Publications by authors named "Claes Lenander"

Background: Tumor budding and a proficient mismatch repair (pMMR) status are considered adverse prognostic factors in colorectal cancer (CRC). The aim of this pilot study was to assess tumor budding in primary CRC with pMMR versus that with deficient mismatch repair (dMMR).

Materials And Methods: Tumor budding was retrospectively examined in the tumor from 134 patients with stage II and stage III CRC with known MMR status.

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The establishment and maintenance of apical-basal cell polarity is essential for the functionality of glandular epithelia. Cell polarity is often lost in advanced tumours correlating with acquisition of invasive and malignant properties. Despite extensive knowledge regarding the formation and maintenance of polarity, the mechanisms that deregulate polarity in metastasizing cells remain to be fully characterized.

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Background: Doppler guidance in hemorrhoidal surgery has become more frequent during the past decade. The method is mainly studied in nonrandomized trials. Data from randomized controlled trials are lacking.

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The genetic susceptibility to colorectal cancer (CRC) has been estimated to be around 35% and yet high-penetrance germline mutations found so far explain less than 5% of all cases. Much of the remaining variations could be due to the co-inheritance of multiple low penetrant variants. The identification of all the susceptibility alleles could have public health relevance in the near future.

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Background: Studying the invading edge of colorectal carcinomas it was previously noticed that the neoplastic glands with pores could contain mucin, inflammatory cells and/or necrotic material.

Aims: To systematically record the type of intraglandular materials found in the neoplastic glands with pores at the invading edge of sporadic colonic carcinomas.

Materials And Methods: Histological sections from 12 adenocarcinomas were selected when the following materials were predominantly found in the neoplastic glands with pores at the invading tumor edge: mucin (3 cases, group I), neutrophilic granulocyes (3 cases, group II), necrotic material (3 cases, group III) and invaginated stroma (3 cases, group IV).

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Purpose: Recently a common variant of the TGFBR1 gene, TGFBR1*6A, has been proposed to act as a low-penetrance tumor susceptibility allele for colorectal cancer, but data from published studies with individually low statistical power are conflicting. To further evaluate the relationship between TGFBR1*6A and colorectal cancer risk, we have conducted a large case-control study and a meta-analysis of previously published studies.

Experimental Design: A total of 1,042 colorectal cancer cases and 856 population controls were genotyped for the TGFBR1*6A polymorphism.

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Background: The size of colorectal polyps is important in the clinical management of these lesions.

Aim: To audit the accuracy in calculating the size of "polyps" by various specialists.

Materials And Methods: Eighteen pathologists and four surgeons measured, with a conventional millimetre ruler, the largest diameter of 12 polyp phantoms.

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Background: The cell cycle checkpoint kinase 2 (CHEK2) 1100delC variant has recently been identified at high frequency in families with both breast and colorectal cancer, suggesting the possible role of this variant in colorectal cancer predisposition.

Patients And Methods: To evaluate the role of CHEK2 ll00delC among Swedish colorectal cancer patients, the variant frequency was determined in 174 selected familial cases, 644 unselected cases and 760 controls, as well as in l8 families used in the genome-wide linkage analysis, where weak linkage was seen for the region harboring the CHEK2 gene.

Results: CHEK2 l100delC was found in 1.

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Ultimately aiming at a more individualized therapeutic approach in epidermoid anal cancer, this study explored the prognostic and predictive impact of a set of tumour markers. From a population-based cohort of 276 patients with epidermoid anal cancer, treated according to prospective protocols, 215 pre-treatment biopsies were investigated using immunohistochemistry. The expression of p53, p21, Cyclin A and CD31 was measured semi-quantitatively.

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