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Rectal polyps
Published in Mark Davenport, James D. Geiger, Nigel J. Hall, Steven S. Rothenberg, Operative Pediatric Surgery, 2020
Most children with juvenile polyps will not have a recurrence of the problem. Pan colonoscopy should be performed, however, for any child with recurrent bleeding. In children with between two and four polyps, juvenile polyposis syndrome, with its increased risk of malignancy, should be considered. These children should undergo pancolonoscopy again a year after their initial polyp removal.
Paper 1
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Cronkhite-Canada syndrome, a type of non-hereditary syndrome, and Cowden syndrome can also affect the entire GI tract with hamartomatous polyps. Familial adenomatous polyposis syndrome (FAPS) is a hereditary condition characterised by hundreds of adenomatous polyps of the large bowel. Juvenile polyposis syndrome also causes hundreds of juvenile hamartomatous polyps affecting the entire GI tract.
Cronkhite−Canada Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Juvenile polyposis syndrome generates hamartomatous polyps containing an inflammatory component mainly in the colon before 10 years of age. Compared to juvenile polyps seen in CCS which show severe architectural changes in the surrounding mucosa, those in juvenile polyposis syndrome have normal-histological appearance in the surrounding mucosa. Further, juvenile polyposis syndrome does not have ectodermal features such as onychodystrophy and skin hyperpigmentation. In addition, juvenile polyposis syndrome is linked to mutation in BMPR1A or SMAD4 gene.
Pharmaceutical advances in the treatment of gastric adenocarcinoma
Published in Expert Opinion on Pharmacotherapy, 2022
Jane E. Rogers, Matheus Sewastjanow D Silva, Rebecca E. Waters, Jaffer A. Ajani
Most GAC are sporadic in nature, but GAC can be associated with a familial risk [1]. There are established inherited risks for GAC that include diffuse hereditary cancer (as a result of CDH1 germline mutation), hereditary non-polyposis colorectal cancer (HNPCC), familial adenomatous syndrome, juvenile polyposis syndrome, Peutz-Jeghers syndrome, Li-Fraumeni syndrome, among others [1,3–5]. H. pylori and Epstein-Barr virus (EBV) infections are linked as probable carcinogens. Other factors linked include high-salt consumption, large intake of smoked or cured food, a deficit in food refrigeration, contaminated drinking water, reduced intake of fruits and vegetables, high body mass index, gastroesophageal reflux, smoking, and exposure to certain occupational factors [1,3]. Gastric cancers are predominately (> 95%) adenocarcinomas and are classified based on anatomic location and Lauren classification histological type (diffuse or intestinal) [1]. Additionally, GAC has been defined into four molecular types: (1) Epstein-Barr virus associated with DNA hypermethylation (2) microsatellite instability having a high mutational load and hypermethylation (3) chromosomal instability with amplification of genes encoding of receptor tyrosine kinases or (4) genomically stable with gene alterations encoding for proteins involved in cell adhesion/cell migration pathways (most diffuse type GACs are in this category) [4–7]. The classification by The Cancer Genome Atlas Research Network does have limitations as it was derived from primary GAC specimens. However, these characteristics show that GAC is a heterogenous group of malignancies, but treatment has yet to differ significantly dependent on these characteristics making it challenging to establish therapeutic breakthroughs.
Juvenile Polyps with Osseous Metaplasia: Report of Two Pediatric Cases and Review of the Literature
Published in Fetal and Pediatric Pathology, 2022
Aileen Azari-Yam, Hosein Alimadadi, Moeinadin Safavi
Colonic/rectal juvenile polyps are gastrointestinal tract lesions that may occur either sporadically or in the heritable juvenile polyposis syndrome (JPS). Histologically, juvenile polyps reveal cystically dilated glands lined by cuboidal to columnar mucus secreting and goblet cells with reactive changes and marked expansion of the stroma which usually contains mixed inflammatory cells. Their surface epithelium is cuboidal, flattened or eroded. Extensive erosion with granulation tissue formation and mixed inflammatory cells infiltration may lead to pyogenic granuloma like changes [1].
Increasing the accuracy of colorectal cancer screening
Published in Expert Review of Anticancer Therapy, 2023
Silvia Pecere, Cristina Ciuffini, Michele Francesco Chiappetta, Lucio Petruzziello, Luigi Giovanni Papparella, Cristiano Spada, Antonio Gasbarrini, Federico Barbaro
This worrying trend is projected to steadily increase, and the incidence of eoCRC is expected to double by 2030 [2]. Moreover, hereditary risk factors play an important role in the development of CRC [3]. Approximately 10–20% of CRC patients have a positive family history, but only 5–7% of CRC cases are sustained by a well-defined hereditary syndrome (Lynch syndrome, Peutz-Jeghers syndrome, familial adenomatous polyposis, polyposis associated with MUTYH gene mutations, juvenile polyposis syndrome) [3,4].