KLF4 Initiates Acinar Cell Reprogramming and Is Essential for the Early Stages of Pancreatic Carcinogenesis.

Ravikanth Maddipati, Jonathan P Katz

Open access · bronzeAbstract readComment

In one paragraph

Article in Cancer cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it

0cells of the map it votes in

4citing papers in PubMed

0.9field-weighted citation impact, top 24% of its field

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

4 citing papers in PubMed, 10 citations in OpenAlex.

KLF4 transcription factor in tumorigenesis.Cell death discovery · 2023
Review
Secretory Mucin 5AC Promotes Neoplastic Progression by Augmenting KLF4-Mediated Pancreatic Cancer Cell Stemness.Cancer research · 2021
Article
KLF4, A Gene Regulating Prostate Stem Cell Homeostasis, Is a Barrier to Malignant Progression and Predictor of Good Prognosis in Prostate Cancer.Cell reports · 2018
Article
CRISPR-ON-Mediated KLF4 overexpression inhibits the proliferation, migration and invasion of urothelial bladder cancerOncotarget · 2017
Article

4 · The record

Corrections and comments

Comment on
KLF4 Is Essential for Induction of Cellular Identity Change and Acinar-to-Ductal Reprogramming during Early Pancreatic Carcinogenesis.2016

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Ravikanth MaddipatiDivision of Gastroenterology, Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104-4863, USA.

Jonathan P KatzDivision of Gastroenterology, Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104-4863, USA. Electronic address: jpkatz@mail.med.upenn.edu.

University of Pennsylvania · US

Funding

Regulation of differentiation in esophageal epitheliaR01DK069984 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATZ, JONATHAN P · 2006 to 2015

$2.8M

NIDDK NIH HHS R01 DK069984

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDA) has a dismal prognosis and is minimally responsive to current chemotherapies. In this issue of Cancer Cell, Xie et al. (2016) identify the transcription factor KLF4 as essential for the early stages of pancreatic carcinogenesis, expanding the repertoire of targets for early intervention strategies.

Indexed as

Acinar CellsAnimalsCarcinogenesisHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsPancreasPancreatic DuctsPrecancerous ConditionsKLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription Factors

Identifiers

PMID26977875

DOI10.1016/j.ccell.2016.02.019

OpenAlexW2299096248

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.