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.

codon 12 K-ras mutations in lung tumors or sputum samples from 102 lung cancer patients

there is an inverse relationship between Kras2 activation and RASSF1A promoter methylation in the majority of human lung adenocarcinomas and large cell carcinomas

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

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.

K-ras mutations are frequently found in surgical margins in non-small-cell lung carcinoma patients.

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

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.

Rna silencing of K-ras(V12) markedly decreased K-ras(V12) gene expression and inhibited cellular proliferation of lung cancer cells.

Circulating KRAS mutations originate from tumors and are prognostically relevant in lung cancer.

Activated K-ras is associated with non-small cell lung cancer

study of EGFR, HER2, TP53& KRAS mutations of p14arf expression of non-small cell lung cancers in relation to smoking

EGFR and K-ras mutations may have a role in progression of resected non-small-cell lung cancer

Kras mutant lung cancer patients have a significantly worse prognosis than wild-type patients.

k-ras codon 12 mutation is associated with non-small cell lung carcinoma

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.

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

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.

both Kras and integrin alpha1beta1 cooperate to drive the growth of non-small cell lung cancer in vivo

KRAS, and CMET mutations are associated with advanced non-small cell lung cancer.

KRAS mutations or TP53 mutations are associated with lung adenocarcinoma.

mutations are associated with post-operative recurrence of lung adenocarcinomas

mutation in KRAS were associated with increased resistance to gefitinib in lung cancer cell lines

There was no significant predictive value for therapeutic response of K-ras mutations for advanced non-small cell lung cancer.

EGFR/KRAS mutation testing of multiple lung adenocarcinomas can assist in differentiating multiple primary lung adenocarcinomas from metastatic lesions.

existing evidence on the relationship between K-ras mutations and tobacco smoking in adenocarcinomas of the pancreas, colorectum and lung [review]

No difference in outcome was seen between patients harboring KRAS transition versus transversion mutations in non-small cell lung cancer.

KRAS mutation is associated with sarcomatoid carcinomas of the lung.

K-RAS mutations were more frequent in males and were associated with smoking habits in 411 lung adenocarcinomas

EGFR and KRAS status of primary lung carcinomas may not predict the status in the corresponding metastases.

LIN28B plays an important role in radiation responses of lung cancer cells through inhibiting let-7g microRNA processing and increasing translation of KRAS.

a sizable subgroup of non-small cell lung carcinomas harbor KRAS amplification, some of which also contain point mutations, and suggest that an increased KRAS copy number may drive p21 overexpression.

KRAS mutations are associated with non-small cell lung cancers.

EGFR and KRAS mutations were found in 33 (10%) and 78 (23%) of lung adenocarcinomas, respectively, whereas 226 (67%) cases were negative for both mutations

These results suggest a role for KRAS mutations in the propensity of primary colorectal tumors to metastasize to the lung.

Molecular studies showed 3 (20%) of 15 oncocytic adenocarcinomas of lung with EGFR mutations and 3 additional cases with KRAS mutations.

Features of KRAS mutations in lung cancer contrast with the features of EGFR mutations.

KRAS mutations were solely and significantly linked to ERK activation in lung adenocarcinoma.

mutations in KRAS is associated with lung adenocarcinoma.

Our results showed significant number of EGFR FISH positive/amplified lung adenocarcinomas harboring KRAS mutation

K-ras mutations did not have any significant effect on Sorafenib treated patients with advanced non-small cell lung cancer.

KRAS mutations are associated with lung adenocarcinomas.

KRAS gene mutations are associated with non-small cell lung cancer.

analysis of EGFR and KRAS mutations in non-small cell lung cancer (NSCLC) patients treated with tyrosine kinase inhibitors

KRAS gene mutations are associated with lung adenocarcinomas with features of the mucinous subtype of bronchioloalveolar carcinoma.

The frequency of K-RAS gene mutations with non-small cell lung cancer in our center is very low and is similar to that in Asia patients, and is lower than that in Caucasian population.

review focused on KRAS gene mutations with special reference to lung cancers, and pointed out important issues remaining to be resolved [review]

KRAS mutation is associated with lung cancer.

Report on the clinical utility of reflex testing of resected stage I through III lung adenocarcinomas for EGFR and KRAS mutatations.

KRAS mutation-positive lung cancer displaying high levels of Myc could be treated by inhibiting Myc transactivation function.

mutations at codon 12 in plasma DNA is not a prognostic factor in advanced non-small cell lung cancer patients

let-7a over-expression represses the expression of k-Ras protein and significantly inhibits the growth of A549 lung cancer cells.

KRAS gene mutations are widely recognized alterations involved in biology and the clinical management of lung adenocarcinoma.This review reports the molecular bases that have led clinical application of detection for such genetic impairments.

Kras mutation plus increased copy number is associated with non-small cell lung cancer.

KRAS mutation analysis helps to differentiate between pulmonary metastasis from colon adenocarcinoma in situ and primary lung adenocarcinoma

In a group of clinically selected patients, EGFR and KRAS analysis was able to define distinct molecular subsets of lung adenocarcinoma.

KRAS mutation seems to be associated with metastasis in specific sites, lung and brain, in colorectal cancer patients

Data show distinct significant correlations between TITF-1 protein expression and DNA copy gain with mutations in the lung adenocarcinoma-prevalent EGFR and KRAS oncogenes.

KRAS-mutated non-small cell lung cancer cells are responsive to either co-treatment with erlotinib or gefitinib and histone deacetylase inhibitors or single treatment with lapatinib.

gene amplification is associated with non-small cell lung carcinoma progression in both Swiss and Amertican cohorts

KRAS mutations in 23 adenosquamous carcinomas of lung

c-Raf plays a unique role in mediating K-Ras signaling in non-small cell lung carcinoma and makes it a suitable target for therapeutic intervention.

Data show that IL-8 overexpression is induced by activating mutations of KRAS or EGFR in non-small cell lung cancer (NSCLC) cells.

the incidence of EGFR and KRAS mutations in Chinese patients with adenosquamous carcinoma of the lung were similar to those of Asian patients with adenocarcinoma

In patients with surgically resected lung adenocarcinomas, the KRAS and EGFR gene mutation status of tumors was not associated with disease-free survival.

KRAS mutations are not associated with response to Bexarotene plus erlotinib therapy in lung carcinogenesis.

the relationship between the mutation of K-ras gene and non-small cell lung cancer

An evaluation of cytomorphologic features of advanced lung adenocarcinomas that might be associated with KRAS mutational status.

KRAS mutation is associated with nonsmall cell lung cancer.

The detection of KRAS mutant allele-specific imbalance in lung adenocarcinomas may identify patients with more aggressive disease.

Data suggest that recurring DNA copy alterations are important for tumor progression in the Kras(LA2) model of lung cancer and that the requirement for these alterations may be dependent on the genetic background of the mouse strain.

The KRAS mutation occurred more frequently in lung tumor patients whose ;ung tumor diameter was >/= 31 mm than in those whose tumor diameter was <30 mm.

KRAS mutation is an early hit in lung adenocarcinoma development.

KRAS mutations are associated with treatment response in non-small cell lung cancer.

KRAS mutation detection may be reliably performed with high accuracy, allowing treatment decisions for lung cancer.

KRAS mutations are associated with non-small cell lung cancer.

KRAS gene may be instable during the metastatic process observed in non-small cell lung cancer, whereas the mutant KRAS genotype in the primary tumor could be more likely to change back to the wild-type after metastasis.

Human lung adenocarcinoma cases lacking EGFR, KRAS, and ALK mutations had a worse prognosis for relapse and death, compared with cases with EGFR, KRAS, or ALK mutations

Data indicate that PIK3CA mutations occur in lung adenocarcinomas, usually concurrently with EGFR, KRAS, and anaplastic lymphoma kinase (ALK).

Report validity EGFR and KRAS mutation analysis in cytologic samples of lung adenocarcinoma enabled by laser capture microdissection.

the activity of myeloblastin was significantly altered in the lung adenocarcinoma biopsies harboring a KRAS gene mutation.

Our findings suggest that EGFR/KRAS mutations do not occur in pure pulmonary squamous cell carcinoma (SQCC).

mutations are good markers of different aetiologies and histopathological forms of lung cancers but have little prognostic value, with the exception of KRAS mutation, which may have a prognostic value in ADC.

KRAS mutations were higher in males compared to females and higher in adenocarcinomas compared to other forms of lung cancers

In the KRAS gene, 10 substitutions at codon 12 were observed in lung adenocarcinomas from a Chiba Prefecture, Japan cohort.

The aim of the present study was to determine the frequency of EGFR and KRAS mutations in non-small cell lung cancer in the West European Dutch population.

Of 26 non-small cell lung cancer cell lines, 14 were KRAS mutant and 12 were wild type; short-term GATA2 knockdown led to specific decreased cell viability and increased apoptosis in KRAS mutant NSCLC cells, comparable to the effect seen with loss of KRAS itself.

Aim of this study was to characterize further the expression of RUNX3 in lung cancers.Inactivation of RUNX3 was observed in 70% of the adenocarcinoma samples, and this was associated with promoter hypermethylation but not biased to EGFR/KRAS mutations.

Authors found that EGFR WT/KRAS mutant advanced non-small cell lung cancer patients are associated with an increased resistance to treatment, specific mutant KRAS may account for differential sensitivity to an EGFR tyrosine kinase inhibitor.

lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1.

KRAS mutations predicted shorter survival for patients with advanced lung adenocarcinoma.

Standard cytology provides adequate material for the assessment of EGFR and Kras mutational status in non-small cell lung cancer and colorectal cancer patients.

Data indicate that epiregulin (EREG) expression significantly correlated with KRAS expression or KRAS copy number in KRAS-mutant non-small-cell lung cancer (NSCLC) cell lines.

KRAS mutation is associated with response to therapy in non-small-cell lung cancer.

Data show that Med23 RNAi specifically inhibits the proliferation and tumorigenicity of lung cancer cells with hyperactive Ras activity.

findings show intratumoral heterogeneity of KRAS mutational status is rare in non-small cell lung cancer (NSCLC); finding is in line with hypothesis that oncogenic activation of KRAS is an early event and a bona fide "driver mutation" in NSCLC

Baseline sPLA(2)IIa expression predicts response to sPLA(2)IIa inhibition in some K-ras mutant lung cancer cells.

KRAS mutations were not detected in lung cancer patients harboring mutations in either EGFR or P53.

a previously unknown link between activated K-Ras and menin, an important interplay governing tumor activation and suppression in the development of lung cancer.

High KRAS expression is associated with the proliferation and invasion of non-small cell lung cancer.

KRAS mutation is associated with lung cancer and is not associated with response to EGFR-tyrosine kinase inhibitors or chemotherapy.

We find that LDHB expression correlates to both KRAS genomic copy number gain and KRAS mutation in lung cancer cell lines and adenocarcinomas.

presence of KRAS mutations in plasma in advanced non-small cell lung cancer may be a marker of poor prognosis and may also hold predictive value.

collegiate smokers (former smokers who smoked between 101 lifetime cigarettes and 5 pack-years)with advanced-stage lung cancers represent a distinct subgroup of patients with a higher frequency of KRAS mutations and lower frequency of EGFR mutations compared with never smokers

EGFR mutation rate is related with gender, smoking history and pathological type in non-small cell lung cancer patients, and is also related with differentiation and smoking history in adenocarcinoma patients.

The status of EGFR and KRAS mutation in serum was not prognostic in patients with advanced non-small cell lung cancer

EGFR and KRAS mutational rates were comparable in primary and unpaired metastatic lung adenocarcinoma in pre-chemotherapy and postchemotherapy groups.

The prevalence of EML4-ALK, EGFR status and KRAS mutations in 208 Chinese patients with non-small cell lung cancer, is reported.

KRAS mutations are associated with lung cancer.

KRAS mutations are associated with solid predominant lung tumors.

KRAS mutations are associated with metastatic lung adenocarcinoma.

KRAS as a prognostic marker of non-small-cell lung cancer (Review)

KRAS mutational status could have an impact to the decision to give chemotherapy or EGFR-TKIs as second-line treatment to patients with non-small cell lung cancer, mainly in patients harboring WT-EGFR.

KRAS mutations are not associated with tyrosine kinase inhibitors treatment efficacy in non-small cell lung cancer.

K-RAS mutations are associated with a worse overall survival in patients with non-small cell lung cancer, especially in patients with adenocarcinoma and early stage.

Identification of a novel association of KRAS mutations with solid growth pattern and tumor-infiltrating leukocytes in non-mucinous lung adenocarcinomas.

KRAS mutation status is not a significant prognostic marker in patients with resected non-small-cell lung cancer.

Cigarette smoking did not influence the frequency of KRAS mutations in lung adenocarcinomas in Korean patients, but influenced qualitative differences in the KRAS mutations.

These results suggested KRAS mutations have an independent prognostic value for chemotherapy in advanced non-small cell lung cancer.

KRAS mutation is not associated with response to chemotherapy in non-small-cell lung cancer.

Race was not statistically significantly associated with KRAS mutational status in patients with non small cell lung cancer.

KRAS mutations are associated with lung cancer.

KRAS mutations,found in smokers, are often activated in lung cancers, with mutations in about 20% of NSCLCs. Most are single amino acid substitutions in codons 12, 13, or 61. It is a negative marker for the efficacy of EGFR TKI in patients with NSCLC

KRAS G12C mutations were associated with primary lung adenocarcinoma, whereas KRAS G12R mutations favored pancreatic adenocarcinoma

evaluated mutations in four driver genes, epidermal growth factor receptor (EGFR), Kirsten ras oncogene (KRAS), c-MET, and echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK), in Chinese lung adenocarcinoma patients

The frequencies of somatic EGFR, KRAS, and ALK gene abnormalities reflect the diverse ethnicity and smoking patterns of non-small-cell lung cancers patients in the United States.

in lung adenocarcinomas, KRAS mutations are prevalent in male smokers; EGFR mutations are associated with female sex, nonsmoking and lepidic and micropapillary growth; TTF1 has a role in survival; BRAF mutations have roles in survival

Report analysis of KRAS mutations in non-small cell lung carcinomas.

Driver mutations among never smoking female lung cancer tissues in China identify unique EGFR and KRAS mutation pattern associated with household coal burning.

KRAS mutations are associated with non-small-cell lung cancer.

Data indicate that coexistence of EML4-ALK fusion or ALK copy number increase and EGFR, MET, and KRAS mutations in tumor tissue from two treatment-naive Chinese non-small cell lung cancer (NSCLC) patients.

overall genomic and transcriptional landscape of lung adenocarcinoma is affected, but only to a minor extent, by EGFR and KRAS mutation status

We show that loss of Scrib and activated oncogenic KRas cooperate in vivo, resulting in more aggressive lung tumors

KRAS mutations are at high risk for early pulmonary recurrence in colorectal carcinoma.

mutation patterns are quantitatively and qualitatively distinct between non-small-cell lung cancer and colorectal cancer

A protumorigenic role for CLPTM1L that is critical for Ras-driven lung cancers, with potential implications for therapy and chemosensitization.

The PI3K/AKT pathway promotes gefitinib resistance in mutant KRAS lung adenocarcinoma by a deacetylase-dependent mechanism.

High KRAS mRNA expression is associated with non-small-cell lung cancer growth and progression.

Sag is a Kras-cooperating oncogene that promotes lung tumorigenesis

Studies suggest the potential predictive role of mutant KRAS in the context of chemosensitivity of non-small-cell lung cancer (NSCLC) which may depend on the individual drug types.

Our findings suggest that IL-8 expression is associated with certain clinicopathological features including age and is a potent prognostic marker in lung adenocarcinoma, especially in oncogenic KRAS-driven adenocarcinoma.

Activating KRAS mutations were associated with lung cancer.

KRAS mutations are more common in heavy smokers, and lung adenocarcinomas with KRAS mutation are more likely to invade the visceral pleura.

While KRAS mutation status per se is neither prognostic nor predictive in stage III-IV lung adenocarcinoma, subtype-specific analysis may indeed identify clinically relevant subgroups of patients that may ultimately influence treatment decisions.

EGFR and KRAS mutations were present in adenocarcinoma of the lung but not squamous tumors.

Simultaneous diagnostic platform of genotyping EGFR, KRAS, and ALK in 510 Korean patients with non-small-cell lung cancer highlights significantly higher ALK rearrangement rate in advanced stage.

KRAS-mutation is associated with non-small cell lung cancer.

miR125a loss may have a role in k-ras dependent lung carcinogenesis

K-RAS mutation is associated with non small cell lung cancer.

The frequency and characteristics of KRAS gene mutation in Turkish non-small cell lung cancer patients

We sought to investigate whether mucinous features, such as signet-ring cell feature and extracellular mucin, are associated with EGFR and KRAS mutations in patients with lung adenocarcinoma

Oncogenic KRAS upregulated mir31 in lung carcinogenesis.

DNA mutational analysis in lebanese population shows that mutations of EGFR and KRAS are present in 8.5% and 37.7% respectivement in lung adenocarcinoma.

KRAS is an independent prognostic marker in resected stage I lung adenocarcinoma. Differential outcomes are associated with codon and amino acid specific KRAS mutations.

KRAS oncogene mutations originated from the guanosine nucleotide and over half of all transversions in lung cancer and colorectal cancer were c.34 G>T and c.35 G>T, respectively. c.35 G>A was the most frequent type of transition in both cancers.

NQO1 expression was significantly more frequent in non-small cell lung carcinoma patients with KRAS mutations, suggesting that oxidative stress may be important in the pathogenesis, worse prognosis, and resistance to treatment reported in these patients.

These findings support a model in which targeting MUC1-C inhibits mutant KRAS signaling in Non-small cell lung cancer cells and thereby reverses the epithelial-mesenchymal transition phenotype and decreases self-renewal.

KRAS mutations are associated with poor prognosis in Non-Small Cell lung cancer patients. Good diagnostic performance obtained from Malignant pleural effusion samples for detecting KRAS mutations.

Our findings illuminate the mechanistic details of KRAS-mediated drug resistance and provide a preclinical rationale to improve the management of lung tumors harboring KRAS mutations with NRF2 pathway inhibitors.

KRAS mutation is associated with metastatic lung adenocarcinomas.

mutations are associated with decreased cancer-specific survival after lung stereotactic body radiation therapy for early-stage non-small-cell lung cancer

Data suggest that the status of p53 and KRAS may be considered for the targeted therapy against NF-kappaappa B in lung cancer patients.

lung metastasis was more likely to develop during the disease course in patients whose tumour had a KRAS mutation than in those whose tumour did not have a KRAS mutation.

an MEK1/2 inhibitor potentiated the anti-tumor effects of cisplatin in KRAS-dependent lung cancer cells and an animal model through inhibition of BIM degradation.

In unselected advanced non-small-cell lung cancer patients, KRAS mutations could be used as a potential negative predictor of clinical benefit from epidermal growth factor receptor tyrosine kinase inhibitors.[meta-analysis]

Results suggest that WT1 and c-MYC expression is important for survival in KRAS mutant tumors as opposed to KRAS wild-type non-small cell lung tumors.

KRAS gene mutation is associated with non small cell lung carcinoma.

Mutated KRAS and mutated BRAF seem to be prognostic factors in patients with Colorectal cancer who undergo lung metastasectomy.

KRAS mutations portend a worse outcome with increased risk of recurrence in early-stage Non-small cell lung cancer and poorer survival in metastatic stage. It is associated with Adenocarcinoma subtype and smoking, and is common in Caucasian patients.

KRAS amplification confers resistance to ROS1 targeting drugs in lung cancer.

KRAS mutations were associated with stage IV lung adenocarcinoma adrenal metastases.

MEK1/2 inhibitor trametinib showed similar PFS and a response rate as docetaxel in patients with previously treated KRAS-mutant-positive non-small cell lung carcinoma.

In multivariable analyses, in both patients with EGFR-mutant and KRAS-mutant lung adenocarcinomas, advanced stage at the time of diagnosis was found to be independently associated with shorter survival.

KRAS and EGFR co-mutation was detected in one case. PPMA patients with ALK rearrangements or KRAS mutation represent a unique subtype in Non-Small-Cell lung Carcinoma

The KRAS gene mutations (especially in codon 12) are the most frequent genetic abnormalities both in primary and in central nervous system metastatic lesions of non-small cell lung cancer.

KRAS mutational status can be determined in biopsies representing bronchial pulmonary carcinomas because when a mutation is present it is generally present in all the histological patterns

EGFR and KRAS mutation were associated with non-small cell lung carcinoma.

Studied the role of PAK1/Crk axis in transduction of the oncogenic KRAS signal in non-small cell lung cancer (NSCLC).

Our results indicate that KRAS mutations are associated with inferior survival benefits for Non-Small Cell lung cancer but not for those treated with chemotherapies integrating cetuximab.

High mesothelin expression was strongly associated with mutant KRAS/wild-type EGFR and poor prognosis in advanced lung cancer.

In transgenic mice programmed to express both mutant oncogenes in the lung epithelium, the resulting tumors express either the KRAS, or the EGFR oncogene.

Elevated calcium levels clinically observed in adenocarcinomas may explain calmodulin's involvement in recruiting and stimulating PI3Kalpha through interaction with its n/cSH2 domains as well as K-Ras4B; importantly, it also explains why K-Ras4B specifically is a key player in ductal carcinomas, such as pancreatic, colorectal, and lung cancers. [Review]

KRAS mutations are associated with nonsmall-cell lung cancer.

data suggest one-step screening platform for KIF5B-RET as well as EGFR, K-RAS, ALK oncogenic mutations be necessary for lung adenocarcinoma patients

KRAS 3'-UTR rs712 polymorphism interfered with has-let-7g/mRNA interaction, and showed that the minor allele was associated with an elevated risk for development of lung cancer in COPD.

Data suggest that Src kinases inhibitors may act with different mechanisms in non-small cell lung cancer (NSCLC) depending on EGF receptor (EGFR)/Ras protein (Ras) mutational profile.

KRAS mutations are indicators of malignant transition in the progression to lung adenocarcinoma.

KRAS mutations are associated with Non-Small-Cell lung cancer.

Findings suggest that COX-2 deletion contributes to the repression of K-ras-induced lung tumorigenesis by reducing tumor cell proliferation, decreasing the production of PGE2, and increasing the production of 13,14-dihydro-15-keto-PGE2, possibly via the MAPK pathway.

KRAS mutations in lung adenocarcinoma were not associated with asbestos exposure.

KRAS mutant lung adenocarcinomas appear to have a more intricate RAS linked signaling network than WT tumors.

EGFR and KRAS mutations were low in lung squamous cell carcinomas, and had no significant correlation with clinical features.

Prognosis impact of KRAS mutations in non-small cell lung cancer.[review]

In lung adenocarcinomas, EGFR mutation was higher in female and non-smoking patients, KRAS mutation only in patients with wild-type EGFR gene was higher.

KRAS mutation is associated with lung cancer.

Kras single nucleotide polymorphisms rs12228277 and rs61761074 of intron 2 result in differential binding patterns of lung nuclear proteins.Rs61761074 demonstrated a significant correlation with allele frequency in non-small-cell lung cancer.

this study shows that combining the analysis of KRAS mutational status and computed tomographic features could better predict survival in patients lung adenocarcinoma

These results indicate that CREG1 is a down-stream effector of KRAS in a sub-type of non-small cell lung cancer cells and a novel candidate biomarker or therapeutic target for KRAS mutant non-small cell lung cancer.

The HSP90 inhibitor, NVP-AUY922, sensitizes KRAS-mutant non-small cell lung cancer with intrinsic resistance to MEK inhibitor, trametinib.

treatment response, survival, and the associations between KRAS mutation status and tumour expression levels of BRCA1, TYMS and SRC retrospectively in a cohort of patients with non-small cell lung cancer, were evaluated.

Results showed that the presence of KRAS activating mutations in patients with metastatic or recurrent non-small cell lung cancer are correlated with worse prognosis.

KRAS mutations are associated with non-small-cell lung cancer.

This study failed to show improvement in ORR or PFS with combination therapy of selumetinib and erlotinib over monotherapy in KRAS mutant and KRAS wild-type advanced nonsmall-cell lung cancer

Case Report: KRAS mutation-positive bronchial surface epithelium type lung adenocarcinoma with strong expression of TTF-1.

KRAS mutations are associated with non-small-cell lung cancer.

Aurora kinases are important KRAS targets in lung cancer.

KRAS mutation is associated with lung adenocarcinomas.

Studied the role of KRAS mutation status as a prognostic factor in surgically resected colorectal cancer patients with liver and lung metastases.

Results show that the presence of KRAS mutation (especially KRAS G12C mutation) correlated with adverse prognosis in non-small cell lung cancer patients treated with second- or third-line pemetrexed or docetaxel.

KRAS point mutations are associated lung cancer.

KRAS mutations are more common in females and smokers, but are not associated with chronic obstructive pulmonary disease status in non-small cell lung cancer patients.

Development of Brain metastases (BM) from colorectal cancer (CRC) is associated with young age, lung metastases, rectal primary and KRAS mutation.

Analysis of KRAS mutation combined with immunohistochemical expression of CD44 and CD166 identified subgroups of patients with colon adenocarcinoma at higher risk of lymph node involvement by the tumor and development of liver and lung metastasis.

Forty-nine paired tissues with both primary adenocarcinoma of lung and matched brain metastasis were collected. Thirteen patients (26.5%) were discordant for the status of EGFR between primary and metastatic sites. K-ras gene could be checked in paired specimens from 33 patients, thirteen patients (39.6%) were discordant for the status of K-ras.

recent years, there has been significant advancement in the understanding of the biology of KRAS and its downstream effectors. This has translated into a multitude of important preclinical studies and clinical trials that are currently underway to find effective therapeutic drugs for KRAS mutant lung cancer recent years, there has been significant advancement in the understanding of the biology of KRAS and its downstream

analysis provides further information on the mutational profiles of pulmonary sarcomatoid carcinoma and demonstrates for the first time a role of KRAS mutations in driving the aggressiveness of this type of cancer

This study demonstrated that KRAS and TP53 mutations are frequently detected in LIFE bronchoscopy samples from former lung cancer patients with early stage lung cancer. These mutations were found not only in abnormal lesions but also in histologically normal tissues in samples from active smokers, from ex-smokers and never smokers.

Reduced insulin receptor substrate-1 (IRS-1) staining in lung adenocarcinoma tissue microarray displayed a significant survival disadvantage, especially within the Kirsten rat sarcoma viral oncogene homolog (KRAS) mutant subgroup.

There is a relationship between KRAS mutation status and local recurrence after image-guided ablation of lung adenocarcinoma. Specifically, KRAS mutation status of the ablated lesion is a significant predictor of time to local recurrence, independent of size and margin.

ACSL3 is essential for mutant KRAS lung cancer tumorigenesis in vivo and is highly expressed in human lung cancer

mutation in KRAS gene is associated with Advanced lung Adenocarcinoma.

KRAS mutations were observed in 255 patients (32%) and were correlated with negative histopathological factors in resected non-small-cell lung cancer.

Inhibition of BET bromodomain-dependent XIAP and FLIP expression sensitizes KRAS-mutated non-small cell lung cancer to pro-apoptotic agents.

In patients with resected stage I lung adenocarcinomas, KRAS mutation was an independent prognostic factor for survival and recurrence, especially in solid predominant tumors.

The in vitro and in vivo inhibitory effect of zoledronic acid was based on the blockade of cell cycle in wild type KRAS-expressing human non-small cell lung cancer cells.

KRAS mutation is associated with lung cancer.

Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer. These data suggested that RMRP might serve as a therapeutic target in lung adenocarcinoma

KRAS exon 2 codon 13 mutations, compared to codon 12 mutations, seem to be associated with better outcomes following lung metastasectomy in colorectal cancer

EGFR and KRAS mutations have a predictive role on brain metastases incidence, recurrence and outcome in Caucasian Non-Small Cell lung cancer patients.

ALK/EGFR mutational co-alterations are associated with response to chemotherapy in Non-Small Cell lung cancer.

microRNA expression profiles had clinicopathological implications that were related to EGFR and KRAS mutations, as well as ALK-rearrangement in lung adenocarcinoma.

This work provides evidence that TP53 and KRAS mutation in lung adenocarcinoma may be served as a pair of potential predictive factors in guiding anti-PD-1/PD-L1 immunotherapy

EGFR and KRAS mutation status was associated with the expression of AKT, p-AKT, DR5, and DcR1 in non-small cell lung cancer

nuclear Ect2 GEF activity is required for Kras-Trp53 lung tumorigenesis in vivo and that Ect2-mediated transformation requires Ect2-dependent rDNA transcription.

KRAS Polymorphism is associated with recurrence in non-small cell lung cancer.

KRAS mutation is associated with colon and lung cancer.

Our studies offer a way forward for Hsp90 inhibitors through the rational design of Hsp90 inhibitor combinations that may prevent and/or overcome resistance to Hsp90 inhibitors, providing an effective therapeutic strategy for KRAS-mutant non-small cell lung cancer .

The mitosis-like condensed chromatin positive phenotype defined a subset of KRAS-mutated lung cancers that were enriched for co-occurring genomic alterations in TP53 and CDKN2A. Results illuminate the basis for the radiation resistance of KRAS-mutated lung cancers.

High FOS-like antigen 1 (FOSL1) expression with mutant KRAS protein lung and pancreatic cancer patients showed the worst survival outcome.

AFR3 cells harbored the secondary EGFR mutation T790M. Our findings constitute the first report showing acquired wild-type KRAS overexpression and attenuation of afatinib resistance following a drug holiday. The heterogeneous mechanisms of afatinib resistance should facilitate the development of more effective therapeutic strategies for non-small cell lung cancer patients

identified focally upregulated FAK and collagen-associated collective invasion in KRAS and LKB1 comutated human lung adenocarcinoma patients. Our results suggest that patients with LKB1 mutant tumors should be stratified for early treatment with FAK inhibitors

G12C mutation associated with reduced progression-free survival in non-small cell lung cancer treated with pemetrexed

KRAS mutation could induce PD-L1 expression through p-ERK signaling in lung adenocarcinoma

TP53 comutation with KRAS or EGFR is not a significant prognostic marker in patients with resected Non-Small-Cell lung cancer. Dual TP53/KRAS mutation seems to be predictive of shortened survival in patients who are treated with platinum-based ACT.

CPS1 maintains pyrimidine pools and DNA synthesis in KRAS/LKB1-mutant lung cancer cells

Studies on the metabolic properties of mutant KRAS protein lung tumors have uncovered unique metabolic features that can potentially be exploited therapeutically [Review].

ALK and KRAS mutations are associated with acquired resistance to crizotinib in ALK-positive non-small cell lung cancer

Taken together these data support a model where PDHK4 regulates KRAS signalling and its tumorigenic properties and suggest that inhibition of PDHK4 could represent a novel therapeutic strategy to target KRAS mutant colorectal and lung cancers

TAZ was positively correlated with EGFR signaling, and coexpression of TAZ/EGFR conferred a poorer prognosis in lung cancer patients. Our findings identify that targeting TAZ-mediated compensatory mechanism is a novel therapeutic approach to overcome gefitinib resistance in KRAS-mutant/EGFR-wild-type non-small-cell lung cancer .

we showed that combination therapy with low concentrations of sorafenib and betulinic acid had the capacity to induce high levels of cell death and abolish clonogenic activity in some non-small cell lung cancer cell lines regardless of KRAS mutations.

The presence of KRAS mutations did not enrich for the activation of IL-6, JAK1 or phosphorylated STAT3 in resected lung adenocarcinoma.

k-RAS gene mutation status was associated with the response of Gefitinib treatment in patients with nonsmall-cell lung cancer

KRAS mutation is associated with lung adenocarcinoma.

KRAS mutations were associated with Primary pulmonary Enteric Adenocarcinomas. KRAS mutations occurred more frequently in Primary pulmonary Enteric Adenocarcinomas , which are cytokeratin 7-negative (P=.032).

provide a rationale for stratification of human patients with lung cancer harboring KRAS/KEAP1- or KRAS/NRF2-mutant lung tumors as likely to respond to glutaminase inhibition

Programmed cell death 1 ligand 1 protein (PD-L1) expression significantly correlates with overall mutational load and KRAS protein mutational status in pulmonary sarcomatoid carcinomas.

FOSL1 is a determinant of lung cancer in vivo and regulates tumor cell proliferation and survival, largely in the context of KRAS mutations through amphiregulin and cell survival gene regulation.

the findings demonstrated that mutated K-ras promotes cathepsin L expression and plays a pivotal role in EMT of human lung cancer. The regulatory effect of IR-induced cathepsin L on lung cancer invasion and migration was partially attributed to the Cathepsin L /CUX1-mediated EMT signaling pathway

Our data provide evidence that blocking TfR could significantly inhibit lung adenocarcinoma (LAC) proliferation by targeting the oncogene KRAS; therefore, TfR may be a therapeutic target for LAC. In addition, our results suggest a new method for blocking the signal from the oncogene KRAS by targeting TfR in LAC.

two major subtypes of KRAS mutant cancers of the lung, pancreas, and large intestine, which reflect different KRAS effector engagement were identified.

The results indicate that lung cancer patients carrying KRAS mutations are prone to multiple metastases in both lungs.

A report of the possible use of abundance measures for K-Ras4A for predicting the survival of lung adenocarcinoma patients with KRAS mutations.

CFTR exhibited an inhibitory role in the malignancy of lung adenocarcinoma A549 cells

An actionable requirement for IKKalpha in KRAS-mutant lung adenocarcinoma.

These findings collectively suggest that the triple combination of survivin knockdown with ABT-263 and trametinib treatment, may be a potential strategy for the treatment of KRAS-mutant lung adenocarcinoma. Furthermore, our findings indicate that the welldifferentiated type of KRAS-mutant lung tumors depends, at least in part, on TTF1 for growth.

Targeting EGFR ligands may benefit patients who carry EGFR-mutant lung tumors but will not benefit patients with KRAS-mutant lung tumors.

mutations in both the p53 tumor suppressor gene and K-ras oncogene are highly frequent in lung tumors from nonsmoking women in China. The predominance of G-->T transversions in both genes and the occurrence of p53 mutations within a specific GC rich region or at specific hotspot codons on the non-transcribed strand are consistent with exposure to smoky coal emissions.

KRAS is one of the most common mutations in Non-small cell lung cancer. [review]

SHP2 inhibition is an unexpected vulnerability of KRAS-mutant non-small-cell lung cancer cells.

KRAS mutational status can affect the immune microenvironment and survival of lung adenocarcinoma patients

These data highlight that MAPK7 represents a promising target for combination treatment with MEK inhibition in KRAS mutant Non Small Cell lung Carcinoma.

Our preclinical study supports further clinical evaluation of combined MEK inhibition and chemotherapy for lung cancer patients harboring KRAS (G12C) and wild-type p53 status.

characteristics of the expression of epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), V-Ki-ras2 Kirsten rat sarcoma viral oncogene homologue (KRAS) in non-small cell lung cancer

mutations of KRAS and DDR2 were found in large cell carcinoma (LCC) and squamous cell carcinoma (SCC) subtypes, respectively, whereas mutations of TP53 were seen in SCC and lung adenocarcinoma subtypes with higher frequencies and LCC subtype with lower frequency in Iranian patients.

results demonstrated that O-GlcNAcylation was sufficient and required to accelerate KrasG12D lung tumorigenesis in vivo, which was reinforced by epithelial plasticity programs.

These results pinpoint mTOR as a mechanism of resistance to chemotherapy in KRAS-mutant lung cancer and validate a rational and readily translatable strategy that combines mTOR inhibitors with standard chemotherapy to treat KRAS-mutant adenocarcinoma, the most common and deadliest lung cancer subset.

Results provide evidence that KRAS and EGFR gene amplifications mediate resistance to the third-generation EGFR TKIs rociletinib and osimertinibin acquired Afatinib-resistant non-small cell lung cancer harboring exon 19 deletion/T790M in EGFR.

KRAS mutation is a recurrent mechanism of primary and secondary resistance to MET tyrosine kinase inhibitors in METex14 lung cancers.

Nivolumab is an effective and safe treatment option for patients with previously treated, advanced non-squamous non-small-cell lung cancer regardless of KRAS mutations.

These data underscore a critical sex-specific role for epithelial Stat3 signaling in K-ras mutant lung adenocarcinomas.

Authors demonstrated that enforced PCDH7 expression significantly accelerates Kras(G12D) -driven lung tumorigenesis and potentiates MAPK pathway activation.

A dual specificity phosphatase, DUSP6, that negatively regulates phosphorylation of (P)-ERK is up-regulated in EGFR- or KRAS-mutant lung adenocarcinoma (LUAD), potentially protecting cells with mutations in the RAS signaling pathway, a proposal supported by experiments with DUSP6-specific siRNA and an inhibitory drug

Findings highlight the prognostic significance of the transcriptional regulator Id1 in KRAS-mutant lung adenocarcinoma and provide mechanistic insight into how it controls tumor growth and metastasis.

Epidermal growth factor receptor (EGFR), KRAS, and BRAF mutations in lung adenocarcinomas: A study from India.

Associations have been identified between radiological features and clinical features with Epidermal Growth Factor Receptor (EGFR)/ Kirsten RAt Sarcoma (KRAS) alterations in an independent group of patients with Non-Small Cell lung cancer (NSCLC).

Results suggest that mutant KRAS promotes RAD51 expression to enhance DNA damage repair and lung cancer cell survival.

Targeting the KRAS, p38alpha, and NF-kappaB in lung adenocarcinoma cancer cells has been reported.

mutational profile of Brazilian lung adenocarcinoma unveils association of EGFR mutations with high Asian ancestry and independent prognostic role of KRAS mutations.

MAPK signaling dependency in epithelial lung cancer cells is due to the scaffold protein interleukin-17 receptor D (IL17RD), which is directly repressed by ZEB1.

KRAS up-regulation is a promising strategy for lung cancer therapy.

Nf1 loss promotes Kras-driven lung adenocarcinoma and results in Psat1-mediated glutamate dependence.

analysis of genetic interactions with a KRAS(G12C) inhibitor in cellular models of KRAS(G12C) mutant lung and pancreatic cancer using CRISPR interference

KRAS exon 3 and PTEN exon 7 mutations had no significant impact on overall survival of small-cell lung cancer patients.

Radioresistance of KRAS/TP53-mutated lung cancer can be overcome by radiation dose escalation or EGFR tyrosine kinase inhibition in vivo.

The prevalence and prognostic value of KRAS co-mutation subtypes in Chinese advanced non-small cell lung cancer patients.

The presence of KRAS mutations in the colorectal cancer specimens, especially G12D or G13D mutations, seems to promote pulmonary metastases formation.

Novel activating KRAS mutation candidates in lung adenocarcinoma.

Loss of heterozygosity (LOH) was analyzed in a cohort of EGFR-mutated non-small-cell lung cancer (NSCLC) patients who were positive or negative for EGFR mutations in their cfDNA. Patients carrying KRAS mutations were also analyzed. No association between KRAS status in cfDNA and number of LOH events was found.

Suppression of the SLC7A11/glutathione axis causes synthetic lethality in KRAS-mutant lung adenocarcinoma.

Simplified molecular classification of lung adenocarcinomas based on EGFR, KRAS, and TP53 mutations.

Actionable mutation Profiles of Non-Small Cell lung cancer patients from Vietnamese population.

Cell-type specific tumorigenesis with Ras oncogenes in human lung epithelial cells.

The cytochrome P450 enzyme CYP24A1 increases proliferation of mutant KRAS-dependent lung adenocarcinoma independent of its catalytic activity.

Early assessment of KRAS mutation in cfDNA correlates with risk of progression and death in advanced non-small-cell lung cancer.

Integrin-linked kinase (ILK) regulates KRAS, IPP complex and Ras suppressor-1 (RSU1) promoting lung adenocarcinoma progression and poor survival.

Outcome of patients with colorectal cancer undergoing lung metastases resection: a single-institution retrospective analysis.

KRAS(Q61H) Preferentially Signals through MAPK in a RAF Dimer-Dependent Manner in Non-Small Cell lung cancer.

KRAS mutation as a prognostic factor and predictive factor in advanced/metastatic non-small cell lung cancer: A systematic literature review and meta-analysis.

DRP1 promotes lactate utilization in KRAS-mutant non-small-cell lung cancer cells.

Weighted gene coexpression network analysis identifies hub genes related to KRAS mutant lung adenocarcinoma.

IKKbeta Kinase Promotes Stemness, Migration, and Invasion in KRAS-Driven lung Adenocarcinoma Cells.

Dysregulated Kras/YY1/ZNF322A/Shh transcriptional axis enhances neo-angiogenesis to promote lung cancer progression.

PLCgamma1 suppression promotes the adaptation of KRAS-mutant lung adenocarcinomas to hypoxia.

Targeting KRAS-Mutant Non-Small-Cell lung cancer: One mutation at a Time, With a Focus on KRAS G12C mutations.

The hexosamine biosynthesis pathway is a targetable liability in KRAS/LKB1 mutant lung cancer.

Functional dissection of the KRAS G12C mutation by comparison among multiple oncogenic driver mutations in a lung cancer cell line model.

Molecular profile of KRAS G12C-mutant colorectal and non-small-cell lung cancer.

KRAS(G12C) Can Either Promote or Impair Cap-Dependent Translation in Two Different lung Adenocarcinoma Cell Lines.

A PCR-Based Approach for Driver mutation Analysis of EGFR, KRAS, and BRAF Genes in lung cancer Tissue Sections.

pulmonary Inflammation and KRAS mutation in lung cancer.

limited clinical usefulness of gene mutation as a selection marker for epidermal growth factor receptor tyrosine-kinase inhibitors sensitivity in non-small cell lung cancer

Kras protein mutation is responsible for the development of mucinous adenocarcinoma of the lung in patient born with congenital pulmonary malformation.

mutations in the K-ras gene are involved in B6C3F1 lung carcinogenesis following BMP- and TNM-exposure.

Kras2 is part of the complex multigenic Pas1 locus, with a functional role for its intragenic polymorphisms in lung tumor susceptibility.

Mice carrying mutant p53 transgene are more sensitive to environmental cigarette smoke(ECS)-induced lung tumors. K-ras mutations are independent of p53 status, but early overexpression of oncogene is related to p53 status in ECS-exposed mice.

model demonstrates that K-ras activation in the lung induces the elaboration of inflammatory chemokines and provides an excellent means to further study the complex interactions between inflammatory cells, chemokines and tumor progression

propose that the Pas1 modifier effect is due to Kras2, and that a sensitive balance between the expression levels of wild-type and mutant alleles determines lung tumor susceptibility

in the context of K-rasG12D-mediated lung tumorigenesis, Sprouty-2 is also up-regulated and functions as a tumor suppressor to limit tumor number and overall tumor burden

cisplatin is partially related to K-ras codon 61 mutations in second primary lung cancer; the mechanism of carcinogenicity by cisplatin is different from that by 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK)or benzo(a)pyrene (BaP)

Loss of a Kras2 allele increases susceptibility to tobacco smoke induced lung tumor development.

roles of endogenous K-ras 4A and K-ras 4B splice variants in tumorigenesis, N-methyl-N-nitrosourea-induced murine lung carcinogenesis.

Pten inactivation cooperated with oncogenic K-ras in promoting lung tumorigenesis.

The lack of Par-4 dramatically enhances Ras-induced lung carcinoma formation in vivo, acting as a negative regulator of Akt activation.

Kras regulatory elements and exon 4A determine mutation specificity in lung cancer

chronic obstructive pulmonary disease-like airway inflammation promotes lung carcinogenesis in a background of a G12D-activated K-ras allele in airway secretory cells.

inhibitors of the PI3K-mTOR pathway may be active in cancers with PIK3CA mutations and, when combined with MEK inhibitors, may effectively treat KRAS mutated lung cancers

The retinoblastoma gene Rb and its family member p130 suppress lung adenocarcinoma induced by oncogenic K-Ras.

Foxp3+ regulatory T cells are required for K-Ras-mediated lung tumorigenesis in mice.

The high incidence of tumors in Nth1-/-Neil1-/- mice together with the activating mutation in the K-ras gene of their pulmonary tumors, reveal for the first time, the existence of mutagenic and carcinogenic oxidative damage to DNA which is not 8-OH-Gua.

p27 is a potent barrier to the growth and malignant progression of Kras-initiated lung tumors.

HIF2alpha cooperates with RAS to promote lung tumorigenesis in mice.

protein prenyltransferase inactivation in mice with K-RAS-induced lung cancer reduced tumor growth and improved survival.

Melphalan inhibits carcinogenesis via modulating K-ras-specific genes and proteins expressed in the lung tissues of K-ras Tg mice.

Overexpression of K-ras and CDK4 is associated with non-small cell lung carcinoma.

Fgfr3 mutation caused papilloma and promoted lung tumorigenesis in cooperation with K-Ras and beta-catenin activation, respectively.

Mmp10 is overexpressed in lung tumors induced by either the smoke carcinogen urethane or oncogenic Kras.

Bronchiolar Clara cells are the origin of cells and tumorigenesis for Kras(G12D)-induced neoplasia in the lungs.

Together, our findings show that MAP Kinase signaling is both necessary and sufficient for KRASG12D induced benign lung tumorigenesis in genetically engineered mouse models.

K-ras mutant is essential for neoplastic transformation and during different stages of lung tumorigenesis

lung carcinomas dissected from KRAS(G12D);NOS2KO mice showed a significantly reduced miR-21 expression.

We combined (L597V)Braf with (G12D)Kras and found that (L597V)Braf modified (G12D)Kras oncogenesis such that fibroblast transformation and lung tumor development were more reminiscent of that driven by the high-activity (V600E)Braf mutant

Data indicate that deletion of Kras enhances lung but attenuates skin tumor development.

Results show that aerosol delivery of osteopontin triple mutant successfully suppresses lung cancer development in the K-ras (LA1) mouse model.

Haploinsufficiency of Nkx2-1 in combination with oncogenic Kras(G12D) caused pulmonary tumors in mice that were phenotypically similar to human mucinous adenocarcinomas.

these results reveal an unrecognized role for CD44 in oncogenic Kras-induced lung adenocarcinoma and suggest that targeting CD44 could be an effective strategy for halting Kras-dependent carcinomas.

Nrf2 deficient mice are sensitive to chemical carcinogens and exhibit a high-level of KRAS mutation independent lung cancer initiation.

Data indicate that forkhead box M1 protein (FOXM1) is required for K-Ras-mediated lung tumorigenesis.

Loss of p53 attenuates the contribution of IL-6 deletion on suppressed tumor progression and extended survival in Kras-driven murine lung cancer.

Kras-4A showed differential allelic expression in lung tumor tissue.

Trim62 loss cooperates with K-Ras mutation in tumourigenesis and metastasis in vivo, indicating that decreased levels of TRIM62 may play an important role in the evolution of lung cancer.

decreased lung tumorigenesis with point mutation at C118

Ras induction of ZEB1 is required for tumour initiation in a lung adenocarcinoma model via Pten repression. A lower threshold of ZEB1 is sufficient for cancer initiation, whereas further induction is necessary for tumour metastasis.

Data suggest that accumulation of proto-oncogene protein Kras mutation occurs later with chronic vanadium pentoxide (VP) exposure and is likely not an early event in VP-induced lung carcinogenesis.

in this overview are the features of various KRAS-driven genetically engineered mouse models (GEMMs) of non-small cell lung cancer--{REVIEW}

mutant Kras lung tumours are not a single disease but rather a heterogeneous group comprising two classes of tumours with distinct metabolic profiles, prognosis and therapeutic susceptibility, depending on their relative mutant allelic content

our results highlight the importance of Pas1 as a tumor-modifier locus, attribute to it a novel role as a major regulator of transcription in lung tumor nodules and strengthen the candidacy of the Kras gene as the effector of this locus.

Data show that cisplatin response was enhanced in human lung cancer cells when Nit1 was knocked down and mice Nit1-/-:KrasG12D/+ tumors showed increased sensitivity to cisplatin in vivo.

the expression of EGFRL858R in KrasG12V-driven lung adenocarcinoma limits tumor progression due to the induction of a transient oncogenic conflict

In a mouse lung model of KRas(G12D)-driven adenomas, co-activation of Myc drives the immediate transition to highly proliferative and invasive adenocarcinomas marked by highly inflammatory, angiogenic, and immune-suppressed stroma.

we conclude that IL22 promotes Kras-mutant lung tumorigenesis by driving a protumor inflammatory microenvironment with proliferative, angiogenic, and stemness contextual cues in epithelial/tumor cells.

Results found that K-ras codon 12-13 mutations occurred at a relatively early age in TP53-175H transgenic mice, which also experienced accelerated lung cancer onset.

Deregulated lncRNA expression profile in the mouse lung adenocarcinomas with KRAS-G12D mutation and P53 knockout.

The stress kinase p38alpha as a nononcogenic signaling molecule that enables the progression of Kras(G12V)-driven lung cancer.

Stromal Hedgehog pathway activation by IHH suppresses lung adenocarcinoma growth and metastasis by limiting reactive oxygen species.

tumor progression and chromatin landscape of lung cancer are regulated by the lineage factor GATA6.

Dispensable role of CCL28 in Kras-mutated non-small cell lung cancer mouse models.

tumor regression and resistance mechanisms upon CDK4 and RAF1 inactivation in KRAS/P53 mutant lung adenocarcinomas.