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The vast number of genomic and molecular alterations in cancer pose a substantial challenge to uncovering the mechanisms of tumorigenesis and identifying therapeutic targets. High-throughput functional genomic methods in genetically engineered mouse models allow for rapid and systematic investigation of cancer driver genes. In this review, we discuss the basic concepts and tools for multiplexed investigation of functionally important cancer genes in vivo using autochthonous cancer models. Furthermore, we highlight emerging technical advances in the field, potential opportunities for future investigation, and outline a vision for integrating multiplexed genetic perturbations with detailed molecular analyses to advance our understanding of the genetic and molecular basis of cancer.
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Download Vivo USB Driver, made by Vivo. Vivo USB Drivers work perfectly with all Vivo devices running Android OS. Therefore, all lines of devices, new and old, are compatible with this latest Vivo USB Driver.
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.
The Vivo USB Driver for Vivo Android devices is available for all computers running on Windows OS, whether a Windows XP or the latest Windows 11. Both 32-bit and 64-bit computers are supported. Unfortunately, it is unavailable for Mac OS X computers or MacOS and Linux.
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.
Vivo USB Drivers are explicitly designed for Vivo smartphones and tablets running on Google's Android operating system. The Vivo USB Driver fully supports all Vivo smartphones and tablets. It may or may not work for other devices.
No. The Vivo USB Driver does not require an active internet connection to be used on a Windows computer or a laptop. You can connect Vivo devices to the computer via a USB cable, so no Wi-Fi or Bluetooth connection is required.
No. Vivo USB Driver provides only the necessary system files, allowing your Vivo devices to communicate effectively with your computer. You cannot view the contents of your phone with the Vivo USB Driver. Once you have installed the Vivo Drivers on the computer, enable USB debugging on your Vivo device and connect it to the computer via a USB cable. Through Windows Explorer, you can view the device contents.
The Vivo USB Driver is designed to be installed on a Windows PC or a laptop to ensure seamless communication between your Vivo device and the Windows computer. But, of course, you need an Vivo device to work with a computer.
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.
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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.
Non-small cell lung cancer (NSCLC) is the leading cause of cancer mortality in the United States, primarily due to the development of metastatic disease1. Recent progress in treating lung cancer has come from identifying patient subpopulations with identifiable oncogenic mutations that can be targeted with small molecule inhibitors (e.g., erlotinib and crizotinib for EGFR-driven and EML4-ALK-driven tumors, respectively)2,3. Unfortunately, the majority of lung cancer cases are driven by unknown genetic events or mutations in genes such as KRAS (30% of patients) for which there are no selective therapeutics4.
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. 152ee80cbc
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