Our research program explores the fundamental question of how immune microenvironments dynamically orchestrate the balance between regenerative repair, homeostatic maintenance, and pathological transformation across diverse biological contexts. Through three interconnected research areas, we investigate the temporal evolution of immune landscapes and their capacity to either promote or suppress disease progression. 

In melanoma, an aggressive skin cancer arising from pigment-producing melanocytes, we examine how innate immune components, particularly macrophages and natural killer cells, regulate the transition between therapy-responsive and therapy-resistant states, seeking to understand why promising targeted therapies often fail over time despite initial efficacy. This work reveals that immune microenvironments undergo critical temporal remodeling that drives treatment failure, suggesting that therapeutic durability depends on maintaining favorable immune dynamics rather than simply eliminating malignant cells.

Our research on vitiligo, an autoimmune condition that destroys pigment-producing melanocytes leading to characteristic white patches on the skin, and melanocyte stem cells explores the complementary question of how immune-mediated inflammation can be harnessed to promote beneficial regenerative rather than destructive responses. We investigate how different immune cell populations create instructive microenvironments that guide melanocyte stem cell proliferation, migration and fate decisions during repigmentation. This work challenges traditional views of inflammation as purely pathological, instead revealing how inflammatory signals can orchestrate controlled regenerative programs when properly regulated.

Our comparative studies with African spiny mice provide a unique evolutionary perspective on these themes by examining a species that has evolved to maintain regenerative microenvironments that override carcinogenic insults. These remarkable animals demonstrate that the same cellular processes (proliferation, migration, and immune activation) can be channeled through fundamentally different networks depending on the context. By investigating how spiny mice transform potentially oncogenic stimuli into controlled regenerative programs, we seek to determine if the mechanisms used for cancer resistance in spiny mice can be applied to cancer-prone animals such as the laboratory mouse and humans.

Collectively, this research addresses the central hypothesis that immune microenvironments function as master regulators that determine whether tissue responses favor regeneration, homeostasis, or pathological transformation. Through understanding the fundamental principles governing these dynamic immune-tissue interactions, we aim to develop therapeutic strategies that can reprogram immune microenvironments to promote favorable outcomes across cancer treatment, autoimmune disease and regenerative medicine.

My teaching centers on bridging fundamental cell biology with clinical medicine, particularly examining how disruptions in normal cellular processes contribute to human disease. In my undergraduate course, I guide students through a systematic exploration that begins with molecular mechanisms within individual cells and progresses to complex tissue functions and pathological states. I am particularly interested in helping students develop the analytical framework necessary to connect basic cellular processes with pharmaceutical interventions and current therapeutic strategies. My approach emphasizes the translational aspects of cell biology, incorporating guest lectures from clinical researchers and encouraging student presentations on disease topics that extend beyond traditional coursework. In this course, students first master fundamental cellular mechanisms, which allows them to meaningfully understand how these systems fail in conditions such as cancer and immune dysfunction. Through this progression, I encourage students to think critically about the molecular basis of disease and to appreciate how research discoveries translate into clinical applications.

• Postdoctoral Research, Adult Stem Cells and their Relationship to Cancer Initiation, UCLA
• PhD, Developmental Biology, Washington University

Andrew is interested in exploring the causes and conditions that facilitate skin cancer initiation and progression from resident stem cell populations.  Andrew received his Ph.D. in Developmental Biology from Washington University in St. Louis.  For his postdoctoral research, he studied adult stem cells and their relationship to cancer initiation at UCLA with Bill Lowry.

Browse PubMed for a complete listing of Dr. White's publications

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