Nathan Redlich's research while affiliated with Medical College of Wisconsin and other places
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Publications (13)
The loss of p16 is a signature event in Human Papilloma Virus (HPV)-negative head and neck squamous cell carcinoma (HNSCC) that leads to increased Cyclin Dependent Kinase 4/6 (CDK) signaling. Palbociclib, a CDK4/6 inhibitor, is active for the treatment of a subset of HNSCC. In this study, we analyzed patient response data from a phase I clinical tr...
ErbB3 has been widely implicated in treatment resistance, but its role as a primary treatment target is less clear. Canonically ErbB3 requires EGFR or ErbB2 for activation, whereas these two established treatment targets are thought to signal independently of ErbB3. In this study, we show that ErbB3 is essential for tumor growth of treatment-naive...
Targeting defects in metabolism is an underutilized strategy for the treatment of cancer. Arginine auxotrophy resulting from the silencing of argininosuccinate synthetase 1 (ASS1) is a common metabolic alteration reported in a broad range of aggressive cancers. To assess the metabolic effects that arise from acute and chronic arginine starvation in...
Citations
... Furthermore, MYC plays an important role in suppressing the host anti-tumor immune response, through various mechanisms involving modifications to the tumor microenvironment via inhibitory cytokines (e.g., TGFβ and immunomodulatory molecules such as PD-L1, CD47, and MHC I) [26][27][28][29] . While the tumorigenic effects of MYC are well known, the molecular mechanisms by which the mutation or amplification of this gene may confer treatment resistance in HNSCC remains under-investigated 30 . A recent case report of a patient with recurrent/metastatic (R/M) HNSCC highlighted a differential response to nivolumab in metastatic lesions secondary to the acquisition of MYC amplification. ...
... In addition, the expression of TROP-2 has been related to aggressive histopathological characteristics of different tumors, such us increased cell tumor growth, deep tumor depth and early vessel invasion [6]. On the other hand, a tumor-suppressive function has been reported for TROP-2 in cervical cancer, head and neck squamous-cell cancer and lung adenocarcinoma [7][8][9][10]. ...
... A lack of ASS1 expression or ASS1 downregulation is very common in cancer, including myxofibrosarcomas, breast cancer, malignant melanoma, liver cancer, prostate cancer, pancreatic cancer, renal cancer, and osteosarcomas [5][6][7][8]. Several reports have shown that ASS1 is underexpressed in a range of tumors and functions as a tumor suppressor [5][6][7][8][9][10][11][12][13]. Furthermore, ASS1 is associated with chemoresistance, invasion, recurrence, and poor clinical outcomes, including breast cancer, HCC, renal cell carcinoma, and prostate cancer [10,13,14], in which ASS1 expression is lost [8,10,11]. ...
