Citations

Abstract Background Serrated polyps are an inhomogeneous group of lesions that harbour precursors of colorectal cancer. Current research has been directed at further defining the histopathological characteristics of these lesions, but definitive treatment recommendations are unclear. The aim was to review the current literature regarding classification, molecular genetics and natural history of these lesions in order to propose a treatment algorithm for surgeons to consider. Methods The PubMed database was searched using the following search terms: serrated polyp, serrated adenoma, hyperplastic polyp, hyperplastic polyposis, adenoma, endoscopy, surgery, guidelines. Papers published between 1980 and 2010 were selected. Results Sixty papers met the selection criteria. Most authors agree that recommendations regarding endoscopic or surgical management should be based on the polyp's neoplastic potential. Polyps greater than 5 mm should be biopsied to determine their histology so that intervention can be directed accurately. Narrow-band imaging or chromoendoscopy may facilitate the detection and assessment of extent of lesions. Complete endoscopic removal of sessile serrated adenomas in the left or right colon is recommended. Follow-up colonoscopy is recommended in 2–6 months if endoscopic removal is incomplete. If the lesion cannot be entirely removed endoscopically, segmental colectomy is strongly recommended owing to the malignant potential of these polyps. Left-sided lesions are more likely to be pedunculated, making them more amenable to successful endoscopic removal. Conclusion Even though the neoplastic potential of certain subtypes of serrated polyp is heavily supported, further studies are needed to make definitive endoscopic and surgical recommendations.

BackgroundThe majority of studies relating amyloid pathology with brain volumes have been cross‐sectional. Apolipoprotein ɛ4 (APOE ɛ4), a genetic risk factor for Alzheimer's disease, is also known to be associated with hippocampal volume loss. No studies have considered the effects of amyloid pathology and APOE ɛ4 together on longitudinal volume loss.MethodsWe evaluated whether an abnormal level of cerebrospinal fluid beta‐amyloid (CSF Aβ) and APOE ɛ4 carrier status were independently associated with greater hippocampal volume loss over 1 year. We then assessed whether APOE ɛ4 status and CSF Aβ acted synergistically, testing the significance of an interaction term in the regression analysis. We included 297 participants: 77 cognitively normal, 144 with mild cognitive impairment (MCI), and 76 with Alzheimer's disease.ResultsAn abnormal CSF Aβ level was found to be associated with greater hippocampal volume loss over 1 year in each group. APOE ɛ4 was associated with hippocampal volume loss only in the cognitively normal and MCI groups. APOE ɛ4 carriers with abnormal CSF Aβ in the MCI group acted synergistically to produce disproportionately greater volume loss than noncarriers.ConclusionBaseline CSF Aβ predicts progression of hippocampal volume loss. APOE ɛ4 carrier status amplifies the degree of neurodegeneration in MCI. Understanding the effect of interactions between genetic risk and amyloid pathology will be important in clinical trials and our understanding of the disease process.

A rapid progression from conventional open surgery to minimally invasive approaches in the surgical management of colorectal cancer has occurred over the last 2 decades. Initial concerns that this new approach was oncologically inferior to open surgery were ultimately refuted when several prospective randomized trials concluded that laparoscopic colectomy could achieve similar oncologic outcomes to open surgery. On the contrary, level 1 data has not yet matured regarding the oncologic safety of minimally invasive approaches for rectal cancer. We review the published literature pertaining to the evolution of minimally invasive techniques used to treat colorectal cancer surgery, including barriers to adoption, and the prospects for future advances related to innovative techniques.

Abstract Triple-negative breast cancers are an aggressive subtype of breast cancer with poor survival, but there remains little known about the etiologic factors that promote its initiation and development. Commonly inherited breast cancer risk factors identified through genome-wide association studies display heterogeneity of effect among breast cancer subtypes as defined by the status of estrogen and progesterone receptors. In the Triple Negative Breast Cancer Consortium (TNBCC), 22 common breast cancer susceptibility variants were investigated in 2,980 Caucasian women with triple-negative breast cancer and 4,978 healthy controls. We identified six single-nucleotide polymorphisms, including rs2046210 (ESR1), rs12662670 (ESR1), rs3803662 (TOX3), rs999737 (RAD51L1), rs8170 (19p13.1), and rs8100241 (19p13.1), significantly associated with the risk of triple-negative breast cancer. Together, our results provide convincing evidence of genetic susceptibility for triple-negative breast cancer. Cancer Res; 71(19); 6240–9. ©2011 AACR.