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494 results on '"Oosterhuis, J. Wolter"'

1. Integrated genomic analysis reveals aberrations in WNT signaling in germ cell tumors of childhood and adolescence

Author

Xu, Lin, Pierce, Joshua L, Sanchez, Angelica, Chen, Kenneth S, Shukla, Abhay A, Fustino, Nicholas J, Stuart, Sarai H, Bagrodia, Aditya, Xiao, Xue, Guo, Lei, Krailo, Mark D, Shaikh, Furqan, Billmire, Deborah F, Pashankar, Farzana, Bestrashniy, Jessica, Oosterhuis, J Wolter, Gillis, Ad JM, Xie, Yang, Teot, Lisa, Mora, Jaume, Poynter, Jenny N, Rakheja, Dinesh, Looijenga, Leendert HJ, Draper, Bruce W, Frazier, A Lindsay, and Amatruda, James F

Subjects
Cancer, Genetics, Pediatric, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Male, Child, Infant, Female, Young Adult, Humans, Adolescent, Infant, Newborn, Child, Preschool, Adult, Wnt Signaling Pathway, Neoplasms, Germ Cell and Embryonal, Teratoma, Testicular Neoplasms, Genomics
Abstract

Germ cell tumors (GCTs) are neoplasms of the testis, ovary and extragonadal sites that occur in infants, children, adolescents and adults. Post-pubertal (type II) malignant GCTs may present as seminoma, non-seminoma or mixed histologies. In contrast, pre-pubertal (type I) GCTs are limited to (benign) teratoma and (malignant) yolk sac tumor (YST). Epidemiologic and molecular data have shown that pre- and post-pubertal GCTs arise by distinct mechanisms. Dedicated studies of the genomic landscape of type I and II GCT in children and adolescents are lacking. Here we present an integrated genomic analysis of extracranial GCTs across the age spectrum from 0-24 years. Activation of the WNT pathway by somatic mutation, copy-number alteration, and differential promoter methylation is a prominent feature of GCTs in children, adolescents and young adults, and is associated with poor clinical outcomes. Significantly, we find that small molecule WNT inhibitors can suppress GCT cells both in vitro and in vivo. These results highlight the importance of WNT pathway signaling in GCTs across all ages and provide a foundation for future efforts to develop targeted therapies for these cancers.

Published
2023

3. Response to letter to the editor: ‘Gonadal tumour screening in XY gonadal dysgenesis’

Author

Pathologie patiënten zorg, Pathologie Groep Van Diest, Hannema, Sabine E., Wolffenbuttel, Katja P., van Bever, Yolande, Bruggenwirth, Hennie T., Hersmus, Remko, Oosterhuis, J. Wolter, Looijenga, Leendert H.J., Pathologie patiënten zorg, Pathologie Groep Van Diest, Hannema, Sabine E., Wolffenbuttel, Katja P., van Bever, Yolande, Bruggenwirth, Hennie T., Hersmus, Remko, Oosterhuis, J. Wolter, and Looijenga, Leendert H.J.

Published
2024

6. Mediastinal germ cell tumors: many questions and perhaps an answer

Author

Oosterhuis, J. Wolter and Looijenga, Leendert H.J.

Subjects
Tumor proteins -- Health aspects, Germinoma -- Diagnosis -- Care and treatment -- Genetic aspects, Gene mutation -- Health aspects, Health care industry
Abstract

Some germ cell tumors (GCTs) in men develop into hematologic malignancies; however, the clonal origins of such malignancies remain unknown. In this issue of the JCI, Taylor, Donoghue, et al. unravel the clonal relationship between primary mediastinal nonseminomas (PMNs) and hematologic somatic-type malignancies (HSTMs). Whole-exome sequencing was used to construct phylogenetic trees of the PMNs and the ensuing HSTM clones. HSTMs were derived from multiple distinct clones not detected within the PMNs. Clones from PMNs and HSTMs shared a common precursor, arguably an embryonal carcinoma cell resulting from a reprogrammed primordial germ cell from the thymus. Mutational and copy number variation analysis of a large cohort of patients with PMNs also demonstrated a high prevalence of TP53 mutations not found in testicular nonseminomas. These data likely explain why patients with PMNs are frequently resistant to platinum-based chemotherapy and provide TP53 mutations as potential targets., Germ cell tumors Earlier studies determined that hematologic somatic-type malignancies (HSTMs) and the primary mediastinal nonseminomas (PMNs) from which they originate (1) may share an isochromosome 12p (duplication of the [...]

Published
2020
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12. Undetectable anti-Mullerian hormone and inhibin B do not preclude the presence of germ cell tumours in 45,X/46,XY or 46,XY gonadal dysgenesis

Author

Hannema, Sabine E., Wolffenbuttel, Katja P., van Bever, Yolande, Brüggenwirth, Hennie T., van den Berg, Sjoerd A.A., Hersmus, Remko, Oosterhuis, J. Wolter, Looijenga, Leendert H.J., Hannema, Sabine E., Wolffenbuttel, Katja P., van Bever, Yolande, Brüggenwirth, Hennie T., van den Berg, Sjoerd A.A., Hersmus, Remko, Oosterhuis, J. Wolter, and Looijenga, Leendert H.J.

Abstract

Objective: Individuals with 45,X/46,XY or 46,XY gonadal dysgenesis are at increased risk of germ cell malignancies. Therefore, prophylactic bilateral gonadectomy is advised in girls and considered in boys with atypical genitalia for undescended, macroscopically abnormal gonads. However, severely dysgenetic gonads may not contain germ cells rendering gonadectomy unnecessary. Therefore, we investigate if undetectable preoperative serum anti-Müllerian hormone (AMH) and inhibin B can predict the absence of germ cells, (pre)malignant or otherwise. Design, Patients and Measurements: Individuals who had undergone bilateral gonadal biopsy and/or gonadectomy because of suspected gonadal dysgenesis in 1999–2019 were included in this retrospective study if preoperative AMH and/or inhibin B were available. Histological material was reviewed by an experienced pathologist. Haematoxylin and eosin and immunohistochemical stainings for SOX9, OCT4, TSPY and SCF (KITL) were used. Results: Thirteen males and 16 females were included, 20 with 46,XY and 9 with 45,X/46,XY DSD. Three females had dysgerminoma alongside gonadoblastoma; two gonadoblastoma, one germ cell neoplasia in situ (GCNIS) and three males had pre-GCNIS and/or pre-gonadoblastoma. Gonadoblastoma and/or dysgerminoma were present in 3/11 individuals with undetectable AMH and inhibin B, one of whom also had non-(pre)malignant germ cells. Of the other 18, in whom AMH and/or inhibin B were detectable, only one had no germ cells. Conclusions: Undetectable serum AMH and inhibin B cannot reliably predict the absence of germ cells and germ cell tumours in individuals with 45,X/46,XY or 46,XY gonadal dysgenesis. This information should help in counselling about prophylactic gonadectomy, taking into account both the germ cell cancer risk and potential for gonadal function.

Published
2023

13. Age-incidence patterns of seminoma and nonseminoma among males and females in Germany and the United States, 2008–2016

Author

Stang, Andreas, Trocchi, Pietro, Kajüter, Hiltraud, Trabert, Britton, Oosterhuis, J. Wolter, McGlynn, Katherine A., Stang, Andreas, Trocchi, Pietro, Kajüter, Hiltraud, Trabert, Britton, Oosterhuis, J. Wolter, and McGlynn, Katherine A.

Abstract

Background & objectives: The comparison of the incidence of gonadal germ cell tumors among males and females can provide insights that cannot be gained by separately studying these tumors. Material and methods: Incidence data on male and female gonadal germ cell tumors were drawn from the cancer registries of North Rhine-Westphalia, Germany, and the United States Surveillance, Epidemiology and End Results program, for non-Hispanic White persons only, for the years 2008–2016. We estimated age-standardized and age-, and histology-specific incidence rates. Results: We included 21,840 male and 716 female gonadal germ cell tumors. Incidence rates among males were higher in Germany (95.8 per million, standard error [SE] 1.1) than in the United States (68.0, SE 0.6), while incidence rates among females were lower in Germany (1.9, SE 0.2) than in the United States (2.6, SE 0.1). The characteristic peak of infantile (age 0–4 years) germ cell tumors among males were missing among females. The age peak of ovarian germ cell tumors occurred 15–20 years earlier (Germany: 10–14 years, United States: 15–19 years) than the age peak of testicular germ cell tumors (30–34 years). The three most common testicular germ cell tumors histologies were seminoma, mixed germ cell tumors, and embryonal carcinoma Among females, the three most common ovarian germ cell tumors histologies were teratoma, yolk sac tumor, monodermal teratomas, and somatic-type tumors arising from dermoid cysts in both countries. Discussion: The characteristic peak of infantile (age 0–4 years) germ cell tumors among males was missing among females. The shapes of the age-specific incidence curves are similar for males and females in Germany and the United States, though with much lower incidence rates in females, suggesting a common pathogenesis. Conclusion: The lower rates among females may be due to the lower number of initiated tumors in the absence of the Y-chromosome, and the earlier peak among females may be

Published
2023

26. Gonadal tumours and DSD

Author

Looijenga, Leendert H.J., Hersmus, Remko, de Leeuw, Bertie H.C.G.M., Stoop, Hans, Cools, Martine, Oosterhuis, J. Wolter, Drop, Stenvert L.S., and Wolffenbuttel, Katja P.

Published
2010
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27. Gonadal Outcome in 17beta-HSD deficiency and 5alpha-reductase deficiency

Author

Boogers, Lidewij S., Bruggenwirth, Hennie T., van Bever, Yolande, Hersmus, Remko, Bryce, Jilian, Ahmed, S. Faisal, Lucas-Herald, Angela K., Baronio, Federico, Cools, Martine, Ellaithi, Mona, Globa, Evgenia, Guran, Tulay, Tosun, Busra Gurpinar, Hiort, Olaf, Holterhus, Paul-Martin, McElreavey, Ken, Niedziela, Marek, Stancampiano, Marianna Rita, Wolffenbuttel, Katja P., Oosterhuis, J. Wolter, Looijenga, Leendert H. J., Hannema, Sabine E., Internal medicine, Amsterdam Gastroenterology Endocrinology Metabolism, Pediatrics, and Amsterdam Reproduction & Development

Published
2021

36. The Y deletion gr/gr and susceptibility to testicular germ cell tumor

Author

Nathanson, Katherine L., Kanetsky, Peter A., Hawes, Rachel, Vaughn, David J., Letrero, Richard, Tucker, Kathy, Friedlander, Michael, Phillips, Kelly-Anne, Hogg, David, Jewett, Michael A.S., Lohynska, Radka, Daugaard, Gedske, Richard, Stephane, Chompret, Agnes, Bonaiti-Pellie, Catherine, Heidenreich, Axel, Olah, Edith, Geczi, Lajos, Bodrogi, Istvan, Ormiston, Wilma J., Daly, Peter A., Oosterhuis, J. Wolter, Gillis, Ad J.M., Looijenga, Leendert H.J., Guilford, Parry, Fossa, Sophie D., Heimdal, Ketil, Tjulandin, Sergei A., Liubchenko, Ludmila, Stoll, Hans, Weber, Walter, Rudd, Matthew, Huddart, Robert, Crockford, Gillian P., Forman, David, Oliver, D. Timothy, Einhorn, Lawrence, Weber, Barbara L., Kramer, Joan, McMaster, Mary, Greene, Mark H., Pike, Malcolm, Cortessis, Victoria, Chen, Chu, Schwartz, Stephen M., Bishop, D. Timothy, Easton, Douglas F., Stratton, Michael R., and Rapley, Elizabeth A.

Subjects
Germ cell tumors -- Research, Germ cell tumors -- Diagnosis, Germ cell tumors -- Risk factors, Human genetics -- Research, Biological sciences
Published
2005

41. Heterogeneous X inactivation in trophoblastic cells of human full-term female placentas

Author

Looijenga, Leendert H. J., Gillis, Ad J. M., Verkerk, Annemieke J.M.H., Putten, Wim L.J. van, and Oosterhuis, J. Wolter

Subjects
Dosage compensation (Genetics) -- Research, Trophoblast -- Genetic aspects, Placenta -- Genetic aspects, Biological sciences
Abstract

Methylation of the androgen receptor in a human full-term placenta is specific for trophoblastic cells, and the X chromosome can be of paternal origin or maternal origin. Methylation status of the polymorphic androgen-receptor gene has been studied using PCR in full-term human female placentas. Sites investigated are methylated specifically on the inactive X chromosome. No methylation was seen in microdissected stromal tissue of the placenta or umbilical cord. X inactivation was preferentially maternal in three of nine placentas for which two closely apposed samples were studied. In one it was preferentially paternal and in five heterogeneous. Two others had regions with balanced preferentially maternal and preferentially paternal X inactivation.

Published
1999

44. Human growth-differentiation factor 3 (hGDF3): developmental regulation in human teratocarcinoma cell lines and expression in primary testicular germ cell tumours

Author

Caricasole, Andrea AD, van Schaik, Ron HN, Zeinstra, Laura M, Wierikx, Cristel DJ, van Gurp, Ruud JHLM, van den Pol, Mirjam, Looijenga, Leendert HJ, Oosterhuis, J Wolter, Pera, Martin F, Ward, Andrew, de Bruijn, Diederik, Kramer, Piet, de Jong, Frank H, and van den Eijnden-van Raaij, Adriana JM

Published
1998
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50. JKT-1 is not a human seminoma cell line

Author

de Jong, Jeroen, Stoop, Hans, Gillis, Ad J. M., van Gurp, Ruud J. H. L. M., van Drunen, Ellen, Beverloo, H. Berna, Lau, Yun-Fai Chris, Schneider, Dominik T., Sherlock, Jon K., Baeten, John, Hatakeyama, Shingo, Ohyama, Chikara, Oosterhuis, J. Wolter, and Looijenga, Leendert H. J.

Published
2007

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