Literature DB >> 19560254

Therapeutic potential of Mdm2 inhibition in malignant germ cell tumours.

Sebastian Bauer1, Thomas Mühlenberg, Michael Leahy, Mathias Hoiczyk, Thomas Gauler, Martin Schuler, Leendert Looijenga.   

Abstract

BACKGROUND: Inadequate response to cisplatin-based chemotherapy is associated with poor prognosis in patients with advanced malignant testicular germ cell tumours (TGCTs), especially of the nonseminomatous type. Novel chemotherapeutic agents have failed so far to significantly improve the outcome of such patients. The majority of these tumours express low levels of p53, and TP53 mutations are rarely observed. Murine double minute 2 (Mdm2) inhibitors enhance apoptosis in tumours harbouring wild-type p53.
OBJECTIVE: We sought to investigate the potential therapeutic value of Mdm2 in TGCT-derived cell lines with the histology of nonseminoma. DESIGN, SETTING, AND PARTICIPANTS: The Mdm2 inhibitor nutlin-3 was evaluated alone and in combination with cisplatin in a panel of germ cell tumour (GCT)-derived cell lines (embryonal carcinomas, being the nonseminomatous stem-cell component) with wild-type (NT2 and 2102EP cells) and mutant (NCCIT cells) p53 status. MEASUREMENTS: Biological consequences of Mdm2 inhibition were determined by analysis of the p53 pathway, cell proliferation, and apoptosis. RESULTS AND LIMITATIONS: Nutlin-3 exhibited significant activity (IC50 2.8 μM) in NT2 and 2102EP (wild-type p53) but not in p53-mutant NCCIT cells (<10% inhibition at 10 μM). At concentrations beyond 500 nM, additive effects were seen for the combination of nutlin-3 and cisplatin in NT2 and 2102EP cells but not in NCCIT cells. This correlated with the induction of p53 and its target p21, suggesting an on-target effect of nutlin-3. Moreover, nutlin-3 (5 μM) and cisplatin (0.5 μM) additively induced caspase cleavage and apoptosis in NT2 cells and 2102-EP cells but not in p53-mutant NCCIT cells.
CONCLUSIONS: These results provide strong evidence for further development of pharmacologic Mdm2 inhibition for the treatment of patients suffering from high-risk nonseminomatous TGCT with wild-type p53 status.
Copyright © 2009 European Association of Urology. Published by Elsevier B.V. All rights reserved.

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Year:  2009        PMID: 19560254     DOI: 10.1016/j.eururo.2009.06.014

Source DB:  PubMed          Journal:  Eur Urol        ISSN: 0302-2838            Impact factor:   20.096


  25 in total

1.  Pro- and anti-apoptotic effects of p53 in cisplatin-treated human testicular cancer are cell context-dependent.

Authors:  Alessandra di Pietro; Roelof Koster; Wytske Boersma-van Eck; Wendy A Dam; Nanno H Mulder; Jourik A Gietema; Elisabeth G E de Vries; Steven de Jong
Journal:  Cell Cycle       Date:  2012-11-19       Impact factor: 4.534

2.  Genetic Determinants of Cisplatin Resistance in Patients With Advanced Germ Cell Tumors.

Authors:  Aditya Bagrodia; Byron H Lee; William Lee; Eugene K Cha; John P Sfakianos; Gopa Iyer; Eugene J Pietzak; Sizhi Paul Gao; Emily C Zabor; Irina Ostrovnaya; Samuel D Kaffenberger; Aijazuddin Syed; Maria E Arcila; Raju S Chaganti; Ritika Kundra; Jana Eng; Joseph Hreiki; Vladimir Vacic; Kanika Arora; Dayna M Oschwald; Michael F Berger; Dean F Bajorin; Manjit S Bains; Nikolaus Schultz; Victor E Reuter; Joel Sheinfeld; George J Bosl; Hikmat A Al-Ahmadie; David B Solit; Darren R Feldman
Journal:  J Clin Oncol       Date:  2016-09-30       Impact factor: 44.544

3.  HDMX-L is expressed from a functional p53-responsive promoter in the first intron of the HDMX gene and participates in an autoregulatory feedback loop to control p53 activity.

Authors:  Anna Phillips; Amina Teunisse; Suzanne Lam; Kirsten Lodder; Matthew Darley; Muhammad Emaduddin; Anja Wolf; Julia Richter; Job de Lange; Matty Verlaan-de Vries; Kristiaan Lenos; Anja Böhnke; Frank Bartel; Jeremy P Blaydes; Aart G Jochemsen
Journal:  J Biol Chem       Date:  2010-07-20       Impact factor: 5.157

4.  MDM2 inhibitor MI-319 in combination with cisplatin is an effective treatment for pancreatic cancer independent of p53 function.

Authors:  Asfar S Azmi; Amro Aboukameel; Sanjeev Banerjee; Zhiwei Wang; Momin Mohammad; Jack Wu; Shaomeng Wang; Dajun Yang; Philip A Philip; Fazlul H Sarkar; Ramzi M Mohammad
Journal:  Eur J Cancer       Date:  2010-02-13       Impact factor: 9.162

Review 5.  Molecular Mechanisms of Cisplatin Chemoresistance and Its Circumventing in Testicular Germ Cell Tumors.

Authors:  Silvia Schmidtova; Katarina Kalavska; Lucia Kucerova
Journal:  Curr Oncol Rep       Date:  2018-09-26       Impact factor: 5.075

Review 6.  Emerging Therapeutic Targets for Male Germ Cell Tumors.

Authors:  Christian Daniel Fankhauser; Friedemann Honecker; Jörg Beyer; Peter Karl Bode
Journal:  Curr Oncol Rep       Date:  2015-12       Impact factor: 5.075

Review 7.  Human germ cell tumours from a developmental perspective.

Authors:  J Wolter Oosterhuis; Leendert H J Looijenga
Journal:  Nat Rev Cancer       Date:  2019-08-14       Impact factor: 60.716

8.  p53 hypersensitivity is the predominant mechanism of the unique responsiveness of testicular germ cell tumor (TGCT) cells to cisplatin.

Authors:  Matthias Gutekunst; Moshe Oren; Andrea Weilbacher; Michael A Dengler; Christiane Markwardt; Jürgen Thomale; Walter E Aulitzky; Heiko van der Kuip
Journal:  PLoS One       Date:  2011-04-21       Impact factor: 3.240

Review 9.  Mechanisms of TP53 Pathway Inactivation in Embryonic and Somatic Cells-Relevance for Understanding (Germ Cell) Tumorigenesis.

Authors:  Dennis M Timmerman; Tessa L Remmers; Sanne Hillenius; Leendert H J Looijenga
Journal:  Int J Mol Sci       Date:  2021-05-20       Impact factor: 5.923

Review 10.  Epigenetic alterations as therapeutic targets in Testicular Germ Cell Tumours : current and future application of 'epidrugs'.

Authors:  Ana Rita Cardoso; João Lobo; Vera Miranda-Gonçalves; Rui Henrique; Carmen Jerónimo
Journal:  Epigenetics       Date:  2020-08-12       Impact factor: 4.528

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