Publications by authors named "M Mossner"

Background: The risk of developing advanced neoplasia (AN; colorectal cancer and/or high-grade dysplasia) in ulcerative colitis (UC) patients with a low-grade dysplasia (LGD) lesion is variable and difficult to predict. This is a major challenge for effective clinical management.

Objective: We aimed to provide accurate AN risk stratification in UC patients with LGD.

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Article Synopsis
  • Patients with inflammatory bowel disease (IBD) face an increased risk of colorectal cancer (CRC), which is heightened for those with low-grade dysplasia (LGD).
  • A study involving 122 patients revealed that the burden of somatic copy number alterations (CNAs) in LGD lesions can significantly predict future cancer development, outperforming traditional clinical risk factors.
  • The research suggests that measuring CNAs in LGD lesions is a cost-effective method for assessing CRC risk, allowing for better management of high-risk patients while reducing unnecessary treatments for those at low risk.
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In low-risk Myelodysplastic Neoplasms (MDS), increased activity of apoptosis-promoting factors such as tumor necrosis factor (TNFα) and pro-apoptotic Fas ligand (CD95L) have been described as possible pathomechanisms leading to impaired erythropoiesis. Asunercept (APG101) is a novel therapeutic fusion protein blocking CD95, which has previously shown partial efficacy in reducing transfusion requirement in a clinical phase I trial for low-risk MDS patients (NCT01736436; 2012-11-26). In the current study we aimed to evaluate the effect of Asunercept therapy on the clonal bone marrow composition to identify potential biomarkers to predict response.

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Immune system control is a major hurdle that cancer evolution must circumvent. The relative timing and evolutionary dynamics of subclones that have escaped immune control remain incompletely characterized, and how immune-mediated selection shapes the epigenome has received little attention. Here, we infer the genome- and epigenome-driven evolutionary dynamics of tumour-immune coevolution within primary colorectal cancers (CRCs).

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Tumor relapse is well recognized to arise from treatment-resistant residual populations. Strategies enriching such populations for in-depth downstream analyses focus on tumor-specific surface markers; however, enrichment using intracellular biomarkers remains challenging. Using B-cell lymphoma as an exemplar, we demonstrate feasibility to enrich B-cell lymphoma 2 (BCL2) populations, a surrogate marker for t(14;18)+ lymphomas, for use in downstream applications.

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