Vivo Y90 Mtp Usb Driver Download !!HOT!!

A USB driver is a small software that allows your computer to recognize and adequately communicate with your Vivo smartphone. Not only does it let your computer recognize your Vivo phone, but it also enables you to transfer files between the two devices, use your phone as a modem, and much more.

Generally, a USB driver for a mobile phone is a small utility that allows users to connect their mobile devices to computers. In this case, we are dealing with Vivo mobile devices. Application developers create mobile applications using a desktop computer, such as a Windows or Mac PC. It isn't easy to thoroughly test the software without installing it on a mobile device. Vivo USB Drivers make this possible for Vivo smartphones running Android OS.

Vivo Y90 Mtp Usb Driver Download

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Yes. The Vivo USB Driver is 100% free since the Vivo community officially releases it for the Vivo Smartphone and Tablet users. Vivo device owners can find the exact Vivo drivers on the Vivo Support forums.

Yes. The Vivo USB Driver is 100% safe for the computer, laptop, and Vivo mobile. Furthermore, since the Vivo community officially releases the driver, it's 100% safe and secure to use on the computer.

You can install the Vivo USB Driver by downloading the .exe file and installing the driver on the Computer. The installation process is quite similar to the standard Windows Application. You can follow the How to install the Vivo Driver page to install the drivers correctly.

Small cell lung cancer (SCLC) is a lethal form of lung cancer. Here, we develop a quantitative multiplexed approach on the basis of lentiviral barcoding with somatic CRISPR-Cas9-mediated genome editing to functionally investigate candidate regulators of tumor initiation and growth in genetically engineered mouse models of SCLC. We found that naphthalene pre-treatment enhances lentiviral vector-mediated SCLC initiation, enabling high multiplicity of tumor clones for analysis through high-throughput sequencing methods. Candidate drivers of SCLC identified from a meta-analysis across multiple human SCLC genomic datasets were tested using this approach, which defines both positive and detrimental impacts of inactivating 40 genes across candidate pathways on SCLC development. This analysis and subsequent validation in human SCLC cells establish TSC1 in the PI3K-AKT-mTOR pathway as a robust tumor suppressor in SCLC. This approach should illuminate drivers of SCLC, facilitate the development of precision therapies for defined SCLC genotypes, and identify therapeutic targets.

Genetic aberrations driving pro-oncogenic and pro-metastatic activity remain an elusive target in the quest of precision oncology. To identify such drivers, we use an animal model of KRAS-mutant lung adenocarcinoma to perform an in vivo functional screen of 217 genetic aberrations selected from lung cancer genomics datasets. We identify 28 genes whose expression promoted tumor metastasis to the lung in mice. We employ two tools for examining the KRAS-dependence of genes identified from our screen: 1) a human lung cell model containing a regulatable mutant KRAS allele and 2) a lentiviral system permitting co-expression of DNA-barcoded cDNAs with Cre recombinase to activate a mutant KRAS allele in the lungs of mice. Mechanistic evaluation of one gene, GATAD2B, illuminates its role as a dual activity gene, promoting both pro-tumorigenic and pro-metastatic activities in KRAS-mutant lung cancer through interaction with c-MYC and hyperactivation of the c-MYC pathway.

KRAS-driven lung cancers are not targetable by currently approved therapies and represent a particularly aggressive form of NSCLC5. Regional or distant metastases are thought to form often and early in KRAS-driven adenocarcinoma leading to high mortality6,7. Subgroups have been identified in KRAS-mutant NSCLC based upon co-mutations that enhance or modulate KRAS tumorigenicity and disease progression, providing biological and molecular context for personalized and targetable treatments for KRAS mutant patients8. New approaches aimed at personalized therapeutic strategies are critical for these patients, as identifying targets downstream of or that work in conjunction with KRAS offer the most promising opportunities to exploit therapeutic vulnerabilities. Therefore, systematic functional characterization of lung cancer genome datasets is needed. The Cancer Genome Atlas (TCGA) and others have generated a compendium of genomic aberrations in lung cancer with the goal of identifying the most promising drug targets and diagnostic biomarkers9. The challenge now is to distinguish the subsets of functional oncogenic and metastatic driver aberrations from passenger mutations that do not offer therapeutic opportunities.

While RNA interference (RNAi)-based and CRISPR/Cas9-based genetic screening platforms have successfully identified new tumor suppressor genes and other genetic vulnerabilities in cancer, several recent studies reveal a complementary approach through developing scalable gain-of-function screening systems for validating over-expressed or mutationally activated oncogenes that, as a class, have served as successful therapeutic targets to date. For example, we previously reported a multi-level functional assessment platform, High-Throughput Mutagenesis and Molecular Barcoding (HiTTMoB), which has identified novel variants of known oncogenes10, as well as elucidating novel drivers of pancreatic ductal adenocarcinoma11. Here we report an adaptation of this platform to identify genetic drivers that synergize with mutant KRAS to advance tumor progression and metastasis in lung adenocarcinoma. In vivo functional screening of a gene library informed by oncogenomics-guided integration of mutant KRAS-specific mouse and human gene signatures reveal several genes whose expression promote tumor growth and/or metastasis, as outlined here and in the companion paper. Among those genes, functional characterization of GATAD2B illuminates its role as a potent driver of tumor growth and metastasis in KRAS-driven lung cancers. We further show here that high GATAD2B expression correlates with worsened outcomes in lung cancer patients and cooperates with KRAS to promote gain-of-function pro-oncogenic and pro-metastatic transcriptional programs including MYC to mediate cell invasion in vitro and tumor progression in vivo.

Because oncogenic pathways can be similarly activated by hyperactivation mutations, an observation first discovered by well-characterized oncogenes such as PIK3CA and ALK19,20,21,22,23, we integrated sequencing results by Ding and colleagues24 that focused on 623 genes with potential relationships to cancer. Filtering copy number amplifications from TCGA with the 1013 non-synonymous somatic mutations identified by their study revealed 31 amplified genes that contain at least one validated missense mutation within the 188 analyzed tumors. Combining these data with the 220 genes described above yielded a total of 251 candidate genes that include several known to play a significant role in lung cancer (e.g., IKK-BETA, KRAS, EGFR, ZEB1, TWIST1), in addition to two potent drivers (FSCN1 and HOXA1) of melanoma transformation and metastasis identified in our previous studies12,25. Of the 251 candidate genes identified, 225 were available in our collection of open reading frame (ORF) clones comprised of the Human ORFeome collection26, as well as other commercially available ORF clones. Conservation analysis was performed to reduce the potential for false negatives in our screening model and confirmed significant homology of the 225 genes between mouse and human (Supplementary Data 1). Included in the 225 ORFs were 28 wild-type ORFs representing mutated genes in Ding et. al studies (Supplementary Data 1). Each ORF was introduced into a lentiviral vector through recombination-mediated cloning. Importantly, each expression vector was uniquely tagged with a 24-nucleotide DNA barcode (Supplementary Data 1) during ORF lentiviral integration using our previously reported High-Throughput Mutagenesis and Molecular Barcoding (HiTMMoB) strategy11, providing a surrogate identifier for each associated ORF.

We sought to determine whether GATAD2B is required for oncogenic growth of KRAS-mutant human NSCLC. To do this, we first validated the efficacy of two independent shRNA hairpins (sh-3 and sh-5) targeting GATAD2B compared to non-targeting vector (shNT) (Supplementary Fig. 5). We next assessed the effect of GATAD2B depletion on anchorage-independent colony growth by five NSCLC cell lines with and without mutant KRAS: NCI-H23, A549, CALU1, NCI-H1437, and NCI-H1568. In all three KRAS mutant lines (H23, A549, CALU1), depletion of GATAD2B using both GATAD2B shRNAs robustly attenuated colony formation compared to shNT control, while no significant differences were observed in KRAS wild-type lines (H1437 and H1568) (Fig. 3g). Taken together, these data support the role of GATAD2B as a KRAS-dependent driver of oncogenesis and metastasis.

While culture-based studies using engineered cell models such as HBEC-iKRASG12D are genetically tractable, they fail to recapitulate the microenvironment critical for the growth of human cancer cells. Therefore, we leveraged a well-established GEM model of lung adenocarcinoma where tumor initiation is achieved by Cre recombinase-mediated activation of a KRASG12D allele (hereafter LSL-KRASG12D;35. In addition to the use of lung-specific Cre driver alleles engineered into mice5,6,7,40, lung tumorigenesis in the LSL-KRASG12D GEM models can be achieved through application of adeno- or lenti-Cre virus through nasal inhalation or intubation41. To build on previous studies that have used this approach for the co-delivery of cDNAs or other genetic elements35,42, we devised a new lentiviral expression construct compatible with HiTMMoB that permits co-expression of barcoded ORFs with Cre recombinase (Fig. 4a). By crossing the LSL-KRASG12D mice with a strain carrying a Cre-inducible Luciferase allele [LSL-Luciferase;43], we generated a mouse strain such that delivery of Cre recombinase permits co-expression of KRASG12D and Luciferase in the same cells (Fig. 4a). To test our lentiviral vector, we recombined ORFs encoding GFP and dominant-negative TP53 (TP53R270H) into separate lentiviral constructs with unique barcodes, followed by virus titering using HEK293-loxP-GFP-RFP Cre reporter cells. Intubation-mediated delivery of high titer virus (500,000 particles) encoding barcoded GFP- and TP53R270H-Cre to LSL-KRASG12D;LSL-Luciferase animals led to formation of lung tumors by 3 months as visualized by bioluminescent imaging (Fig. 4b). Animal necropsies confirmed numerous focal lesions throughout the lungs of animals intubated with either GFP-Cre or TP53R270H-Cre (Fig. 4c). In contrast to mice exposed to GFP-Cre, those intubated with TP53R270H-Cre exhibited gross metastases to proximal and distant lymph nodes (Fig. 4c) consistent with other reports demonstrating metastatic activity of the TP53R270H allele in the LSL-KRASG12D model44. As expected, immunoblot analysis confirmed increased expression of TP53 in tumor-infiltrated lung and lymph node tissues from mice intubated with TP53R270H-Cre vs. mice who received GFP-Cre (Fig. 4e). NGS analysis of these tissues confirmed robust enrichment for TP53R270H-associated barcode consistent with the presence of TP53R270H-Cre transduced cells (Fig. 4f). 17dc91bb1f