blood-cancer

CRISPR gene-editing screens are mapping the genetic roots of treatment failure in blood cancer.

This protocol describes using CRISPR-Cas9 knockout screens to systematically identify genes mediating drug resistance in AML. Cells surviving better when a particular gene is deleted implicate that gene in resistance to cytarabine or venetoclax.

CRISPR gene-editing screens are mapping the genetic roots of treatment failure in blood cancer.

Key Findings

CRISPR-Cas9 screens identify drug resistance genes in AML systematically
Genes whose knockout increases drug tolerance implicated as resistance drivers
Applicable to cytarabine and venetoclax resistance
Identified genes provide rational targets for combination therapies

Implications

Methodology accelerates AML resistance discovery, potentially enabling combination therapies that prevent relapse.

Caveats

Methods protocol paper; abstract-only. Results require extensive experimental and clinical validation.

Source: Methods in cell biology — 2026-01-01

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CRISPR gene-editing screens are mapping the genetic roots of treatment failure in blood cancer.

Key Findings

Implications

Caveats

Read more

Landmark DCIS trial, CRC microbiome & AML combos

Colorectal Cancer Microbiome Discovery Platform

GBM Tumor Microenvironment Drug Target Atlas

BET Inhibitor Target Selectivity Database