irinotecan in colorectal cancer patients(4% v 27% in nonmutated patients; P = .021) and shorter PFS (3.0 v 5.3 months; P = .021).
- Overexpression and mutations of Kras lead to common altered gene expression patterns in NIH3T3 cell.
- KRAS2 mutations in human pancreatic acinar-ductal metaplastic lesions are limited to those with pancreatic intraepithelial neoplasia.