Evidence map›Paper›PMID 28057848›Full record

ReviewCold Spring Harbor symposia on quantitative biology2016

A Pipeline for Drug Target Identification and Validation.

Eusebio Manchado, Chun-Hao Huang, Nilgun Tasdemir, Darjus F Tschaharganeh, John E Wilkinson, Scott W Lowe

Open access · diamondAbstract readReview
In one paragraph

Review in Cold Spring Harbor symposia on quantitative biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Eusebio ManchadoDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065.
Chun-Hao HuangDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065.
Nilgun TasdemirDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065.
Darjus F TschaharganehDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065.
John E WilkinsonULAM/Department of Pathology, University of Michigan School of Medicine, Ann Arbor, Michigan 48109.
Scott W LoweDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10065.
Cornell University · USMemorial Sloan Kettering Cancer Center · USCold Spring Harbor Laboratory · USMichigan Medicine · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
VIRAL TRANSACTIVATIONP01CA013106 · NCI · COLD SPRING HARBOR LABORATORY · PI William Richard McCombie · 1985 to 2026
$116.8M
The Role of Focal Oncogene Amplifications in Lung CancerP01CA129243 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Piro Lito · 2007 to 2026
$31.2M
COMPUTATIONAL AND FUNCTIONAL APPROACHES TO VALIDATING CANCER GENOME TARGETSU01CA168409 · NCI · COLD SPRING HARBOR LABORATORY · PI POWERS, SCOTT · 2012 to 2016
$7.3M
A scalable platform for target validation in GEMM models of gastrointestinal malignancies.R01CA195787 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LOWE, SCOTT W. · 2015 to 2017
$2.0M
NCI NIH HHS P01 CA013106NCI NIH HHS P01 CA129243NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA195787NCI NIH HHS U01 CA168409
6 · The paper itself

Abstract

Rapid and affordable tumor profiling has led to an explosion of genomic data that is facilitating the development of new cancer therapies. The potential of therapeutic strategies aimed at inactivating the oncogenic lesions that contribute to the aberrant survival and proliferation of tumor cells has yielded remarkable success in some malignancies such as BRAF-mutant melanoma and BCR-ABL expressing chronic myeloid leukemia. However, the direct inhibition of several well-established oncoproteins in some of these cancers is not possible or produces only transient benefits. Functional genomics represents a powerful approach for the identification of vulnerabilities linked to specific genetic alterations and has provided substantial insights into cancer signaling networks. Still, as inhibition of gene function can have diverse effects on both tumor and normal tissues, information on the potency of target inhibition on tumor growth as well as the toxic side effects of target inhibition are also needed. Here, we discuss our RNA interference (RNAi) pipeline for cancer target discovery based on our optimized short-hairpin RNA (shRNA) tools for negative selection screens and inducible RNAi platform that, in combination with embryonic stem cell (ESC)-based genetically engineered mouse models (GEMMs), enable deep in vivo target validation.

Indexed as

Disease Models, AnimalEmbryonic Stem CellsAnimalsCell ProliferationHumansRNA InterferenceRNA, Small InterferingSignal TransductionRNA, Small Interfering

Identifiers

PMID28057848
PMCPMC5469697
OpenAlexW2570501153

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.