scholarly journals NPC-Exosome Carry Wild and Mutant-type p53 among Nasopharyngeal Cancer Patients

2021 ◽  
Vol 13 (4) ◽  
pp. 403-8
Author(s):  
Hamsu Kadriyan ◽  
Eka Sunarwidhi Prasedya ◽  
Nova Audrey Luetta Pieter ◽  
Masyita Gaffar ◽  
Amsyar Akil ◽  
...  
Keyword(s):  
Nasopharyngeal Cancer ◽  
P53 Mutation ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Sequencing Analysis ◽  
Wild Type ◽  
Rt Pcr ◽  
Mutant Type ◽  
Expression Levels ◽  
Mutation Type

BACKGROUND: Nasopharyngeal cancer (NPC) is known to release a specific exosome. NPC-derived exosome (NPC-Exo) could carry p53. However, information regarding the type of p53 carrier on NPC-Exo remains limited. This study aims to introduce our important findings regarding the type of p53 NPC-Exo cargo.METHODS: Serum from patients with NPC were prepared for exosome isolation with Seramir Exoquick by following the manual instructions. RT-PCR was conducted to determine the expression levels of latent membrane protein 1 (LMP-1) and p53 in the exosome isolate. Partial sequencing of p53 amplicon was conducted to determine mutation type of p53.RESULTS: There were 8 patients enrolled in this study. According to RT-PCR results, the expression levels of LMP-1 and p53 varied in the NPC-Exo isolate. Based on sequencing analysis, 1 case of p53 mutation was noticeable.CONCLUSION: According to current results, the NPC-derived exosome potentially carries not only wild type but also mutant type p53. Further research is needed to explore deeper the effect of the mutant type p53 as an exosome carrier in the clinical application.KEYWORDS: Nasopharyngeal cancer, exosome, p53, mutation

Mutation profiles in circulating tumor DNA (ctDNA) to predict the efficacy of sorafenib treatment in patients with advanced hepatocellular carcinoma (HCC).

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e15648-e15648
Author(s):  
Ping Yang ◽  
Guanghui Ji ◽  
Qionghui Jiang ◽  
Zejun Lu ◽  
Yao Yu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Gene Mutation ◽  
Therapeutic Efficacy ◽  
Genomic Dna ◽  
Mutation Frequency ◽  
Advanced Hepatocellular Carcinoma ◽  
Sequencing Analysis ◽  
Wild Type ◽  
Blood Samples ◽  
Mutation Type

e15648 Background: To find biomarkers from blood samples through ctDNA and leucocyte genomic DNA sequencing to predict the efficacy of sorafenib. Methods: CtDNA and leucocyte genomic DNA were extracted from patients with advanced hepatocellular carcinoma for sequencing analysis before and after targeted therapy with sorafenib. Mutation profiles were obtained by deep sequencing of 620 selected genes for further bioinformatics analysis. Gene mutation frequency and status were further integrated with clinical data to dynamically monitor and predict the efficacy of sorafenib. Results: Twelve patients with advanced hepatocellular carcinoma admitted to our hospital from March 2017 to September 2018 were enrolled. A total of 27 blood samples were collected for further analysis. The results showed that there were significant differences in BRD4 and FANCG gene mutation abundance between therapeutic effect group and poor effect group (p = 0.014). The mutations of BRD4, FANCG and TP53 were associated with shorter PFS (BRD4 mutation type vs wild type: 12 weeks vs 32 weeks, p = 0.0011; FANCG mutation type vs wild type: 16 weeks vs 32 weeks, p = 0.0103; TP53 mutation type vs wild type: 8 weeks vs 32 weeks, p = 0.0095). Furthermore, we found another 19 genes (SDHA, OTUD7A, TMPRSS2, NAV3, AKT1, EIF2S2, DICER1, MAP3K1, RAD9A, TCF3, IRS1, PIK3C2G, CTCF, TSHZ2, ITPKB, KDM5C, STAG2, AMER1, CDC27) associated with therapeutic efficacy, and dynamic changes of these 19 genes mutation alleys could predict therapeutic efficacy. Conclusions: Our results showed that mutations in ctDNA could predict the efficacy and prognosis of sorafenib for advanced hepatocellular carcinoma, and that dynamic monitoring of mutation frequency in ctDNA of peripheral blood samples could be an additional method to monitor therapeutic efficacy of sorafenib. The clinical significance of the mutations of BRD4, FANCG, TP53 and another 19 genes we found needs to be confirmed on a larger scale.

scholarly journals Upregulation of special AT-rich-binding protein 1 by Epstein–Barr virus latent membrane protein 1 in human nasopharyngeal cells and nasopharyngeal cancer

2013 ◽  
Vol 94 (3) ◽  
pp. 507-513 ◽  
Author(s):  
Kazuhira Endo ◽  
Julia Shackelford ◽  
Mitsuharu Aga ◽  
Tomokazu Yoshizaki ◽  
Joseph S. Pagano
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Binding Protein ◽  
Nasopharyngeal Cancer ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Tissue Samples ◽  
Multifunctional Protein ◽  
Barr Virus ◽  
Epstein Barr

A global regulator of chromatin remodelling and gene expression, special AT-rich-binding protein 1 (SATB1) has been implicated in promotion of growth and metastasis of a number of cancers. Here, we demonstrate that the principal oncogene of Epstein–Barr virus (EBV), latent membrane protein 1 (LMP1) upregulates SATB1 RNA and protein expression in human nasopharyngeal cell lines. Silencing of endogenously expressed SATB1 with specific short hairpin RNA decreases cell proliferation and resistance to apoptosis induced by growth factor withdrawal. Additionally, we provide evidence that LMP1-mediated expression of Survivin, a multifunctional protein involved in promoting cell growth and survival, is mediated at least in part by SATB1 in human nasopharyngeal cells. Finally, we show that SATB1 protein levels are elevated in tissue samples from patients with nasopharyngeal carcinoma (NPC), and are directly correlated with the expression of LMP1. Taken together, our results suggest that SATB1 functions as a pro-metastatic effector of LMP1 signalling in EBV-positive NPC.

scholarly journals Sequence Analysis of the Epstein-Barr Virus (EBV) Latent Membrane Protein-1 Gene and Promoter Region: Identification of Four Variants Among Wild-Type EBV Isolates

Blood ◽  
1997 ◽  
Vol 90 (1) ◽  
pp. 323-330 ◽  
Author(s):  
Kristian Sandvej ◽  
Jan W. Gratama ◽  
Mette Munch ◽  
Xiao-Ge Zhou ◽  
Reinder L.H. Bolhuis ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Latent Membrane Protein ◽  
Wild Type Virus ◽  
Latent Membrane Protein 1 ◽  
Wild Type ◽  
Barr Virus ◽  
Sequence Variations ◽  
Epstein Barr ◽  
Viral Isolates

Abstract Sequence variations in the Epstein-Barr virus (EBV) encoded latent membrane protein-1 (LMP-1) gene have been described in a Chinese nasopharyngeal carcinoma-derived isolate (CAO), and in viral isolates from various EBV-associated tumors. It has been suggested that these genetic changes, which include loss of a Xho I restriction site (position 169425) and a C-terminal 30-base pair (bp) deletion (position 168287-168256), define EBV genotypes associated with increased tumorigenicity or with disease among particular geographic populations. To determine the frequency of LMP-1 variations in European wild-type virus isolates, we sequenced the LMP1 promoter and gene in EBV from lymphoblastoid cell lines from healthy carriers and patients without EBV-associated disease. Sequence changes were often present, and defined at least four main groups of viral isolates, which we designate Groups A through D. The widespread prevalence of LMP-1 sequence variations, particularly the Xho I polymorphism and the 30-bp deletion, indicate that they cannot be used as simple markers for oncogenic viruses related to particular forms of EBV-associated tumor. Several of the structural changes detected occur, however, at sites where they may affect transcription, translation, or function of LMP-1. Future in vitro studies should aim to establish the functional importance of variations at these sites.

scholarly journals GGR (Geranylgeranyl Reductase) Expression Affects the Allelopathic Response to Arabidopsis Allelochemicals

2018 ◽  
Vol 10 (7) ◽  
pp. 122
Author(s):  
Debora Almeida Alcântara da Silva ◽  
Juliane Laner de Toledo ◽  
Flaviani Gabriela Pierdoná ◽  
Gabriel Sergio Costa Alves ◽  
Michelle de Souza Fayad André ◽  
...  
Keyword(s):  
Growth And Development ◽  
Pcr Analysis ◽  
Enzyme Complex ◽  
Wild Type ◽  
Geranylgeranyl Diphosphate ◽  
Rt Pcr ◽  
Leaf Extracts ◽  
Expression Levels ◽  
Transgenic Lines ◽  
Allelopathic Effects

Allelopathy involves the release of compounds into the environment that affects the growth and development of other organisms. This phenomenon may lead to the production of compounds less harmful to the environment than traditional herbicides used in weed control. In plants, terpenes have been identified as components of allelochemicals and are synthesized by enzymes named as geranylgeranyl diphosphate synthases (GGPPS). There are about 12 GGPPS genes in Arabidopsis, among which is GGR. This work aims to study the association between the expression levels of GGR and the allelopathic response of sesame seedlings to Arabidopsis leaf extracts. Hence, the GGR gene was inserted into Arabidopsis with the purpose to investigate the allelopathic effects of GGR expression levels on sesame seedlings. GGR expression levels were quantified by RT-PCR in both transgenic and non-transgenic [wild-type (WT)] lines. It has been observed that both wild-type and GGR expressing transgenic lines inhibited the growth of sesame seedlings. However, it is noteworthy that the phytotoxicity of extracts from GGR lines were greater than WT extracts. RT-PCR analysis of GGR expression revealed that WT plants had higher levels of GGR expression than GGR transgenic lines, which suggests that a homologous-dependent gene silencing (HDGS) occurred in GGR lines. GGR is part of an enzyme complex that works as a hub that determines the types of terpenes produced in Arabidopsis chloroplasts. The present data indicates that decreases in GGR expression may have favoured the production of terpenes with stronger allelopathic capacity in Arabidopsis leaves.

Detection of wild type and deleted latent membrane protein 1 (LMP1) of Epstein-Barr virus in clinical biopsy material

2004 ◽  
Vol 116 (1) ◽  
pp. 79-88 ◽  
Author(s):  
John Nicholls ◽  
Peter Hahn ◽  
Elisabeth Kremmer ◽  
Thomas Fröhlich ◽  
Georg J Arnold ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Wild Type ◽  
Biopsy Material ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Preliminary Study On Latent Membrane Protein-1 (LMP-1) And Bcl-2 Associated X (BAX) In Exosomes Of Patients With Nasopharingeal Cancer In NTB Provincial Hospital

2021 ◽  
Vol 1 (2) ◽  
pp. 117-130
Author(s):  
Puput Angrayany Sapar ◽  
Hamsu Kadriyan ◽  
Didit Yudhanto
Keyword(s):  
Membrane Protein ◽  
Nasopharyngeal Cancer ◽  
Tumor Necrosis Factor Receptor ◽  
Signs And Symptoms ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Barr Virus ◽  
Epstein Barr ◽  
Bax Gene ◽  
Necrosis Factor

Nasopharyngeal cancer is one of the most common types of cancer in Indonesia, especially head and neck cancer. One of the etiology of this cancer is infection with Epstein-Barr virus. Early diagnosis is difficult to establish because the early signs and symptoms of nasopharyngeal carcinoma are not specific. Examination of latent membrane protein-1 (LMP1) oncogene expression and BCL2-associated X (BAX) gene expression proved to be useful in the identification of nasopharyngeal cancer. LMP1 oncogene is an oncogene that functions as a tumor necrosis factor receptor (TNFR), so that apoptosis does not occur and promotes invasion and metastasis. The BAX gene is a pro-apoptotic gene that inhibits cancer development, but its regulation will be downregulated by LMP1 because LMP can protect B-cells from apoptosis.

scholarly journals Role of the TRAF Binding Site and NF-κB Activation in Epstein-Barr Virus Latent Membrane Protein 1-Induced Cell Gene Expression

1998 ◽  
Vol 72 (10) ◽  
pp. 7900-7908 ◽  
Author(s):  
Odile Devergne ◽  
Ellen Cahir McFarland ◽  
George Mosialos ◽  
Kenneth M. Izumi ◽  
Carl F. Ware ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Gene Induction ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Wild Type ◽  
Barr Virus ◽  
Epstein Barr

ABSTRACT In this study, we investigated the induction of cellular gene expression by the Epstein-Barr Virus (EBV) latent membrane protein 1 (LMP1). Previously, LMP1 was shown to induce the expression of ICAM-1, LFA-3, CD40, and EBI3 in EBV-negative Burkitt lymphoma (BL) cells and of the epidermal growth factor receptor (EGF-R) in epithelial cells. We now show that LMP1 expression also increased Fas and tumor necrosis factor receptor-associated factor 1 (TRAF1) in BL cells. LMP1 mediates NF-κB activation via two independent domains located in its C-terminal cytoplasmic tail, a TRAF-interacting site that associates with TRAF1, -2, -3, and -5 through a PXQXT/S core motif and a TRADD-interacting site. In EBV-transformed B cells or transiently transfected BL cells, significant amounts of TRAF1, -2, -3, and -5 are associated with LMP1. In epithelial cells, very little TRAF1 is expressed, and only TRAF2, -3, and -5, are significantly complexed with LMP1. The importance of TRAF binding to the PXQXT/S motif in LMP1-mediated gene induction was studied by using an LMP1 mutant that contains alanine point mutations in this motif and fails to associate with TRAFs. This mutant, LMP1(P204A/Q206A), induced 60% of wild-type LMP1 NF-κB activation and had approximately 60% of wild-type LMP1 effect on Fas, ICAM-1, CD40, and LFA-3 induction. In contrast, LMP1(P204A/Q206A) was substantially more impaired in TRAF1, EBI3, and EGF-R induction. Thus, TRAF binding to the PXQXT/S motif has a nonessential role in up-regulating Fas, ICAM-1, CD40, and LFA-3 expression and a critical role in up-regulating TRAF1, EBI3, and EGF-R expression. Further, D1 LMP1, an LMP1 mutant that does not aggregate failed to induce TRAF1, EBI3, Fas, ICAM-1, CD40, and LFA-3 expression confirming the essential role for aggregation in LMP1 signaling. Overexpression of a dominant form of IκBα blocked LMP1-mediated TRAF1, EBI3, Fas, ICAM-1, CD40, and LFA-3 up-regulation, indicating that NF-κB is an important component of LMP1-mediated gene induction from both the TRAF- and TRADD-interacting sites.

scholarly journals Sequence Analysis of the Epstein-Barr Virus (EBV) Latent Membrane Protein-1 Gene and Promoter Region: Identification of Four Variants Among Wild-Type EBV Isolates

Blood ◽  
1997 ◽  
Vol 90 (1) ◽  
pp. 323-330 ◽  
Author(s):  
Kristian Sandvej ◽  
Jan W. Gratama ◽  
Mette Munch ◽  
Xiao-Ge Zhou ◽  
Reinder L.H. Bolhuis ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Latent Membrane Protein ◽  
Wild Type Virus ◽  
Latent Membrane Protein 1 ◽  
Wild Type ◽  
Barr Virus ◽  
Sequence Variations ◽  
Epstein Barr ◽  
Viral Isolates

Sequence variations in the Epstein-Barr virus (EBV) encoded latent membrane protein-1 (LMP-1) gene have been described in a Chinese nasopharyngeal carcinoma-derived isolate (CAO), and in viral isolates from various EBV-associated tumors. It has been suggested that these genetic changes, which include loss of a Xho I restriction site (position 169425) and a C-terminal 30-base pair (bp) deletion (position 168287-168256), define EBV genotypes associated with increased tumorigenicity or with disease among particular geographic populations. To determine the frequency of LMP-1 variations in European wild-type virus isolates, we sequenced the LMP1 promoter and gene in EBV from lymphoblastoid cell lines from healthy carriers and patients without EBV-associated disease. Sequence changes were often present, and defined at least four main groups of viral isolates, which we designate Groups A through D. The widespread prevalence of LMP-1 sequence variations, particularly the Xho I polymorphism and the 30-bp deletion, indicate that they cannot be used as simple markers for oncogenic viruses related to particular forms of EBV-associated tumor. Several of the structural changes detected occur, however, at sites where they may affect transcription, translation, or function of LMP-1. Future in vitro studies should aim to establish the functional importance of variations at these sites.

FLT3-ITD+ AML Stem/Progenitor Cells Demonstrate Increased SIRT1 Expression and Enhanced Sensitivity to SIRT1 Inhibition

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1368-1368
Author(s):  
Ling Li ◽  
Tinisha McDonald ◽  
Liang Li ◽  
Sookhee Chun ◽  
Cedric Dos Santos ◽  
...  
Keyword(s):  
Cell Growth ◽  
Growth Inhibition ◽  
Progenitor Cells ◽  
P53 Mutation ◽  
Wild Type ◽  
Expression Levels ◽  
Sirt1 Expression ◽  
Enhanced Sensitivity ◽  
Cd34 Cells ◽  
Induced Apoptosis

Abstract Abstract 1368 In acute myeloid leukemia (AML) small populations of leukemia stem and progenitor cells are resistant to available therapies and represent an important barrier to response and cure. There is pressing need to develop new treatment approaches to target AML stem/progenitor cells. The NAD-dependent deacetylase SIRT1 plays an important role in protection of stem cells from stress. We have recently shown that SIRT1 inhibition enhances elimination of CML LSC via acetylation and activation of p53 (Cancer Cell 2012, 21:266). Here we evaluated the role of SIRT1 in growth and maintenance of AML stem/progenitor cells. We observed higher levels of SIRT1 expression in AML compared to normal CD34+CD38− and CD34+CD38+ cell, with highest expression levels in samples from patients with poor-risk cytogenetic abnormalities. We tested the effects of the SIRT1 inhibitor Tenovin-6 (TV-6) on CD34+ cells from high-risk AML patients (n=12) and healthy controls (n=4). AML CD34+ cells demonstrated varying degrees of sensitivity to TV-6, but TV-6 treatment did not significantly reduce viability of AML CD34+ cells taken as a group, compared to normal cells (p=0.8). However, we observed significantly reduced viability of a subset of samples bearing the FLT3-ITD mutation following TV-6 treatment (p=0.01). We therefore tested the effects of TV-6 on a larger set of poor risk AML samples with the FLT3-ITD mutation (n=11), or wild-type FLT3 (FLT3-WT, n=11). The FLT3-ITD mutation was associated with significantly enhanced sensitivity of AML CD34+ cells to TV-6 induced apoptosis (LD50 for FLT3-ITD=1.9μM; FLT3-WT=3.9μM, p=0.009), and inhibition of cell growth measured using the CellTitre Glo luminescent cell viability assay (FLT3-ITD IC50=0.73μM; versus FLT3-WT IC50=1.4μM, p=0.01). Therefore the presence of the FLT3-ITD mutation identifies a subset of AML samples that are very sensitive to SIRT1 inhibition. Tenovin-6 treatment increased acetylated as well as total p53 levels in FLT3-ITD+ AML CD34+ cells. Tenovin-6 also induced apoptosis and inhibited growth of the FLT3-ITD+ and p53 wild type cell line MV4-11. SIRT1 knock-down reduced TV-6-induced apoptosis and growth inhibition in MV4-11 cells confirming that TV-6 effects are related to SIRT1 inhibition. The growth inhibitory and pro-apoptotic effects of TV-6 in MV4-11 cells were also significantly reduced by p53 knock-down (TV-6 1μM, p53 shRNA 39±8% inhibition, control ShRNA 66±2% inhibition, p=0.04, n=3). Taken together these results support a potential role for p53 activation in mediating the effects of TV-6 treatment in FLT3-ITD+ AML cells. Sequencing studies indicated that only one sample in the FLT3-WT group harbored a p53 mutation, suggesting that their resistance to SIRT1 inhibitors is related to mechanisms other than p53 mutation. Flow cytometry analysis demonstrated increased SIRT1 levels in FLT3-ITD (n=7) compared to FLT3-WT (n=9) AML CD34+ cells (p=0.01). We used lentivirus vectors to ectopically express a FLT3-ITD construct in human cord blood CD34+ cells. Expression of FLT3-ITD resulted in significantly increased SIRT1 expression levels compared to FLT3-WT or vector controls. Consistent with results obtained with samples from AML patients, FLT3-ITD transformed CB CD34+ cells demonstrated enhanced sensitivity to TV-6 mediated apoptosis (TV6 1μM, FLT3-ITD 44±3% survival, n=5; FLT3-WT 59±2% survival, n=5, p=0.04; empty vector 64±4% survival, p=0.02, n=5) and cell growth inhibition. These results indicate that FLT3-ITD-mediated SIRT1 overexpression may contribute to the increased sensitivity of FLT3-ITD AML CD34+ cells to SIRT1 inhibition. In conclusion, our studies indicate that AML stem/progenitor cells demonstrate varying degrees of sensitivity to SIRT1 inhibition reflecting underlying genetic lesions. Importantly the poor prognosis FLT3-ITD mutation is associated with increased SIRT1 expression and enhanced sensitivity to SIRT1 inhibition. In view of the limited success of small molecule FLT3 inhibitors so far, the use of SIRT1 inhibitors may offer an attractive approach to target FLT3-ITD+ AML stem/progenitor cells. Disclosures: No relevant conflicts of interest to declare.

Clinical benefits of bevacizumab in metastatic colorectal cancer depending on KRAS status.

2014 ◽  
Vol 32 (3_suppl) ◽  
pp. 636-636
Author(s):  
Keisuke Kurimoto ◽  
Kiyoshi Ishigure ◽  
Yoshiyasu Kato ◽  
Yasuyuki Asai ◽  
Nobutake Tanaka ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Adverse Events ◽  
Metastatic Colorectal Cancer ◽  
Reduction Rate ◽  
Wild Type ◽  
Mutant Type ◽  
Drug Benefits ◽  
Kras Status ◽  
Clinical Benefits ◽  
Mutation Type

636 Background: KRAS status is the therapeutic marker of anti-EGFR drug, and may be the prognostic marker of metastatic colorectal cancer (mCRC). However, there is no consensus whether bevacizumab (anti-VEGF drug) benefits patients with mutated KRAS in mCRC. We investigated the clinical benefits of bevacizumab treatment in mCRC depending on KRAS status, retrospectively. Methods: We investigated 49 patients who received chemotherapies with bevacizumab as first-line treatment for mCRC from May 2008 through June 2013. We evaluated response rate (RR), disease control rate (DCR), progression-free survival (PFS), overall survival (OS), tumor reduction rate and the adverse events (CTCAE v4.0 - JCOG) depending on KRAS status. Results: The median age of the patients was 66 years (range; 36 - 80). Forty-five patients received oxaliplatin-based chemotherapies with bevacizumab and four patients received irinotecan-based chemotherapies with bevacizumab. KRAS status of 30 patients was wild type and that of 19 patients was mutation type. There was no difference in patient characteristics between KRAS wild type (WT) and mutation type (MT). In all 49 patients, RR was 62.5%. DCR was 91.7%. The median PFS was 10.9 months. In RR, patients with KRAS wild type tumors had better outcome than patients with mutant type tumors (WT : MT, 69.0% : 52.6%, no statistically difference). A similar tendency was seen in DCR (WT : MT, 96.6% : 84.2%, no statistically difference). The average reduction rate in KRAS WT was 42.7% and in KRAS MT was 32.3% (p = 0.309). In the KRAS wild patients, the median PFS was longer than that in the KRAS mutant patients (WT : MT, 11.8 : 8.9 months, Log Rank p = 0.583), but there is no statistically difference between two groups. In median OS, there was no difference between two groups (WT : MT, 21.0 : 20.8 months, Log Rank p = 0.393). The incidence of severe adverse events was not statistically different between KRAS WT group and MT group. Conclusions: Regardless of KRAS status, bevacizumab provides clinical benefits for patients with mCRC.

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