Timeframe: 2019 -2020
Goal: Assess whether supressing checkpoints or signaling by a specific chemokine (CXCL12) can enhance immune response
Principal Investigator: Venu Pillarisetty, MD, Associate Professor, Division of General Surgery [Extension after CRI Fellowship grant to Kevin Sullivan in Dr. Pillarisetty’s lab, 2016-2019]
Immunotherapy, harnessing the patient’s immune system to precisely target cancer cells, has emerged as a promising approach to treat many cancers. It has been discovered that fibrolamellar carcinoma (FLC) tumors contain a class of immune cells called T cells that potentially could recognize and destroy the cancer cells. However, the therapeutic ability of T cells can be limited by suppressive factors made by both cancer cells and other cells in the tumor such as the abundant fibroblastic stromal cells that give FLC its name. Suppressive molecules in the tumor microenvironment that may limit anti-cancer immune responses include “immune checkpoints” and signaling molecules known as cytokines. The latter include chemokines, small protein chemical messengers that influence cell migration.
This study aimed to determine whether blockade of checkpoints and/or signaling by a specific chemokine (CXCL12) can enhance T cell mediated immunity against fibrolamellar cancer cells, using slice cultures of human FLC tumors.