Spontaneous Regression Of Melanoma - Letting Us Reaffirm The Significance Of Immunotherapy
Miyagawa, T., Kadono, T., Yamada, D., & Sato, S. (2017). spontaneous regression of melanoma-letting us reaffirm the significance of immunotherapy. Japanese journal of clinical oncology, 47(5), 469–470. https://doi.org/10.1093/jjco/hyx035
View Original Source →Case Details
Disease Location
Lip
Personal Characteristics
46 -year-old male
Clinical Characteristics
Primary cutaneous anaplastic large cell lymphoma (c-alcl), CD4+/CD8+ double-positive phenotype patient was found to have a steadily enlarging nodule, which had been present for 3 weeks on his upper lip the lesion was biopsied and malignant lymphoma was suspected. Physical exam revealed an ulcerated reddish tumor measuring 1.5x1.5cm in diameter on his upper lip and the patient said that the tumor had flattened slightly after the biopsy histopathology of the first biopsy at the referring hospital revealed that the tumor was composed of large anaplastic cells arranged in large clusters with scattered eosinophils ihc revealed most tumor cells expressed CD4, 8, and 30, and expressed partial loss of CD3. Approx. 50% of cells were ki-67 positive. A second biopsy detected clonally rearrange t-cell receptor beta and lambda chain genes ihc of the second specimen revealed that most inflammatory lymphocytes were positive for CD3 and 4, and a small number of cells were positive for CD8. The number of CD30 positive cells was very small
Remission Characteristics
Histopathology of the second biopsy showed a mixture of a large number of inflammatory infiltrating lymphocytes and a small number of large anaplastic cells, suggesting that the tumor was regressing after the second biopsy the tumor started to regress rapidly and completely disappeared within a week the patient remained free of disease 14 months later
Treatment & Mechanisms
Proposed Remission Mechanisms
CD30-cd30l interactions might play a role in the pathophysiology of regression in c-alcl massive infiltrates of t cells in the second biopsy might have been triggered by the damage caused by the first biopsy, the second biopsy may have accelerated this process
Clinical Treatment
None reported
Non-Clinical Treatment
None reported