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Jeudi 20 Juin 2024
Centre de recherche - Paris - Amphithéâtre Hélène Martel-Massignac (BDD)

Lineage- and species-specific sensitivity or resistance to cancer - Insights from RB loss and KRAS activation

It is known but poorly understood why the common effect of “oncogenic” mutations is not cancer.  Lineages that are cancer-prone are far outweighed by those that are cancer-resistant.  On another level, cancer susceptibility of orthologous lineages is also species-specific. For example, human RB null cone photoreceptor precursors are cancer-prone, but cancer resistant in other mammals.  We have deduced the underlying molecular network explaining this difference, generating the first cone-derived murine model of retinoblastoma.  As well as species specificity, RB mutation also provides striking examples of lineage specific susceptibility to transformation. Why one lineage is cancer-prone and another cancer resistant is unknown.  We uncovered a hallmark of lineage-specific susceptibility to RB loss. Remarkably, a tissue can exhibit numerous hallmarks of mature cancer, but if the initiation hallmark is not present, the tissue remains cancer-free. In lung, RB loss or KRAS activation render distinct lineages cancer-prone.  Our cancer initiation hallmark predicts the cancer-prone lineage in both scenarios.  Together our work provides insight into species and lineage specific resistance or susceptibility to neoplastic transformation, raising new strategies for therapeutic intervention.

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Lunenfeld Tanenbaum Research Institute, Canada

Invité(e)(s) par

Biologie cellulaire et Cancer (UMR144)

Institut Curie

Génétique et biologie du développement (UMR3215 / U934)

Institut Curie



Institut Curie

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