Non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related mortality worldwide, accounting for approximately 18% of all cancer deaths.1 Despite treatment with platinum-based chemotherapy, the standard of care for first-line therapy, patients with metastatic NSCLC have a median survival of approximately 10 months, and a 5-year survival rate of less than 5%. Immunotherapeutic approaches have demonstrated clinical efficacy in several cancer types, including melanoma, hormone-refractory prostate cancer, and lung cancer.3,4.

Personalized medicine provides a unique opportunity for patients to receive optimized treatment efficacy through individually tailored and targeted therapies. The ability to control the release of therapeutics in targeted tissues with a desired spatial distribution and at an adjustable rate is essential for personalized medicine. However, it is extremely challenging to control the release of a therapeutic drug with the desired timing, while also monitoring the real-time drug distribution in optically turbid deep tissue.

This is a randomized, double-blind, placebo-controlled phase 3 study designed to compare the OS between patients treated with HMA plus vadastuximab talirine (experimental arm) versus patients treated with HMA plus placebo (comparator arm). Patients will be randomized in a 1:1 manner to one of the study arms. Investigators may select either HMA (azacitidine or decitabine).

Applied Research

Aberrant activation of the B cell receptor (BCR) is an emerging hallmark of mature B cell tumors. The BCR initiates a signaling cascade that activates multiple kinases, including SYK, BTK and PI3K?, leading to engagement of the NF-?B, PI3K/AKT, RAS and MAPK pathways, thus promoting proliferation/survival of B cells. Considering this pro-growth outcome, it is not surprising that malignant B cells hijack this signaling module for their benefit.

Factors in the tumor microenvironment promote immunosuppression that permits tumor escape from immune destruction. Our data show that tumor PD-L1 (CD274, B7-H1) is a major regulator of tumor inflammatory lymphocyte (TIL) infiltrate. PD-L1 is widely expressed in many tumors and is the target of two successful new cancer immunotherapy approaches, but is a poor predictor of treatment efficacy.