p53 · Mutant gain of function · Cancer vulnerabilities

Prives Laboratory

Columbia University

Welcome to our lab

Understanding p53 in every molecular context

The Prives Laboratory investigates how the p53 tumour suppressor senses stress, selects transcriptional programmes and prevents malignant transformation—and how cancer-associated p53 mutants acquire new functions that promote tumour progression.

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Principal investigator

Carol Prives, Ph.D.

Da Costa Professor of Biology

Carol Prives, Ph.D., is the Da Costa Professor of Biology at Columbia University and an internationally recognised leader in p53 biology. Her laboratory has made foundational contributions to understanding p53 DNA binding, transcriptional regulation, protein interactions and mutant gain of function. The programme connects fundamental biochemistry with cancer mechanisms, including MDM2/MDMX control, metabolic pathways, chromatin regulation, invasion and therapeutic strategies for tumours carrying TP53 mutations.

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Research programmes

What we investigate

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Wild-type p53 tetramer engagement with DNA and chromatin can support distinct transcriptional programmes, including arrest, metabolic adaptation and cell death.

Wild-type p53 structure and transcriptional choice

We define how p53 recognises chromatin, binds response elements and selects context-specific programmes of arrest, repair, metabolism and cell death.

A conceptual model of mutant-p53 stabilisation, altered protein partnerships, clonal selection and the emergence of invasive tumour states.

Mutant p53 gain of function and tumour evolution

We investigate when missense p53 mutants acquire oncogenic activities and how those activities depend on cellular lineage, cooperating pathways and tumour architecture.

MDM2 and MDMX form a regulatory circuit that controls p53 ubiquitination, degradation and stress-dependent activation, creating distinct therapeutic interfaces.

MDM2, MDMX and p53 protein stability

We study the regulatory circuitry that keeps wild-type p53 low in unstressed cells while permitting mutant p53 to accumulate in tumours.

The mevalonate pathway supports protein prenylation and Rho/ROCK-dependent cytoskeletal signalling, linking p53 status to invasion and targetable metabolic dependencies.

Metabolism, invasion and therapeutic vulnerabilities

We trace how p53 status rewires the mevalonate pathway, cytoskeletal signalling and tumour invasion to identify mutation-selective treatment opportunities.

Selected publications