Doubling Down on Mutant RAS Can MEK or Break Leukemia.

Zuzana Tothova, Benjamin L Ebert

Abstract read

In one paragraph

Article in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it

0cells of the map it votes in

2citing 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

2 citing papers in PubMed.

Phase II Trial of MEK Inhibitor Binimetinib (MEK162) in RAS-mutant Acute Myeloid Leukemia.Clinical lymphoma, myeloma & leukemia · 2019
Trial
Mechanistic regulation of epithelial-to-mesenchymal transition through RAS signaling pathway and therapeutic implications in human cancer.Journal of cell communication and signaling · 2018
Review

4 · The record

Corrections and comments

Commented on by
KRAS Allelic Imbalance Enhances Fitness and Modulates MAP Kinase Dependence in Cancer.2017

5 · Who and what money

Authors and funding

2 authors.

Zuzana TothovaBrigham and Women's Hospital, Division of Hematology, Boston, MA 02115, USA; Dana Farber Cancer Institute, Department of Medical Oncology, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.

Benjamin L EbertBrigham and Women's Hospital, Division of Hematology, Boston, MA 02115, USA; Dana Farber Cancer Institute, Department of Medical Oncology, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: bebert@partners.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting of the RAS pathway has long been a critical therapeutic challenge in oncology. Burgess et al. examine how the relative expression of mutant and wild-type KRAS modulates clonal fitness and sensitivity to MEK inhibitors in a model of Kras

Indexed as

Genes, rasHumansLeukemia, Myeloid, AcuteMutationProtein Kinase Inhibitorsras ProteinsProtein Kinase Inhibitorsras Proteins

Identifiers

PMID28235190

DOI10.1016/j.cell.2017.02.013

What OpenQuestion holds

Textmetadata

Read underepoch 390

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.