English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Peutz–Jeghers syndrome (PJS) is an autosomal dominant cancer susceptibility syndrome characterised by mucocutaneous melanin pigmentation, hamartomatous polyps, and an 18-fold increase in intestinal and extraintestinal cancer risk.1 PJS is caused by a germline mutation in LKB1 , a gene that plays a role in cellular polarity.2 Proper cellular polarity is critical for accurate asymmetrical stem cell division.3 The pathogenesis and neoplastic risk, if any, of hamartomatous Peutz–Jeghers polyps remain unclear.Based on rare observations of neoplastic changes in PJS polyps and the finding of biallelic inactivation of the gene involved in PJS, the existence of a unique hamartoma–carcinoma sequence has been proposed in this disorder.4,5 This concept suggests that PJS polyps are clonal premalignant lesions responsible, at least in part, for the high rates of gastrointestinal cancer in these patients. However, dysplastic changes have been found rarely. Clarification of the risk of neoplastic transformation in PJS polyps would assist …

Peutz Jeghers syndrome polyps are polyclonal with expanded progenitor cell compartment