A link between the p53 germ line polymorphisms and white blood cells apoptosis in lung cancer patients

aberrent expresion correlates with VEGF and IL-8 mRNA expression and neoangiogenesis in non-small-cell lung cancer

MYCL1, FHIT, SPARC, p16(INK4) and TP53 genes associated to lung cancer in idiopathic pulmoary fibrosis

lung-specific expression of human point mutant p53-273H (under the SP-C promoter) is associated with a high frequency of lung adenocarcinoma in transgenic mice. This mutation is frequent in human lung tumors.

The restoration of wild-type p53 expression and function in human autologous lung carcinoma IGR-Heu cells results in a significant potentiation of target cell susceptibility to cytotoxic T cell-mediated lysis.

p53 mutations in exon 7 might be associated with increased radiosensitivity in certain SCLC & NSCLC human lung cancer cell lines. No correlation concerning mutations in separate exons & response towards different chemotherapeutic agents could be found.

p53 alteration is an independent and significant indicator to predict unfavorable prognosis in patients with unresectable non-small cell lung cancer.

value of this tumor marker regarding relapse, metastasis and death in resectable non-small cell lung cancer

Adenovirus-p53 induces the expression of a variety of proapoptotic genes and that lack of induction in one of these genes does not block Ad/p53-mediated cell killing in human lung cancer cells.

Detection of P53 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.

A point mutation of p53 in a lung cancer patient simultaneously can elicit not only a humoral immune response against overexpressed p53 protein, but also a specific cytotoxic T lymphocyte response against the mutated epitope of p53 in the same patient.

P53 gene mutations were frequently found in surgical margins in patients with non-small-cell lung carcinoma.

Results link p53 status with POLkappa expression and suggest that loss of p53 function may in part contribute to the observed POLkappa upregulation in human lung cancers.

survivin can reduce the cell growth inhibition and apoptosis, and p53 elevates the p21 level, which may attenuate the cell death in the quercetin-treated human lung carcinoma cells

Rb and p53 have roles in progression of primary non-small cell lung carcinoma

The p53 Pro allele is associated with an increased frequency of p53 mutations in non-small cell lung cancer.

The combination of mutation with the codon 72 proline variant predicts poorer patient survival in non-small cell lung cancer.

In operable non-small lung cell cancers, there may be different relationship of this protein with paatient outcome.

A significant correlation between YB-1 and PCNA-LI was found, but none was found between p53 expression and PCNA in lung cancer.

an aberrant p53 status was related to IL-8 expression in patients with non-small cell lung carcinoma

evidence that in lung carcinomas, non-CpG methylation is frequently observed in certain GC rich regions of the p53 gene; evidence presented from the p53 mutation databases which corroborates the reported experimental results

p53 mutation in lung cancers was closely correlated with the expression of drug-resistance associated proteins.

Genetic polymorphisms in cell cycle regulatory genes MDM2 and TP53 contribute to the risk of developing lung cancer.

The expression rate of p53 was relatively high in small cell lung cancer without any prognostic significance.

Increased risk of non-small cell lung cancer and frequency of somatic TP53 gene mutations in Pro72 carriers of TP53 Arg72Pro polymorphism

p53 inhibits protein synthesis in human lung carcinoma cells;The mechanism involves dephosphorylation and accumulation of the translational inhibitor 4E-BP1, and increased association of 4E-BP1 with initiation factor eIF4E.

HER-2/neu and p53 may have a role in chemoresistance in patients with non-small cell lung cancer

identification of polymorphisms in lung carcinoma of never smokers

Data show that the acrolein-DNA binding pattern is similar to the p53 mutational pattern in human lung cancer, and suggest that it contributes to lung carcinogenesis through DNA damage and inhibition of DNA repair.

The expression of p53, Bcl-2 and Bax was altered in lung cancer tissue compared to histologically normal bronchial epithelium.

somatic alterations in p53 and EGFR have roles in progression of primary lung cancer

study reveals that the TP53 Arg allele, active smoking and human papillomavirus infection infection are the important risk factors in lung cancer development in the north part of Iran, Mazandaran province

Most non-small cell lung cancers (NSCLCs) have mutations of p53.[Review]

Mutant p53 may contribute to its 'gain of function' effects which accelerate the oncogenesis and promotion of lung adenocarcinoma.

Lack of evidence that p53 Arg72pro influences lung cancer prognosis: an analysis of survival in 619 female patients.

Non-small cell lung cancer cells with nonfunctional TP53 might be sensitized against radiation by genistein or estradiol.

high and low P-glycoprotein, glutathione S-transferase pi expression, excision repair cross-complementing 1 alterations, and tumor suppressor p53 mutation were candidates for future clinical trials of chemosensitivity tests in lung cancer patients.

These observations demonstrate a novel regulatory role for p53 as a uPAR mRNA binding protein that down-regulates uPAR expression, destabilizes uPAR mRNA, and thereby contributes to the viability of human airway epithelial or lung carcinoma cells.

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

In lung cancer patients, p53 accumulation could be due to a decrease in full-length MDM2 isoform together with an increase of the 57-kDa MDM2 isoform that was unable to stimulate p53 degradation.

Data suggest that p53 regulates cellular responses to environmental carcinogen benzo[a]pyrene-7,8-diol-9,10-epoxide in human lung cancer cells.

study investigated the correlation of p53 abnormalities in 15 patients with pulmonary large cell carcinomas; 5/15 expressed p53 and none had mutant p53 sequences; there was a negative survival correlation with positive p53 immunostaining (P = 0.05)

p53 and Ki-67, but not bcl-2, cyclin D1 or HER-2 may have roles in the process of tumor genesis in non-small cell lung carcinoma

Loss of TP53-DNA interaction induced by p.C135R point mutation in lung cancer

Loss of heterozygosity (LOH) of the hDMP1 gene was detectable in approximately 35% of human lung carcinomas, which was found in mutually exclusive fashion with LOH of INK4a/ARF or that of P53. DMP1 is a pivotal tumor suppressor for human lung cancers.

HPV16/18 E6 is expressed in HPV DNA-positive lung tumors and is involved in p53 inactivation to contributing to HPV-mediated lung tumorigenesis

levels of p53/p21waf1 mRNA in blood lymphocytes collected before chemotherapy may predict the chemoresponses of lung cancer patients.

p53 mutation is associated with non-small cell lung carcinoma

p53 Arg72Pro heterozygous genotype was overall an independent prognostic factor...of lung cancer

p53 codon 72 and intron 3 polymorphisms are associated with non-small cell lung cancer

p53 mutation spectra and differences with histology in lung cancers.

polymorphism at codon 72 modulates the risk of lung cancer in Brazilian patients with African ethnical background

The p53 Pro72 homozygous non-small cell lung cancer patients often presented high-grade tumours and had significantly poorer survival rates than patients with R72 homozygotes or heterozygotes.

Hibiscus syriacus extract exhibits a cytotoxic effect on lung cancer cells by activation p53 and AIF.

Polymorphism Arg72Pro in tumor suppressor gene TP53 increases the risk of lung cancer, especially for small cell lung cancer and heavy smokers.

polymorphisms and haplotypes in the TP53 gene, including Arg72Pro, were not significantly associated with lung cancer in a Korean population

a high level of p53 downregulates the beta-catenin expression, but this effect is attenuated by non-functional AXIN2 or betaTrCP in lung cancer.

Microsatellite alterations, and p53 tumor mutations are associated with non-small cell lung cancer patients

a novel role for p53 as an mRNA-binding protein that regulates increased PAI-1 expression and stabilization of PAI-1 mRNA in human lung epithelial and carcinoma cells

MGMT promoter methylation modulated by p53 status could partially promote p53 mutation occurrence in advanced lung tumors

TP53 gene mutations of lung cancer patients in upper northern Thailand and environmental risk factors are reported.

TP53 mutation is associated with metastatic pulmonary adenocarcinomas.

Results suggest that the Arg/Arg genotype polymorphism of p53 may represent a potential risk factor for the development of lung cancer independent of the human papillomavirus infection.

three different COX-2 mutations and five different P53 mutations are associated with non-small-cell lung carcinoma

integrin beta4 is implicated in and associated with p53 in autophagy of lung cancer cells

Doublets in the EGFR and TP53 genes in human lung cancer are elevated about eight- and three-fold, respectively, relative to spontaneous doublets in mouse

p53 nucleolar association occurs in lung and bladder carcinomas.

p53 mutations are frequent in tumor-surrounding histologically normal tissue, and some of them might be involved in lung carcinogenesis

The Snail-p53 binding as the new therapeutic target for K-Ras-mutated cancers including pancreatic, lung, and colon cancers.

Suggest a synergistic effect between smoking and TP53 genetic polymorphisms on lung cancer risk compared with each risk factor alone.

a risk factor for lung cancer

lung adenocarcinoma occurring in young patients tends to have a poorer prognosis, and angiogenesis of lung adenocarcinoma in young patients is more closely correlated with p53 expression than in elderly patients.

Report role of p53 in the induction of cyclooxygenase-2 by cisplatin or paclitaxel in non-small cell lung cancer cell lines.

The Pro allele at codon 72 of p53 was a risk factor for developing lung cancer.

review of literature analysing influence of radon exposure on mutations TP53 in lung cancer patients; results are not consistent in order to support existence of a radon hotspot in TP53 gene [review]

Findings suggest that the influence of NAT2 genotype, alone or in combination with p53 genotype, may confer increased susceptibility to lung cancer.

Elevated association between the TP53 G12139C polymorphism and the stage I lung cancer was found under dominant genetic model.

Characterized the p53-dependent secretome of H358(human nonsmall cell lung adenocarcinoma cell line with a homozygous deletion of p53) and demonstrate the modulation of exported proteins can also be detected in vivo in the plasma of tumor-bearing mice.

TP53 tumour suppressor gene mutations have a role in development of smoking-related bulky DNA adducts in a lung cancer study population from Hungary

Our data show the first valid clinical evidence of the deregulation of HIC1-SIRT1-p53 loop in lung tumorigenesis and prognosis

Upregulation of survivin in non-small cell lung cancer is associated with its neoplasm staging and correlated with p53 and Bcl-2 level.

Novel mutations in the TP53 gene are associated with lung adenocarcinoma.

Egr1 is a novel regulator of stathmin expression and p53 mediates the transcriptional repression of stathmin by Egr1 in human lung cancer cells.

These results suggest that altered and deficient p53 affects the cellular response to freshly fractured silica exposure, and thereby enhances susceptibility and augments cell proliferation and lung cancer development.

simultaneous detection of p53, Rb, p16, and EGFR in a suspension microarray facilitates rapid diagnosis of lung cancer

p53 wild type cells are protected from taxol by nutlin-3 in a combined lung cancer treatment

Investigated maspin, p53 and VEGF expression in patients with squamous cell carcinoma (SCC), adenocarcinoma (AC) and small cell lung carcinoma (SCLC).

Polymorphism-polymorphism interaction (both multiplicative and additive) between TP53BP1 and TP53 SNPs was suggested for lung cancer risk in a Japanese population.

Loss of TP53 and increased incidence of autosomal aneuploidy and chromatid breaks, along with other chromosomal alterations, can contribute to the progression of lung cancer.

mutations may predict the biological nature of pulmonary adenocarcinomas and facilitate new therapies.

p53 overexpression is a late event during tumor development and plays a role in the progression of the peripheral pulmonary adenocarcinoma.

results indicate that latitude may modify the effect of Arg72Pro polymorphism on the risk of breast cancer and possibly on the risk of lung cancer

Inhibition of the mTOR signal may be a promising strategy for radiosensitization with no relevance to p53 gene status from the aspects of lung cancer cell lethality and cell growth depression.

Tp53 and EGFR mutations usually precede lymph node metastasis and that these gene statuses in matched primary non-small cell lung cancers and lymph node metastasis show predominantly a concordant pattern

The loss of expression of MGMT may lead to activation of the wild-type p53 in lung carcinomatosis, and may predict prognosis in patients with non-small cell lung cancer.

Data indicated that interaction of betel quid with p53 genotypes in lung cancer was significant increase for all the three genotypes.

the 4 SNPs (XPA rs1800975, OGG1 rs1052133, ADPRT rs1136410, and NBS1 rs1805794) may modulate the occurrence of TP53 mutations and contribute to lung carcinogenesis

mutation of p53 gene and HPV infection may facilitate each other in the generation of lung squamous cell carcinoma

Relevance of the combinatorial inactivation of p53 in non-small cell lung carcinoma progession.

iASPP regulates the proliferation and motility of lung cancer cells. This effect is intimately associated with the p53 pathway.

codon 72 polymorphism is associated with the risk of lung cancer in a Korean population

Loss of p53-related suppression of lung resistance-related protein through Y-box binding protein 1 may be the reason for LRP expression increase, and, therefore, chemotherapy resistance in tumor cells.

combination of TP53 variant genotypes and XRCC1 variant genotype is associated with the increased lung cancer risk in younger, but not elderly, smokers.

TIM50, was upregulated in a non-small cell lung carcinoma cell line (H1299) that expressed the p53 mutants R175H and R273H compared to cells lacking p53.

Polymorphisms in TP53 gene is associated with lung squamous cell carcinoma.

HSA-miR-125a-5p induces apoptosis via a p53-dependent pathway in human lung cancer cells.

Genetic polymorphisms in TP53, P73, and MDM2 are associated with non-small cell lung cancer

Increased expression of 14-3-3 gamma in lung cancer coincides with loss of functional p53.

Data suggest that TP53 expression in lung cancer cells (A549 cells) can be down-regulated by miR-98 (and miR-453); this mechanism involves targeting of the 3-prime-UTR of TP53.

found that HDGF was overexpressed also in primary gastric, breast, and lung cancer tissues harboring mutant p53 genes

relationship between potentially functional polymorphisms of apoptosis-related genes and TP53 mutations in non-small cell lung cancer; none of the polymorphisms was significantly associated with occurrence of TP53 mutations suggesting apoptosis-related genes may not play an important role in occurrence of TP53 mutations in lung cancer

the pro-oncogenic activity of TR3 in lung cancer cells was due to inhibition of p53 and activation of mTORC1

TP53 mutation and CDKN2A methylation specifically interact to promote lung tumorigenesis in subjects with CYP1A1 risk genotype.

This study indicates that p53 mutation and HPV 16/18 infection might coordinate in the development of lung squamous cell carcinomas, and their coexistence is associated with poor prognosis.

suggest that mutations of TP53 are good markers of different aetiologies and histopathological forms of lung cancers but have little prognostic value

p53 overexpression may be a possible predictive marker for adjuvant chemotherapy using cisplatin in non-small-cell lung cancer

The expression of TIMP-3 in the non-small cell lung cancer and metastasis groups was upregulated.

Studied the expression of RUNX3 in lung cancers.Results suggest RUNX3 is downregulated in ADCs, however normally expressed in SCC. EGFR and KRAS mutations and EGFR and p53 protein expression were not correlated with the RUNX3 downregulated ADC samples.

This report shows that much of the 682-gene signature of this murine skin carcinoma transcriptome is also present in breast and lung cancer mouse models in which p53 is inhibited.

Arg/Pro polymorphism in p53 gene is associated with lung cancer.

The p53 target gene desmocollin 3 acts as a novel tumor suppressor through inhibiting EGFR/ERK pathway in human lung cancer.

results showed that several of the polymorphisms and their haplotypes in CHRNA5/CHRNA3 genes may have functional effects on susceptibility to lung cancer

p53 codon 72 polymorphisms play a role in the development of lung cancer and modifies the risk for smoking-related lung cancer in a Chinese population.

The tumor suppressor, p53, contributes to radiosensitivity of lung cancer cells by regulating autophagy and apoptosis.

Genetic variation Arg72Pro of the p53 gene may contribute to higher risk of squamous cell carcinoma of lung in the North Indian population.

In COPD patients, the presence of serum p53 antibodies was found to be associated with smoking level and lung function impairment, both risk factors of cancer development.

in non-small cell lung cancer patients the increase of transversions in TP53 gene is consistent with a synergistic effect of asbestos

the HPV 16/18 E6 protein, which is involved in the p53 inactivation that contributes to HPV-infected lung tumorigenesis, is associated with the p53 codon 72 genotype; the combination of HPV 16/18 E6 status and p53 codon72 polymorphism in lung tumors is an important biologic and prognostic parameter

It has been shown that p53 expression is more frequently registered in patients with lung adenocarcinoma with paraneoplastic rheumatic syndrome than in patients with lung adenocarcinoma without this syndrome.

Results suggest that the TP53 Pro allele acts as a risk factor for development of lung cancer, especially for smokers and Asians.

The p53 codon 72 polymorphism may weakly modify the risk for lung cancer among the adenocarcinoma patients and non-smokers. [Meta-analysis]

analysis of a rare TP53 variant, rs78378222, that may have a protective role against squamous cell carcinoma of head and neck, but not in melanoma or lung cancer.

TP53 codon 72 Arg/Pro polymorphism is a risk factor for lung cancer in the Asian population. [Meta-analysis]

special function of p53 family members in the development, chemosensitivity and target treatment of lung cancer

PIAS3 activates the intrinsic apoptotic pathway in non-small cell lung cancer cells independent of p53 status.

we demonstrated that a polyclonal antibody raised against mouse p53 could cross-react with human glucosidase II, which was found to be frequently overexpressed in human lung tumor tissues and exhibited a stress response similar to p53.

Results suggest that intratumor genetic heterogeneity may be an important factor in determining the role of TP53 mutations on the prognosis of non-small cell lung cancer patients.

data suggest that hsa-miR-125a-3p induces apoptosis not only via the p53 pathway in human lung cancer cells

p53 mutation is associated with smoking-induced lung cancer. Smokers with lung cancer had a higher risk for p53 mutation than non-smokers (Meta-Analysis)

A rare G>C mutation in TP53 is associated with arsenic-related lung tumor.

mutation of TP53 is associated with lung adenocarcinomas.

TP53 Arg72Pro polymorphism is associated with an increased lung adenocarcinoma risk.

Report high frequency of coexpression of maspin and p63, as well as maspin and p53, in squamous cell carcinoma of the lung.

There is a significant association between lung cancer risk and intron 3 16 bp polymorphism in a dominant model. [Meta-analysis]

53BP1 and TP53 gene interactions were not associated with lung cancer risk.

A high frequency of somatic mutations in p53 (44.3%; 43/97) and/or EGFR (51.5%; 50/97) resulted in a high discrimination rate of tumor clonality (77.3%; 75/97) in metachronous multiple lung cancers.

TP53 rs2078486 SNP is potentially a novel TP53 SNP that may affect lung cancer risk. Our study also suggested potential synergetic effects of TP53 rs2078486 SNP with smoking and indoor air pollution exposure on lung cancer risk.

functional characterization of a radiation-induced p53 mutation in the H460 lung cancer cell line does not implicate it in the development of radiation resistance

Nondisruptive mutations in the TP53 gene are an independent prognostic factor of shorter survival in advanced non-small cell lung cancer

WT-p53 is a potent suppressor of TGF-beta-induced Nox4 in p53-null lung epithelial cells. tumour-associated mutant p53 (R175H or R280K) caused enhanced Nox4 expression in both TGF-beta-dependent and TGF-beta-independent pathways.

Results show that p53 loss is insufficient to drive lung adenocarcinoma dissemination but rather enables rare cancer cells in a small fraction of primary adenocarcinomas to gain alterations that drive dissemination.

The presence of individual and multiple alterations of p53, p16 and PTEN were compared in in non-small cell lung carcinoma (NSCLC), glioma and breast carcinoma.

EGFR/p53 mutations were associated with tumor size >1 cm, and p53 mutations were frequently observed in moderately differentiated lung adenocarcinoma. p53 mutation was significantly correlated with tumor relapse in patients with stage I disease.

Results suggest that p53-regulated TUG1 is a growth regulator, which acts in part through control of HOXB7 in non-small cell lung cancer.

The current evidence suggests that s-p53 antibody has potential diagnostic value for cancer, especially for breast, colorectal, esophageal, gastric, hepatic, lymphoma, lung and ovarian cancer.

Both p53 wildtype and mutant human lung adenocarcinoma tumors rely on MIF family members for maximal cell growth and survival.

p53, KLF4, and p21 showed altered expression patterns in pulmonary neuroendocrine neoplasms. Lack of KLF4 and p21 expression was associated with accumulation of aggressive features in typical carcinoids.

We conclude that not Pro47Ser SNP but Arg72Pro p53 SNP is involved in susceptibility to developing lung cancer, at least in Bangladeshi population.

Cigarette smoke condensate decreased AP-2alpha expression by suppressing its transcription in human lung cancer cell lines, particularly in p53-deficient NCI-H1299 cells.

Study demonstrates a link between p53 and Bcl-2 proteins as regulators of ROS production and cellular invasiveness, and reveals complex-I, especially ND5, as their functional target in lung tumor cells.

TP53 reponse element polymorphisms are associated with increased risk of lung cancer in smokers.

focuses on lung cancer stem cells, p53 mutations noted in these cells, and importance of MDM2 interactions

Cigarette smoking and overexpression of p53 or p21 are associated with poor prognosis in non-small cell lung cancer.

Loss of p53 function may result in upregulation of 14-3-3gamma in lung cancers.

TP53 expression was not associated with prognosis in limited-stage small cell lung cancer.

SHMT1 knockdown in lung cancer cells leads to cell cycle arrest and to p53-dependent apoptosis.

PDZ-binding kinase/T-LAK cell-originated protein kinase correlates with mutant p53 and affects cell proliferation and viability as well as prognosis in lung adenocarcinoma

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

Mir-660 inhibits lung tumorigenesis by targeting MDM2-p53 interaction.

Our results indicate that the screening approach used in this study can identify clinically relevant synthetic lethal interactions and that vitamin D receptor agonists may show enhanced efficacy in p53-negative lung cancer patients.

Bcl-X(L) and p53-mediated amplification mechanisms played important roles in the sensitization of non-small-cell lung carcinoma cells to TRAIL-mediated apoptosis

we evaluated the association of gene polymorphisms, including the repair genes of XRCC1, ERCC1, ERCC2 (XPD), and TP53, with RFS in patients with non-small cell lung cancer

Tp53 codon 72 gene polymorphism with environmental factors is associated with risk of lung cancer.

Selective inhibition of HDAC2 in lung tumor cell causes survivin downregulation through activation of p53, which is mediated by downregulation of Mdm2.

MDM2 polymorphism may be one of the important factors for the increased expression mdm2, which was associated with down-regulation of p53 at and ultimately may contribute in the poor clinical outcome of the non-small cell lung cancer patients

Transcriptomic data in patients with non-small cell lung cancer indicate that TP53 mutations are associated with higher VEGF-A expression.

highly reliable association of combined susceptible genotypes of polymorphic markers Arg72Pro and T309G of TP53 and MDM2 genes with non small cell lung cancer and both its subtypes.

Our results collectively suggested that JARID1B expressed in lung cancer played a role in lung cancer cells proliferation and invasion, which may be partly associated with the p53 expression

Authors suggest that NKX2-1 as a tumour suppressor or a tumour promoter in lung adenocarcinoma progression is dependent on p53 status.

Detection of serum p53 antibodies in non-small cell lung cancer patients was useful in identifying subsets of patients with poor prognosis.

High P53(Mut) protein expression is associated with lymph node metastasis in lung adenocarcinoma.

The Pro/Pro (BB) genotype and the B allele are risk factors for lung cancer among Bangladeshis, particularly for people under age 50, women and smokers.

authors identified TP53-mutated tumor cells in the xenografts derived from the primary RCC, and in a lung metastasis developed in one patient. The mutation enabled us to track back their origin to a minority sub-clone in the primary heterogeneous RCC.

Mutant p53 protein increased in all the patients with proliferative and precancerous changes and lung cancer, suggesting p53 protein dysfunction.

demonstrate that the effect of TP53 mutational status on TLR4 activity may extend to ovarian, colon, and lung cancers, among others, suggesting that the viability of TLR4 as a therapeutic target depends on TP53 status in many different tumor types

Overexpression of microRNA125a3p effectively inhibits the cell growth and invasion of lung cancer cells by regulating the mouse double minute 2 homolog/p53 signaling pathway

ZNF322A overexpression transcriptionally dysregulates genes involved in cell growth and motility therefore contributes to lung tumorigenesis and poor prognosis

TP53 mutations are indicators of malignant transition in the progression to lung adenocarcinoma.

Mutant p53 may confer cisplatin resistance via upregulation of Nrf2 expression in non-small cell lung carcinoma.

Studied effects of X-radiation in lung cancer cell lines. Cell death and role of reactive oxygen species, mitochondrial membrane potential, BAX, BCL-2 and cell cycle were analyzed. Total and phosphorylated P53 were assessed by western blotting.

A Novel Naphthalimide Compound Restores p53 Function in Non-small Cell lung cancer by Reorganizing the Bak.Bcl-xl Complex and Triggering Transcriptional Regulation.

This prompts for further studies on the mechanisms behind the TP53-induced regulation of SOX2 expression and the possible importance of hsa-miR-145 in lung cancer.

Report TP53 overexpression in non-small cell lung carcinomas.

The repair capacity of lung cancer cell lines A549 and H1299 depends on HMGB1 expression level and the p53 status.

TP53 mutation is associated with Non-Small Cell lung cancer.

Results show that monoubiquitination of mutant p53 increases following DNA damage in lung cancer cells and is dependent on the DNA damage checkpoint.

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.

In this paper, the authors found that miR-138 showed a pronounced increase after p53 activation in human non-small cell lung cancer (NSCLC) cells, which is mediated by p53 binding sites in the promoter region of its host gene, but this did not happen with rat and mouse cells.

Together these findings suggest that evodiamine is a strong inducer of apoptosis in lung epithelial cancer cells independent of their p53 status and that could involve both intrinsic as well as extrinsic pathway of apoptosis. Thus evodiamine could be a potential anticancer agent against lung cancer.

Low TP53 expression is associated with lung and colonic cancer.

There is no association between P53 codon 72 polymorphism and increased risk of lung cancer in patients and controls but according to results of adenocarcinoma in never-smoker patients

p53 codon 72 polymorphism could play a role as a prognostic marker in lung cancer patients.

Results revealed the universal spatial heterogeneity of driver mutations in non-small cell lung cancer and demonstrated that the molecular timing of acquisition of driver mutations, such as TP53 mutation, varies in different tumors during tumor formation and progression.

ENTPD5 is a mediator of mutant p53 gain of function activity in clonogenic growth, architectural tissue remodeling, migration, invasion, and lung colonization in lung cancer and its mouse models

p53 overexpression may help judge the prognosis of patients who undergo pulmonary metastasectomy for metastatic colorectal cancer.

A significant increase in the risk of non-small cell lung cancer was observed for the following combinations: TP53 codon72 variant with GSTM1 null (OR 2.22, 95 % CI 1.23-4.04; p=0.009), GSTT1 null (OR 2.98, 95 % CI 1.49-5.94; p=0.002), and GSTP1 (Ala114Val) variant genotypes (OR 3.38, 95 % CI 1.54-7.41; p=0.002).

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

Low TP53 expression is associated with non-small-cell lung cancer.

mir-486-5p is positively regulated by mir-660-5p in lung cancer cell lines, through the mir-660-MDM2-p53 pathway.

findings show an important role for TP53 variants as negative predictors for the outcome of non-small cell lung cancer adenocarcinoma patients, especially for TP53 inactivating mutations in advanced stage tumors treated with DNA-damaging agents, and provide the first evidence of the R213R G-allele as possible risk factor for non-small cell lung cancer

The expression of p53 fulllength transcript and Delta133p53 isoforms alpha, beta and gamma transcripts, MDM2 and p21 transcripts were determined by reverse transcriptionquantitative polymerase chain reaction, in total RNA isolated from 17 lung carcinoma specimens and 17 corresponding adjacent noncancerous tissues.

This study reveals a critical link between two keys factors in tumourigenesis and autophagy, and suggests a potential important role of p53-TFEB signaling axis in lung cancer.

high A1AT expression correlated with increased tumor stage, elevated p53 staining and shorter overall survival in lung adenocarcinoma patients.

TP53 mutation is associated with lung Adenocarcinoma.

WDR79 colocalized and interacted with USP7 in the nucleus of non-small cell lung cancer cells. This event, in turn, reduced the ubiquitination of Mdm2 and p53, thereby increasing the stability and extending the half-life of the two proteins.

Studied association of tumor protein p53 and drug metabolizing enzyme polymorphisms with clinical outcome in patients with advanced nonsmall cell lung cancer.

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.

Germline TP53 mutation p.Pro190Arg is associated with lung and bilateral breast cancers.

PKCzeta was specifically involved in ACOT7 depletion-mediated cell cycle arrest as an upstream molecule of the p53-p21 signaling pathway in MCF7 human breast carcinoma and A549 human lung carcinoma cells.

tumor suppressor p53 protein mutation from lung carcinoma patients stimulates cell spreading and migration. Mutant p53 (R175H) decrease the expression of Rho GTPase activating protein 44 in both mRNA and protein level.

These findings support the existence of a direct link between the p53(DEL), proliferation, epithelial-mesenchymal transition, and invasiveness in human lung cancer cells. So the p53(DEL) is a promising target for prevention and treatment of lung cancer.

High TP53 expression is associated with Non-Small Cell lung cancer.

Using integrated analysis of genome-wide short hairpin RNA (shRNA) screening data in combination with genome-wide gene expression data, the study identified GSK3 as one of the key factors in p53-mediated apoptosis in human lung cancer cells.

p53 was over expressed in 82% of the non-small cell lung cancer cases studied.

Data demonstrate a causative role for TRP53 mutants in development of chemoresistant lung cancer.

Our findings showed novel regulatory mechanisms of p53 in regulating Aurora-A gene expression in non-small cell lung carcinoma cells.

These data suggested that Annexin A2 induces cisplatin resistance of non-small cell lung cancer (NSCLC)via regulation of JNK/c-Jun/p53 signaling, and provided an evidence that blockade of Annexin A2 could serve as a novel therapeutic approach for overcoming drug resistance in NSCLCs

Increased Cdc7-dependent replication initiation is a hallmark of p53 gain-of function mutations in lung adenocarcinoma.

miR-300 regulates the cellular sensitivity to ionizing radiation through targeting p53 and apaf1 in lung cancer cells.

these results suggested that Aloin may induce apoptosis in A549 cells via the ROSmitogen activated protein kinase signaling pathway, with p53 phosphorylation. These results implicate Aloin as a potential therapeutic agent for the treatment of lung cancer.

The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone may increase the risk of lung cancer progression and poorer outcomes in patients with p53 mutations by perturbing proper mitotic progression and chromosome integrity.

These investigations demonstrated etoposide-induced NMI can suppress tumor proliferation and promote cell apoptosis by activating the ARF-p53 signaling pathway in lung carcinoma. Our results provide an alternative mechanism for etoposide in lung carcinoma and suggest NMI has a critical role in suppressing lung carcinoma progression.

P53-deficiency gene signature defined based on RNA-seq provides a significant prognostic predictor in lung adenocarcinoma that is applicable to both RNA-seq and microarray platforms.

the TP53 R72P genotype may serve as a clinical prognostic factor in lung carcinomas

These results demonstrate a previously unrecognized relationship between p53 and REV3L in cancer cell metabolism and may lead to improvements in chemotherapy treatment plans that reduce cisplatin resistance in lung cancer.

Findings suggest the mechanisms by which tumor protein p53 (p53) operates to enhance vascular endothelium barrier function by mediating the opposing actions of Rac family small GTPase 1 (Rac1) and ras homolog family member A (RhoA) in pulmonary tissues.

High expression of synthesis of cytochrome c oxidase 2 and TP53-induced glycolysis and apoptosis regulator can predict poor prognosis in human lung adenocarcinoma

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.

TP53 mutations define a subset of ALK-translocated non-small cell lung carcinoma tumours with recurrent MYC amplication that harbour chromosomal instability, leading to the co-occurrence of pathogenic aberrations.

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.

Inactivation of HUWE1 in a human lung cancer cell line inhibited proliferation, colony-forming capacity, and tumorigenicity. Mechanistically, this phenotype was driven by increased p53, which was due to attenuated proteasomal degradation by HUWE1.

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.

TP53 represses the expression of SETDB1 via increasing miR-29s expression in non-small cell lung cancer.

to reveal the prognostic value of TP53 in advanced non-small cell lung cancer,as well as the correlation with EGFR mutation

TP53 mutations V157, R158, and A159 are enriched in lung cancer and may confer a biological gain-of-function to TP53.

p53R245W tumors are the most aggressive and exhibit metastases to lung and liver.

The TP53 codon 72 Arg allele and XRCC1 codon 399 Gln allele are likely to have a protective effect against lung adenocarcinoma, especially in individuals older than 50 years of age. XRCC1 and TP53 genotyping might be a useful low-cost tool for evaluating individual lung cancer risk

Results find that p53 activity is regulated through its binding to AHNAK to regulate stemness-related-gene transcription thereby controlling non-small-cell lung cancer (NSCLC) cell stemness.

Ferritin heavy subunit enhances apoptosis of non-small cell lung cancer cells through modulation of miR-125b/p53 axis.

Study results revealed that the expression of LOC285194 was significantly lower in non-small cell lung cancer (NSCLC) tumor tissues when compared with the corresponding non-tumor tissues. Its expression was correlated with the tumor size, disease-free survival, and overall survival rates. RNA protein interaction analysis revealed that p53 was the direct binding target of LOC285194 in NSCLC.

Study data indicated that exogenous p53wt mediates the regulation of Op18/stathmin signaling through the p53NFkappaBCDC2/ERKOp18/stathmin pathway, and that p53 deficiency is associated with high malignancy levels of nonsmall cell lung cancer NCIH1299 cells.

SYT7 interacted with P53 and enhanced the interaction between P53 and MDM2 in lung cancer.

The study confirmed the prognostic value of poor overall survival and progression free survival of TP53 commutation in EGFR mutant lung cancers.

TP53 and protein kinase D Co-mutations are associated with lung Adenocarcinoma.

the p53 wild-type cell lines were more sensitive to volasertib treatment, suggesting that p53 might be a predictive biomarker for Plk1 inhibition in non-small-cell lung cancer. Moreover, our results pave the way for new combination strategies with Plk1 inhibitors to enhance antitumor activity.

Data report the development of a new transgenic lung cancer mice model in which a Type II conformational human TP53 mutation (175H) is expressed in a lung-specific manner. The observation of accelerated tumor and early onset, and high frequency of K-ras codon 12-13 mutations in these mice suggests an enhanced oncogenic function of conformational TP53 mutations, and gains in early genetic instability for these tumors.

Low expressions of TP53 is associated with non-small cell lung cancer.

SPAG5 is upregulated in lung adenocarcinoma. SPAG5 knockdown suppresses proliferation, colony forming, and migration. SPAG5 is regulated in a p53-and p21-dependent manner.

One of only few reports demonstrating the mutated p53 gainoffunction (GOF) activity resulting in a decrease of a malignant trait in human cancer revealed that expression of GOF mutant p53R248Q decreased the motility and invasiveness of the breast and lung cancer cells in a p53 transactivationdependent manner.

These results demonstrated that JSK could trigger cell cycle arrest at the G2/M phase and apoptosis in A549 and H460 cells, which was likely mediated via the p53/p21WAF1/CIP1 and p27KIP1 pathways. Overall, the results indicated that JSK may be used as an anticancer agent for the treatment of nonsmall cell lung cancer (NSCLC)

The lung-enriched p53 mutants V157F and R158L/P regulate a gain of function transcriptome in lung cancer.

The present study demonstrated that the transfection of the Delta133p53 (an amino-terminally truncated isoform of p53) gene in lung adenocarcinoma cell line (H1299) led to the reduction of chemosensitivity.

this study provides evidence for the existence of a p53/miR-30a-5p/SOX4 feedback loop, which likely plays a key role in the regulation of proliferation, apoptosis, and migration in non-small-cell lung cancer, highlighting a new therapeutic target.

p16 and p53 were detected in 50.7 and 57.3% of lung adenocarcinomas (ADCs; n = 75), and 35.2 and 63.6% of lung squamous cell carcinomas (n = 88).

LIMCH1 is a negative regulator involved in a new molecular mechanism for the pathogenesis of lung cancer with HUWE1 and p53

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.

TP53 mutation is associated with lung cancer risk.

this study shows that p53 suppresses tumor growth by prompting pyroptosis in non-small-cell lung cancer

Sirtuin 3 induces apoptosis and necroptosis by regulating mutant p53 expression in smallcell lung cancer.

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

Study found that SIRT3 can deacetylate mutant p53, thus reducing its expression, inducing apoptosis in small-cell lung cancer (SCLC) cells, and increasing SCLC cisplatin chemosensitivity. The relationship between SIRT3 and mutant p53 could be the basis of a new SCLC treatment approach.

mutation in the tumor suppressor gene TP53 can be detected in the CSF of patients with lung cancer associated meningitis. Patients with such mutation have earlier meningeal metastasis and shorter median survival time

The USP10-HDAC6 axis confers cisplatin resistance in non-small cell lung cancer lacking wild-type p53.

The p53-53BP1-Related Survival of A549 and H1299 Human lung cancer Cells after Multifractionated Radiotherapy Demonstrated Different Response to Additional Acute X-ray Exposure.

Micheliolide Enhances Radiosensitivities of p53-Deficient Non-Small-Cell lung cancer via Promoting HIF-1alpha Degradation.

Evolutionary Action Score of TP53 Enhances the Prognostic Prediction for Stage I lung Adenocarcinoma.

Molecular characterisation of TP53 mutated squamous cell carcinomas of the lung to identify putative targets for therapy.

RNF115-mediated ubiquitination of p53 regulates lung adenocarcinoma proliferation.

Biomarker-driven phase 2 umbrella trial study for patients with recurrent small cell lung cancer failing platinum-based chemotherapy.

Association of TP53 Codon 72 Arg>Pro Polymorphism with Breast and lung cancer Risk in the South Asian Population: A Meta-Analysis.

TP53 somatic mutations are associated with poor survival in non-small cell lung cancer patients who undergo immunotherapy.

TP53 Arg72Pro and XPD Lys751Gln Gene Polymorphisms and Risk of lung cancer in Bangladeshi Patients.

Novel evidence for retinoic acid-induced G (Rig-G) as a tumor suppressor by activating p53 signaling pathway in lung cancer.

Prognostic value of TP53 co-mutation status combined with EGFR mutation in patients with lung adenocarcinoma.

NT5DC2 suppression restrains progression towards metastasis of non-small-cell lung cancer through regulation p53 signaling.

Survival of lung cancer Patients Dependent on the LOH Status for DMP1, ARF, and p53.

Knocking down USP39 Inhibits the Growth and Metastasis of Non-Small-Cell lung cancer Cells through Activating the p53 pathway.

Antrodia cinnamomea Inhibits Growth and Migration of lung cancer Cells through Regulating p53-Bcl2 and MMPs pathways.

Systems Immunology Analysis Reveals an Immunomodulatory Effect of Snail-p53 Binding on Neutrophil- and T Cell-Mediated Immunity in KRAS Mutant Non-Small Cell lung cancer.

These results suggest that p53 function is important for protecting mice from both spontaneous and BaP-induced lung cancers.

Mutant p53(R270H) in bi-transgenic mice enhanced transition from intraepithelial neoplasia to invasive carcinoma, resulting in a higher frequency of invasive carcinoma per gland and per mouse, a more severe phenotype, more frequent pulmonary metastasis

restoration of p53 in established murine lung tumours leads to significant but incomplete tumour cell loss specifically in malignant adenocarcinomas, but not in adenomas

p53 subcellular localization resulting from CRM1 alterations may play an important role in lung tumorigenesis

loss of Trp53 and Rb1 can efficiently transform neuroendocrine and SPC-expressing cells leading to small cell lung cancer.

This report shows that much of the 682-gene signature of this murine skin carcinoma transcriptome is also present in breast and lung cancer mouse models in which p53 is inhibited.

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

Mir-660 inhibits lung tumorigenesis by targeting MDM2-p53 interaction.

The WAP-Cre:Pten(f/f):p53(lox.stop.lox_R270H) mice develop basal-like breast cancer that is enriched in TICs, can readily form lung metastasis, and provides a preclinical model to study both basal-like and claudin-low TNBC in immune-competent mice.

NFIB overexpression interacts with Rb/p53 deletion to promote small cell lung cancer in a mouse model

Results provide evidence for a critical role of mutations in TP53 and KEAP1 during lung squamous cell carcinoma (LSCC oncogenesis, because deletion of either gene leads to increased self-renewal of airway basal stem cells. Also, KEAP1/NRF2 mutations increase radioresistance and predict local tumor recurrence in radiotherapy treated LSCC patients.

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

Authors show that p53 loss before oncogene induced senescence is permissive for the transition from lung adenoma to adenocarcinoma.

Data demonstrate a causative role for TRP53 mutants in development of chemoresistant lung cancer.

Increased Cdc7-dependent replication initiation is a hallmark of p53 gain-of function mutations in lung adenocarcinoma.

p53R245W tumors are the most aggressive and exhibit metastases to lung and liver.

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

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

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