Abstract:
Malignant melanoma, the most aggressive form of skin cancer, is characterized
by unpredictable growth patterns, and its mortality rate has remained alarmingly
high over recent decades, despite various treatment approaches. One promising
strategy for improving outcomes in melanoma patients lies in the early use of
biomarkers to predict prognosis. Biomarkers offer a way to gauge patient outlook
early in the disease course, facilitating timely, targeted intervention. In recent
years, considerable attention has been given to the immune response’s role in
melanoma, given the tumor’s high immunogenicity and potential responsiveness
to immunologic treatments. Researchers are focusing on identifying predictive
biomarkers by examining both cancer cell biology and immune interactions
within the tumor microenvironment (TME). This approach has shed light on
tumor-infiltrating lymphocytes (TILs), a type of immune cell found within the
tumor. TILs have emerged as a promising area of study for their potential to serve
as both a prognostic indicator and therapeutic target in melanoma. The presence
of TILs in melanoma tissue can often signal a positive immune response to the
cancer, with numerous studies suggesting that TILs may improve patient
prognosis. This review delves into the prognostic value of TILs in melanoma,
assessing how these immune cells influence patient outcomes. It explores the
mechanisms through which TILs interact with melanoma cells and the potential
clinical applications of leveraging TILs in treatment strategies. While TILs present
a hopeful avenue for prognostication and treatment, there are still challenges.
These include understanding the full extent of TIL dynamics within the TME and
overcoming limitations in TIL-based therapies. Advancements in TIL
characterization methods are also critical to refining TIL-based approaches. By
addressing these hurdles, TIL-focused research may pave the way for improved
diagnostic and therapeutic options, ultimately offering better outcomes for
melanoma patients.