Evidence map›Paper›PMID 36351408›Full record

ArticleCell reports2022

NF1 loss of function as an alternative initiating event in pancreatic ductal adenocarcinoma.

Gopalakrishnan Ramakrishnan, Parash Parajuli, Pura Singh, Creighton Friend, Eric Hurwitz, Celine Prunier, Mohammed S Razzaque, Keli Xu, Azeddine Atfi

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.3field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 22 citations in OpenAlex.

  1. Impact of Tumor Genomic Profile on Adjuvant Chemotherapy Efficacy in Resected Pancreatic Adenocarcinoma: Results From the PRODIGE-24/CCTG PA6 Study.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. New Therapeutic Targets in RAS Wild-type Pancreatic Cancer.Current treatment options in oncology · 2024
    Review
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  8. Article
  9. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Gopalakrishnan RamakrishnanCancer Institute, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Parash ParajuliCancer Institute, University of Mississippi Medical Center, Jackson, MS 39216, USA; Department of Biochemistry & Molecular Biology and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA.
Pura SinghCancer Institute, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Creighton FriendDepartment of Biochemistry & Molecular Biology and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA.
Eric HurwitzDepartment of Biochemistry & Molecular Biology and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA.
Celine PrunierSorbonne Université, INSERM, CRSA, 75012 Paris, France.
Mohammed S RazzaqueDepartment of Pathology, Lake Erie College of Osteopathic Medicine, Erie, PA 16509, USA.
Keli XuCancer Institute, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Azeddine AtfiCancer Institute, University of Mississippi Medical Center, Jackson, MS 39216, USA; Department of Biochemistry & Molecular Biology and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA; Sorbonne Université, INSERM, CRSA, 75012 Paris, France. Electronic address: azeddine.atfi@vcuhealth.org.
Virginia Commonwealth University · USUniversity of Mississippi Medical Center · USLake Erie College of Osteopathic Medicine · USSorbonne Université · FR

Funding

Targeting the TGIF/Twist1 network in osteosarcomaR01CA210911 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI ATFI, AZEDDINE · 2017 to 2021
$1.8M
Exploiting the Twist1 network in cancer cachexiaR01CA240484 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI ATFI, AZEDDINE · 2019 to 2023
$1.7M
Targeting Transglutaminase 2 in cancer cachexiaR01CA251405 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI ATFI, AZEDDINE · 2020 to 2024
$1.6M
NCI NIH HHS R01 CA210911NCI NIH HHS R01 CA240484NCI NIH HHS R01 CA251405
6 · The paper itself

Abstract

A long-standing question in the pancreatic ductal adenocarcinoma (PDAC) field has been whether alternative genetic alterations could substitute for oncogenic KRAS mutations in initiating malignancy. Here, we report that Neurofibromin1 (NF1) inactivation can bypass the requirement of mutant KRAS for PDAC pathogenesis. An in-depth analysis of PDAC databases reveals various genetic alterations in the NF1 locus, including nonsense mutations, which occur predominantly in tumors with wild-type KRAS. Genetic experiments demonstrate that NF1 ablation culminates in acinar-to-ductal metaplasia, an early step in PDAC. Furthermore, NF1 haploinsufficiency results in a dramatic acceleration of Kras

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsHumansMutationNeurofibromin 1Pancreatic DuctsProto-Oncogene Proteins p21(ras)Neurofibromin 1Proto-Oncogene Proteins p21(ras)alternative genetic drivers in pancreatic ductal adenocarcinomaCP: Cancermosaic analysis with double markersmutant KRASpancreatic ductal adenocarcinoma initiationtumor-suppressor gene NF1tumor-suppressor gene PMLtumor-suppressor gene TP53

Identifiers

PMID36351408
PMCPMC9716579
OpenAlexW4308515104

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.