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Working model for CAMKK2’s proposed tumor-extrinsic role in prostate cancer. We propose that Camkk2 KO in the liver and/or pancreas protects against metabolic syndrome. One consequence of this is lowered circulating insulin (or some insulin-like molecule), which slows early primary tumor growth and later metastatic colonization through decreasing cancer cell-intrinsic, oncogenic mTOR signaling.
