On an SSA, low and high grade cytological dysplasia may appear Predominance of mature goblet cells in the upper part of the cryptĪbnormal architecture that extends to the base of the crypts: dilatation and serration, horizontal growth, goblet cells at the baseĪbnormal proliferation: focal nuclear stratification can be observed. Microvesicular mucin in the upper part of the crypt Normal architecture and proliferation in the lower third of the crypt serration in the middle to upper part of the crypt 7,8 This group of lesions has a common histologic characteristic, which is the appearance of serrated teeth in the epithelium of the crypt due to an accumulation of colonocytes secondary to inhibited apoptosis ( Fig. However, hyperplastic polyps are only a part of the spectrum of serrated polyps, and today we know that some subtypes have the potential to transform into colorectal carcinoma through the serrated pathway. Traditionally, hyperplastic polyps have been considered benign lesions with no risk of neoplastic progression. Serrated Polyps: Concept and Classification
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Search MethodologyĪ search was performed in PubMed of scientific articles (original articles and reviews) in English with the following words: “serrated polyps”, “hyperplastic polyposis”, “serrated polyposis” and “hyperplastic polyps”. The objective of this article is to describe the concept of the serrated carcinogenesis pathway, serrated polyps and serrated polyposis syndrome (SPS), as well as explaining the clinical implications for the diagnosis, treatment and follow-up of these lesions.
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In addition, recent studies have demonstrated that patients with multiple and/or large serrated polyps have an increased risk for developing CRC. 7–9 These lesions, with specific endoscopic, anatomic and pathologic characteristics that differentiate them from adenomas, have an important clinical relevance, as it has been observed that the majority of interval CRC detected in patients participating in CRC screening programs (tumors detected between 2 colonoscopies) are this type of lesion. 7 One of the most significant advances in recent years in the field of digestive oncology related with CRC has been recognizing serrated lesions as precursors to CRC, through the so-called “serrated” carcinogenesis pathway, which is responsible for 20%–30% of all CRC. Nevertheless, today we know that this model is implicated in only 70%–80% of CRC. This lesion, although benign, can potentially become malignant through the so-called “traditional” carcinogenesis model, related to chromosome instability and initiated by means of the inactivation of the APC gene. Until a few years ago, it was believed that the majority of CRC came from a common precursor lesion known as an adenomatous polyp, or adenoma. In recent decades, the prognosis of patients with CRC has improved, due to screening programs aimed at detecting asymptomatic individuals that present precancerous lesions (polyps) or adenocarcinomas in initial tumor phases, and thus decreasing the incidence and mortality of CRC. 4,5 This is because its natural history is known (most CRC originate from a premalignant lesion known as an adenoma), there are many means for its early detection (colonoscopy, fecal occult blood testing) and detection in early phases significantly improves prognosis. 1–3 These data contrast with the fact that CRC is the paradigm of a preventable neoplasm.
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Estos pacientes y sus familiares requieren una evaluación multidisciplinar en unidades de alto riesgo de cáncer colorrectal.Ĭolorectal cancer (CRC) is currently the most frequent neoplasm in Spain when both sexes are included, and it represents the second cause of death by cancer.
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El síndrome de poliposis serrada es una entidad clínico-patológica asociada a un aumento del riesgo de padecer cáncer colorrectal. La evidencia actual indica que estas lesiones deben ser resecadas completamente y que el paciente requiere un programa de vigilancia endoscópica. Los principales factores que se asocian a un mayor riesgo de malignizaciónen los pólipos serrados son el tamaño ≥10 mm, la multiplicidad, la histología de adenoma serrado sésil, la presencia de displasia asociada y la localización proximal. El descubrimiento de estas lesiones ha supuesto un cambio de paradigma en el concepto de la secuencia adenoma-carcinoma, de modo que hasta un 30% de los tumores se desarrollan por esta vía. Los pólipos serrados del colon constituyen un grupo heterogéneo de lesiones con potencial de transformación a cáncer colorrectal a través de la “vía serrada” de la carcinogénesis.