Long-term Morbidity of Testicular Cancer Treatment

Fung, Chunkit; Fosså, Sophie D.; Williams, AnnaLynn; Travis, Lois B.

doi:10.1016/j.ucl.2015.05.002

Cited by 54 publications

(24 citation statements)

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“…The chemotherapeutic agent cisplatin, known to accumulate DNA adducts in blood cells of treated patients during the course of multiple therapy cycles [Reed et al, 1986], has also been shown to persist long-term (1.5 to 22 months) in organs of cancer patients after the cessation of chemotherapy [Poirier et al, 1987;Poirier et al, 1992]. Because cisplatin is considered responsible for secondary malignancies occurring in testicular cancer patients [Fung et al, 2015], the long-term persistence of cisplatin-DNA adducts may contribute to tumor induction. Human DNA adduct levels may be modulated by an individual's metabolic capacity.…”

Section: Dna Damage In Humans: Exposure Documentation and Molecular Dmentioning

confidence: 99%

Linking DNA adduct formation and human cancer risk in chemical carcinogenesis

Poirier

2016

Environ and Mol Mutagen

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Over two centuries ago, Sir Percival Pott, a London surgeon, published a pioneering treatise showing that soot exposure was the cause of high incidences of scrotal cancers occurring in young men who worked as chimney sweeps. Practicing at a time when cellular pathology was not yet recognized, Sir Percival nonetheless observed that the high incidence and short latency of the chimney sweep cancers, was fundamentally different from the rare scrotal cancers typically found in elderly men. Furthermore, his diagnosis that the etiology of these cancers was related to chimney soot exposure, was absolutely accurate, conceptually novel, and initiated the field of "occupational cancer epidemiology." After many intervening years of research focused on mechanisms of chemical carcinogenesis, briefly described here, it is clear that DNA damage, or DNA adduct formation, is "necessary but not sufficient" for tumor induction, and that many additional factors contribute to carcinogenesis. This review includes a synopsis of carcinogen-induced DNA adduct formation in experimental models and in the human population, with particular attention paid to molecular dosimetry and molecular cancer epidemiology. Environ. Mol. Mutagen. 57:499-507,

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Section: Dna Damage In Humans: Exposure Documentation and Molecular Dmentioning

confidence: 99%

Linking DNA adduct formation and human cancer risk in chemical carcinogenesis

Poirier

2016

Environ and Mol Mutagen

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“…Up to 20% of patients have cisplatin‐resistant tumors and will eventually die of their disease (Einhorn, ). Furthermore, there is significant therapy‐related toxicity in patients treated for GCTs, including pulmonary complications, hearing loss, early onset cardiovascular disease, and second malignancies (Fung et al ., , ).…”

Section: Introductionmentioning

confidence: 99%

Identification of testicular cancer driver genes by a cross‐species comparative oncology approach

Sanchez

Pierce

et al. 2019

Andrology

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Background: Germ cell tumors arise in the testis, ovary, or extragonadal locations and have a wide range of histopathological and clinical presentations. The relative lack of animal models of germ cell tumors has impeded functional assessment of candidate driver genes. Previously, we described the development of testicular germ cell tumors in zebrafish carrying a mutation in bmpr1bb, a BMP family receptor, and demonstrated that human germ cell tumors have defects in BMP signaling. Objective: To further credential the zebrafish model for studies of human germ cell tumor, and to elucidate conserved genetic programs underlying the development of germ cell tumor. Materials and Methods: We used genetic techniques to ablate the germ cell lineage in developing fish and tested tumors for lossof-heterozygosity of the wild-type allele of bmpr1bb. We performed comparative gene expression profiling of zebrafish and human germ cell tumors and carried out functional studies of selected genes. Results: Ablation of germ cells completely prevents testis tumor formation in the fish, definitively establishing the germ cell origin of the tumors. Germ cell tumors in bmpr1bb heterozygous mutants retain the wild-type allele, indicating haploinsufficiency of bm-pr1bb as the mechanism of tumor formation. Comparison of RNA-Seq and microarray data from human and zebrafish germ cell tumors revealed a unique overlapping signature shared by the zebrafish tumors with human seminomas, yolk sac tumors, and embryonal carcinomas. The most highly conserved gene set in this cross-species analysis included potential driver genes such as JUP, which we show to be essential for germ cell tumor cell growth. Conclusion: Our findings highlight the value of cross-species comparative oncology for the identification of candidate human cancer genes.

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“…GCT survivors cured with surgery, cisplatin combination chemotherapy, and/or radiotherapy live for decades and may experience late toxicities derived from such treatments. These include secondary malignancies, cardiovascular, neuro‐, renal, and pulmonary toxicity, hypogonadism, infertility, and a decline in quality of life (QoL) . Cognitive abilities were reported to decline with cancer treatment in multiple cancer diagnoses; however, available studies mostly evaluated immediate to short‐term cognitive functioning .…”

Section: Introductionmentioning

confidence: 99%

Long-Term Cognitive Functioning in Testicular Germ-Cell Tumor Survivors

et al. 2018

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In this study, long-term survivors of germ-cell tumors have reported cognitive impairment after curative treatment with radiotherapy and chemotherapy compared with controls who had treatment with orchiectomy only. These data provide an argument against the use of adjuvant radiotherapy for stage I seminoma. Unnecessary overtreatment with chemotherapy and additional radiotherapy after chemotherapy should be avoided.

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Long-term Morbidity of Testicular Cancer Treatment

Cited by 54 publications

References 100 publications

Linking DNA adduct formation and human cancer risk in chemical carcinogenesis

Linking DNA adduct formation and human cancer risk in chemical carcinogenesis

Identification of testicular cancer driver genes by a cross‐species comparative oncology approach

Long-Term Cognitive Functioning in Testicular Germ-Cell Tumor Survivors

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