Progression or recurrence of cancer occurred in only 25 percent
of palbociclib plus fulvestrant treated patients versus 50 percent of patients treated with fulvestrant alone.
► In a news feature in this week's Science, Ken Garber described the surprisingly, frustratingly messy path
of palbociclib, one of the most promising cancer treatments to come along in years, from its conception in 1995 through its recent, successful phase - II clinical trial.
Not exact matches
While MEK inhibitors are part
of treatment protocols for melanoma,
palbociclib is entering clinical trials for use in melanoma populations.
While one drug, MEK inhibitor, is usually used in advanced - stage melanoma, the other drug, CDK4 / 6 inhibitor,
palbociclib, is currently FDA - approved for treatment
of Estrogen Receptor - positive breast cancer patients.
The treatment arm received
palbociclib together with standard
of care for this population, fulvestrant, a drug that blocks the hormone receptor via a different mechanism than first - line therapies.
«The PALOMA - 3 study showed that
palbociclib extends the time to progression
of disease while maintaining very good quality
of life.»
PALOMA - 1 showed that
palbociclib in combination with the estrogen - production blocker, letrozole, doubled the time it took for metastatic cancer to recur from a median
of 10 months with letrozole plus placebo, to 20 months for
palbociclib plus letrozole.
A new phase 3 study in some
of the most difficult - to - treat patients, women with endocrine - resistant disease, showed that the newly approved drug,
palbociclib, more than doubled the time to cancer recurrence for women with hormone - receptor (HR +) positive metastatic breast cancer.
«While it was known that
palbociclib stalls proliferation by inhibiting CDK4 / 6, inducing proteasomal activity may be an additional mechanism that ensures the completeness
of the cell cycle arrest,» says Dr. Mikael Björklund, one
of the lead authors
of the study.
«Our work suggests that proteasome inhibitors and
palbociclib are a not a good combination, given that they act in opposite directions,» says Professor Matthias Trost
of the Institute
of Cell and Molecular Biosciences at Newcastle University, who co-led the study.
Thermal proteome profiling
of breast cancer cells reveals proteasomal activation by CDK4 / 6 inhibitor
palbociclib, The EMBO Journal (2018).
Mass spectrometry ‐ based cellular thermal shift assay (MS ‐ CeTSA) analysis
of CDK4 / 6 inhibitor
palbociclib targets in MCF7 human breast cancer cells identifies protein complexes including the 20S proteasome.