Dr. Jhaveri on Acquired Resistance to CDK 4/6 Inhibitors in Breast Cancer

Komal L. Jhaveri, MD
Published: Thursday, May 24, 2018



Komal L. Jhaveri, MD, FACP, medical oncologist, Memorial Sloan Kettering Cancer Center, discusses acquired resistance to CDK 4/6 inhibitors in breast cancer.

Preclinical data may justify combination regimens to address acquired resistance to CDK 4/6 inhibitors, says Jhaveri. Some adaptive responses to CDK 4/6 inhibition may lead to activation of the PI3K pathway. That, Jhaveri says, has justified a triplet combination to be evaluated in the clinic. That is an ongoing effort.

Some data suggest that FGFR1 amplification could be 1 mechanism of resistance. An early data set from the MONALEESA-2 trial showed that FGFR1 amplification from baseline circulating tumor DNA has limited progression-free survival benefit. Though small in number, Jhaveri says it parallels the data that show that FGFR1 amplification is a resistance mechanism.
 
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Komal L. Jhaveri, MD, FACP, medical oncologist, Memorial Sloan Kettering Cancer Center, discusses acquired resistance to CDK 4/6 inhibitors in breast cancer.

Preclinical data may justify combination regimens to address acquired resistance to CDK 4/6 inhibitors, says Jhaveri. Some adaptive responses to CDK 4/6 inhibition may lead to activation of the PI3K pathway. That, Jhaveri says, has justified a triplet combination to be evaluated in the clinic. That is an ongoing effort.

Some data suggest that FGFR1 amplification could be 1 mechanism of resistance. An early data set from the MONALEESA-2 trial showed that FGFR1 amplification from baseline circulating tumor DNA has limited progression-free survival benefit. Though small in number, Jhaveri says it parallels the data that show that FGFR1 amplification is a resistance mechanism.
 



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