Evidence map›Paper›PMID 34599002›Full record

ReviewGenes & development2021

Anticipating resistance to KRAS inhibition: a novel role for USP21 in macropinocytosis regulation.

Howard C Crawford

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Genes & development, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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

1 author at 1 institution in 1 country.

Howard C CrawfordHenry Ford Pancreatic Cancer Center, Henry Ford Health System, Detroit, Michigan 48202, USA hcrawfo1@hfhs.org.ORCID 0000-0001-9360-3019
Henry Ford Health System · US

Funding

Interrupting Cellular Crosstalk in the Immunosuppressive Microenvironment of Pancreas CancerU01CA224145 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CRAWFORD, HOWARD C., PASCA DI MAGLIANO, MARINA · 2017 to 2021
$2.6M
Metaplastic Tuft Cells in Pancreatic CancerR01CA247516 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CRAWFORD, HOWARD C. · 2020 to 2024
$2.3M
NCI NIH HHS R01 CA247516NCI NIH HHS U01 CA224145
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers. Virtually all PDAC harbors an oncogenic mutation in the KRAS gene, making it the prime target for therapy. Most previous attempts to inhibit KRAS directly have been disappointing, but recent success in targeting some KRAS mutants presages a new era in PDAC therapy. Models of PDAC have predicted that identifying KRAS inhibitor resistance mechanisms will be critical. In this issue of

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsCell Line, TumorCell ProliferationHumansMutationProto-Oncogene Proteins p21(ras)Ubiquitin ThiolesteraseKRAS protein, humanProto-Oncogene Proteins p21(ras)Ubiquitin ThiolesteraseUSP21 protein, humanKRASmacropinocytosisMARK3targeted therapy resistanceUSP21

Identifiers

PMID34599002
PMCPMC8494204
OpenAlexW3204420358

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.