The inflammatory disorders of the pancreas have two forms, acute and chronic. Acute pancreatitiscauses severe illness and reduces life expectancy. However, besides supportive care, there is no effectivetreatment for the disease due to a lack of understanding of the early cellular events important in thepathophysiology of this disease. Not only is chronic pancreatitis as bad in that it does not heal or improve andonly gets worse over time leading to permanent damage of the pancreas, it is also the top risk factor forpancreatic adenocarcinoma (PDAC).

Prostate cancer is the most common non-cutaneous cancer in American men. In May of 2012, the U.S. Preventive Task Force recommended that serum prostate specific antigen (PSA) screening no longer be recommended as standard clinical practice. A factor contributing to this recommendation is that many prostate cancers diagnosed via PSA-screening are indolent disease that will never progress. Current American Urologic Association recommendations stress informed decision making.

Uterine fibroids (UFs; leiomyomas) are the most important benign neoplastic threat to women's healthworldwide, but disproportionately affect women of color, particularly African American (AA) women, who have athreefold higher incidence rate and relative risk of UFs than Caucasian (CC) women. While the underlyingcause for this risk disparity is not fully understood, recent studies implicate hypovitaminosis D as a majorcontributor.

We respond to PQ3 with our data showing that tumor PD-L1 (CD274, B7-H1) is a major regulator of tumorinflammatory infiltrates. Our preliminary data show that melanoma PD-L1 regulates TIL through severalpreviously unknown tumor-intrinsic and extrinsic mechanisms. We define novel effects of tumor intrinsic PD-L1signaling on tumor proliferation, sensitivity to immune killing, in vivo growth independent of anti-tumorimmunity, and regulation of mTOR signals.

Estrogen receptor (ER)? exhibits an antitumor activity in multiple cancer types in both tumor-intrinsicand -extrinsic manners. However, little is known as to how such activity can be harnessed with high efficacyand precision, nor is it clear which host cell type(s) mediates the tumor-extrinsic function of ER?. These majorknowledge gaps hamper efforts to unleash ER? antitumor activity for cancer therapies. We recently discovereda phosphotyrosine-dependent signaling axis that controls ER? antitumor activity.