Adam Telerman, M.D., Ph.D. Director of research CNRS

Director of research CNRS
 

Tumor Reversion project: Reprogramming the tumor cells

EMBO Rep (2024)25: 1962 - 1986 https://doi.org/10.1038/s44319-024-00108-7

The main interest in the field of cancer research is to understand how a normal cell becomes malignant. Undoubtedly this is already a complex question and today, many of the molecular events leading to the transformed phenotype have been, and are thoroughly investigated, with every day delivering new and exciting answers.

We asked a different question: how does a tumor cell quit its malignant status, and thus, revert?

This question has been quite neglected and much if not most of the work remains to be done. In order to study this issue, we first established a series of biological models of tumor reversion. From human leukemia and solid tumor cell lines (breast, colon, lung and melanoma) we derived cells with a highly suppressed malignant phenotype. These revertants enabled us to trace the molecular modifications that are implicated in the process of tumor reversion. Today we are investigating the genetics and epigenetics leading to tumor reversion. More specifically, we are working on material from cancer patients and are investigating how the molecular pathways of tumor reversion are switched on. Understanding these “molecular switches” could lead to a different treatment of cancer than the one proposed today.

 

Selected publications

TCTP regulates genotoxic stress and tumorigenicity via intercellular vesicular signaling. Amson R, Senff-Ribeiro A, Karafin T, Lespagnol A, Honoré J, Baylot V, Banroques J, Tanner NK, Chamond N, Dimitrov JD, Hoebeke J, Droin NM, Job B, Piard J, Bommer UA, Choi KW, Abdelfatah S, Efferth T, Telerman SB, Geyer FC, Reis-Filho J, Telerman A. EMBO Rep. 2024 Apr;25(4):1962-1986.

TCTP/tpt1 Remodeling Signaling from Stem Cell to Disease. Telerman, A and Amson, R, Editors; Springer International Publishing AG, 2017, Cham, Switzerland ; Volume 64, pp. 1–309.  

TPT1/TCTP-regulated pathways in phenotypic reprogramming. Amson R, Pece S, Marine JC, Di Fiore PP and Telerman A. Trends in Cell Biology 2013 January.                           

Reciprocal repression between P53 and TCTP. Amson R, Pece S, Lespagnol A, Vyas R, Mazzarol G, Tosoni D, Colaluca I, Viale G, Rodrigues-Ferreira S, Wynendaele J, Chaloin O, Hoebeke J, Marine JC, Di Fiore PP, Telerman A. Nature Med 2012 Jan18 (1): 91-100 

The molecular programme of tumour reversion: the steps beyond malignant transformation. Telerman A, Amson R. Nat Rev Cancer 2009 Mar;9(3):206-16.

Exosome secretion, including the DNA damage-induced p53-dependent secretory pathway, is severely compromised in TSAP6/Steap3-null mice. Lespagnol A, Duflaut D, Beekman C, Blanc L, Fiucci G, Marine JC, Vidal M, Amson R, Telerman A. Cell Death Differ 2008 Nov 15 (11):1723-33

Translationally controlled tumor protein is a target of tumor reversion. Tuynder M, Fiucci G, Prieur S, Lespagnol A, Geant A, Beaucourt S, Duflaut D, Besse S, Susini L, Cavarelli J, Moras D, Amson R, Telerman A. Proc Natl Acad Sci USA 2004; 101: 15364-15369

Biological models and genes of tumor reversion: Cellular reprogramming through tpt1/TCTP and SIAH-1. Tuynder M, Susini L, Prieur S, Besse S, Fiucci G, Amson R, Telerman A. Proc. Natl. Acad. Sci. USA 2002; 99: 14976-14981  

Inhibition of Presenilin 1 expression is promoted by p53 and p21WAF-1 and results in apoptosis and tumor suppression. Roperch JP, Alvaro V, Prieur S, Tuynder M, Nemani M, Lethrosne F, Piouffre L, Gendron MC, Israeli D, Dausset J, Oren M, Amson R, Telerman A. Nature Med 1998; 4, 835-838

A model for tumor suppression using H-1 parvovirus. Telerman A, Tuynder M, Dupressoir T, Robaye B, Sigaux F, Shaulian E, Oren M, Rommelaere J, Amson R. Proc. Natl. Acad. Sci. USA 1993; 90, 8702-8706