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Comparative genomic profiling of glandular bladder tumours
Angela Maurer1, Nadina Ortiz-Bruechle1, Karolina Guricova1
1Institute of Pathology, University Hospital RWTH Aachen University, Pauwelsstrasse 30, 52074, Aachen, Germany.
Virchows Archiv : an International Journal of Pathology
|March 22, 2020
Summary
Primary glandular bladder tumors share molecular similarities with colorectal cancer, suggesting common pathways in their development. This research analyzed bladder adenocarcinomas (BAC), urachal adenocarcinomas (UAC), and urothelial carcinomas with glandular differentiation (UCg).
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Primary glandular bladder tumors, including bladder adenocarcinoma (BAC), urachal adenocarcinoma (UAC), and urothelial carcinoma with glandular differentiation (UCg), are rare and poorly understood malignancies.
- These tumors often exhibit histological similarities to colorectal adenocarcinoma (CORAD), but limited molecular data hinders understanding of their pathogenesis.
- Existing knowledge on muscle-invasive bladder cancer (BLCA) and CORAD provides a comparative basis for investigating these rare bladder tumors.
Purpose of the Study:
- To conduct an in-depth molecular analysis of BAC, UAC, UCg, and non-invasive glandular lesions.
- To identify novel genetic alterations and pathways involved in the tumorigenesis of primary glandular bladder tumors.
- To compare the molecular profiles of these bladder tumors with established data from BLCA and CORAD.
Main Methods:
- Comprehensive analysis of 12 BAC, 13 UAC, 11 UCg, and 19 non-invasive glandular lesions.
- Identification of mutations in key cancer-related genes and pathways (TP53, Wnt, MAP kinase, MTOR, SMAD4, ARID1A, BRAF, TERT, FBXW7).
- Immunohistochemical analysis for DNA mismatch repair deficiency, PD-L1 expression, and protein loss of ARID1A, SMARCA1, and PBRM1.
Main Results:
- Mutations in SMAD4, ARID1A, and BRAF were identified in BAC, alongside known alterations.
- UCg showed frequent 'urothelial-like' alterations, while BAC and UAC displayed 'colorectal-like' mutational patterns.
- No DNA mismatch repair deficiency or PD-L1 tumor cell positivity was observed; PD-L1 immune cell expression varied by tumor type and antibody.
Conclusions:
- Similar molecular pathways may drive tumorigenesis in BAC, UAC, and CORAD, irrespective of tissue origin.
- The distinct molecular profiles of UCg ('urothelial-like') versus BAC/UAC ('colorectal-like') suggest different etiological mechanisms.
- Alterations in TERT and FBXW7 in intestinal metaplasia suggest a potential precancerous role, aligning with previous findings.
Keywords:
Bladder adenocarcinomaMolecular geneticsUrachal carcinomaUrothelial carcinomaUrothelial carcinoma with glandular differentiation
