Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Early KRAS oncogenic driver mutations in nonmucinous tissue of congenital pulmonary airway malformations as an indicator of potential malignant behavior.

Human pathology - 1 Sept 2020

Hermelijn Sergei M, Wolf Janina L, Dorine den Toom T, Wijnen René M H, Rottier Robbert J, Schnater J Marco, von der Thüsen Jan H

Abstract excerpt

The potential for malignant degeneration is the most common reason for some practitioners to resect asymptomatic congenital pulmonary airway malformations (CPAMs). We aimed to investigate the potential of various immunohistochemical (IHC) and genomic biomarkers to predict the presence of mucinous proliferations (MPs) in CPAM. Archival CPAM tissue samples were re-assessed and underwent IHC analysis using a panel...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adenocarcinoma, Mucinous
Share to Biomarkers, Tumor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Transformation, Neoplastic

Share to Infant

Share to Infant, Newborn

Share to Lung Neoplasms

Share to Precancerous Conditions

Share to Proto-Oncogene Proteins p21(ras)

Source

Identifiers

PMID: 32681943
DOI: 10.1016/j.humpath.2020.07.015

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Early KRAS oncogenic driver mutations in nonmucinous tissue of congenital pulmonary airway malformations as an indicator of potential malignant behavior.PMID 32681943Read ↗

Activating KRAS mutations mark premalignant cystic structures in congenital pulmonary airway malformations.Semantic proximity Read ↗

Defining the spatial landscape of KRAS mutated congenital pulmonary airway malformations: a distinct entity with a spectrum of histopathologic features.Semantic proximity Read ↗

Expression of epidermal growth factor receptor, but not K-RAS mutations, is present in congenital cystic airway malformation/congenital pulmonary airway malformation.Semantic proximity Read ↗

Mucinous Adenocarcinoma With Intrapulmonary Metastasis Harboring KRAS and GNAS Mutations Arising in Congenital Pulmonary Airway Malformation.Semantic proximity Read ↗

A case report of an unusual non-mucinous papillary variant of CPAM type 1 with KRAS mutations.Semantic proximity Read ↗

Frequent EGFR exon 20 insertion in the so-called peripheral-type squamous cell neoplasm of uncertain malignant potential: a variant of bronchiolar adenoma or under-recognised entity?Semantic proximity Read ↗

A comprehensive review of benign tumors in the lung.Semantic proximity Read ↗

Mucinous adenocarcinoma arising in congenital pulmonary airway malformation: clinicopathological analysis of 37 cases.Semantic proximity Read ↗

Mucinous cells in type 1 pulmonary congenital cystic adenomatoid malformation as mucinous bronchioloalveolar carcinoma precursors.Semantic proximity Read ↗

Clinicopathologic and Molecular Characteristics of Resected Thoracic Mass Lesions in the Pediatric Population: A 25-Year Institutional Experience From a Tertiary Care Center.Semantic proximity Read ↗

Clinical Characteristics, Diagnosis, and Management of Primary Malignant Lung Tumors in Children: A Single-Center AnalysisSemantic proximity Read ↗

Neonatal congenital pulmonary airway malformation associated with mucinous adenocarcinoma and KRAS mutations.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.