ArticleBritish journal of cancer2019
Molecular heterogeneity and early metastatic clone selection in testicular germ cell cancer development.
Article in British journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Report From the International Society of Urological Pathology (ISUP) Consultation Conference on Molecular Pathology of Urogenital Cancers: IV: Current and Future Utilization of Molecular-Genetic Tests for Testicular Germ Cell Tumors.The American journal of surgical pathology · 2020Guideline
- Pediatric malignant testicular germ cell tumors: a developmental and comparative perspective.Diagnostic pathology · 2026Review
- Driving precision medicine in testicular germ cell tumors: from preclinical models to clinical applications.Therapeutic advances in medical oncology · 2026Review
- NanoString profiling of DNA repair and apoptosis genes in testicular germ cell tumours with divergent chemotherapy outcomes.Therapeutic advances in medical oncology · 2026Article
- Differences of sex development.Nature reviews. Disease primers · 2025Review
- A Thiopurine-like Mutagenic Process Defines TGCT Subtypes.bioRxiv : the preprint server for biology · 2025Article
- Genomic landscape of adult testicular germ cell tumours in the 100,000 Genomes Project.Nature communications · 2024Article
- Successful Multimodal Treatment of Intracranial Growing Teratoma Syndrome with Malignant Features.Current oncology (Toronto, Ont.) · 2024Article
- Integrated genomic analysis reveals aberrations in WNT signaling in germ cell tumors of childhood and adolescence.Nature communications · 2023Article
- Impact of tumor markers on diagnosis, treatment and prognosis in CNS germ cell tumors: correlations with clinical practice and histopathology.Brain tumor pathology · 2023Article
- ZFP281 drives a mesenchymal-like dormancy program in early disseminated breast cancer cells that prevents metastatic outgrowth in the lung.Nature cancer · 2022Article
- Chromosome 3p25.3 Gain Is Associated With Cisplatin Resistance and Is an Independent Predictor of Poor Outcome in Male Malignant Germ Cell Tumors.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2022Article
- Whole genome duplication in oral squamous cell carcinoma in patients younger than 50 years: implications for prognosis and adverse clinicopathological factors.Genes, chromosomes & cancer · 2022Article
- Clonal diversification and histogenesis of malignant germ cell tumours.Nature communications · 2022Article
- 12p gain is predominantly observed in non-germinomatous germ cell tumors and identifies an unfavorable subgroup of central nervous system germ cell tumors.Neuro-oncology · 2022Article
- Combining HypermethylatedCancers · 2021Article
- Review
- In Utero Programming of Testicular Cancer.Journal of developmental biology · 2021Review
- Differential methylation EPIC analysis discloses cisplatin-resistance related hypermethylation and tumor-specific heterogeneity within matched primary and metastatic testicular germ cell tumor patient tissue samples.Clinical epigenetics · 2021Article
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTesticular germ cell cancer (TGCC), being the most frequent malignancy in young Caucasian males, is initiated from an embryonic germ cell. This study determines intratumour heterogeneity to unravel tumour progression from initiation until metastasis.
methodsIn total, 42 purified samples of four treatment-resistant nonseminomatous (NS) TGCC were investigated, including the precursor germ cell neoplasia in situ (GCNIS) and metastatic specimens, using whole-genome and targeted sequencing. Their evolution was reconstructed.
resultsIntratumour molecular heterogeneity did not correspond to the supposed primary tumour histological evolution. Metastases after systemic treatment could be derived from cancer stem cells not identified in the primary cancer. GCNIS mostly lacked the molecular marks of the primary NS and comprised dominant clones that failed to progress. A BRCA-like mutational signature was observed without evidence for direct involvement of BRCA1 and BRCA2 genes.
conclusionsOur data strongly support the hypothesis that NS is initiated by whole-genome duplication, followed by chromosome copy number alterations in the cancer stem cell population, and accumulation of low numbers of somatic mutations, even in therapy-resistant cases. These observations of heterogeneity at all stages of tumourigenesis should be considered when treating patients with GCNIS-only disease, or with clinically overt NS.
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