Key result
In the presence of platelets, P2Y12 inhibition and recombinant apyrase reduced platelet-enhanced ovarian cancer cell proliferation, suggesting P2Y12 affects primary tumor growth in mice.
Why the study?
Does P2Y12 inhibition reduce tumor growth and cancer cell proliferation in ovarian cancer models?
Does P2Y12 inhibition reduce tumor growth and cancer cell proliferation in ovarian cancer models?
Inhibition of P2Y12 on platelets reduces platelet-enhanced ovarian cancer cell proliferation, suggesting a potential novel adjuvant therapeutic option for ovarian cancer.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for P2Y12 blockade in ovarian cancer; leaves open clinical translation from preclinical models.
mice. Finally, knockdown of ecto-apyrase (CD39) on ovarian cancer cells increased tumor growth in tumor-bearing mice. Although in the absence of platelets, ADP, the P2Y12 inhibitor, recombinant apyrase, or knockdown of CD39 did not affect cancer cell proliferation, in the presence of platelets, the P2Y12 inhibitor and recombinant apyrase reduced and knockdown of CD39 increased platelet-enhanced cancer cell proliferation. These results suggest that P2Y12 on platelets and ADP concentration at the interface between cancer cells and platelets affect the growth of primary ovarian cancer tumors in mice. If additional studies in mice and in pilot human trials confirm our results, inhibition of P2Y12 might be a new therapeutic option that can be used in adjuvant to the traditional surgery and chemotherapy in patients with ovarian cancer.
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Cho et al. (2017) studied Ovarian cancer. P2Y12 inhibitor, recombinant apyrase, or CD39 knockdown was evaluated on Tumor growth and cancer cell proliferation. In the presence of platelets, P2Y12 inhibition and recombinant apyrase reduced platelet-enhanced ovarian cancer cell proliferation, suggesting P2Y12 affects primary tumor growth in mice.
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