Background: Biomarkers for clinical response to immunotherapy in melanoma patients had been explored. Intrinsically, a higher melanoma tumor mutational load and a specifically neoantigen peptide landscape is associated with clinical benefit in anti-CTLA-4 therapy [1]. Extrinsically, an active immune microenvironment as well as a lower tumor burden favors clinical response to immunotherapy[2,3,4]. Furthermore, tumors growing in different sites are biologically heterogeneous in growth potential, as well as in tumor response to anti-cancer therapies[5].
Methods: Characterize immune cell subsets that infiltrate tumor microenvironments in sites of metastatic disease at rapid autopsy by using histochemical methods and characterize immune-related gene expression in different tumors using NanoString technology. Identify within-patient spatio-temporal differences in the above immune parameters and correlate them with differences in patients’ clinical course.
Preliminary data: In all the autopsy metastasis samples of 7 patients (median metastasis sites, 9; range, 4-20), surprisingly, there is unanimously scant tumor infiltrating leukocytes (TILs) compared with plentiful of TILs in their pre-mortal biopsies. Those patients had all been received glucocorticoids in the late-stage of the disease for the symptom control of brain metastasis.
Conclusion: Glucocorticoids might have the potential of eliminating the immune cells in melanoma. Mice model should be established to identity the exact role of glucocorticoids in melanoma as the response of immunotherapy largely depends on TILs and in clinical setting, physicians should be more careful of using glucocorticoids on immunotherapy candidates.
Disclosures: The authors declare that they have no conflict.