Immunological heterogeneity in human melanoma: immunogenic alloantigen expression in autologous host.
نویسندگان
چکیده
A patient presented with a primary melanoma, Level IV, 2.5 mm thick; 30 excised lymph nodes were all negative for tumor. Four local recurrences followed in the ensuing 17 months. Tumor cells cultured at this time were epithelioid. Autoimmunization was followed by a disease-free interval of 15 months. Postimmunization, the patient's lymphocytes destroyed his melanoma cells in culture and were stimulated in mixed cell culture by his irradiated tumor cells. Cells grown from the relapsing tumor were spindle/dendritic with bizarre morphology and were not attacked by his lymphocytes in culture. Using a C' fixation technique, DR antigen profiles of the patient's B-cells and both tumor cell types showed that the immunizing tumor was positive for DR antigens 3, 5, and 8, none of which were present on his B-cells which had DR 2 and 4. Both B-cells and immunizing tumor cells were positive for DQ antigens. The relapsing tumor cells were positive for DR2 and negative for all other D region antigens tested. The evidence suggests that given a melanoma of heterogeneous cell population, autoimmunization against the predominant immunogenic cell inhibits tumor growth but allows the ascendance of a nonimmunogenic tumor cell type.
منابع مشابه
HLA-G in skin cancer: a wolf in sheep's clothing?
Despite well-defined and immunogenic tumor antigens, and even in the presence of tumor antigen-specific cytotoxic cells, the immune system does not appear to be very effective in eradicating cells that have undergone malignant transformation. Tumor cells, even though invading and representing a threat, are not truly "foreign" but autologous cells that have become transformed in a subtle way, en...
متن کاملInduction of antigen-specific cytolytic T cells in situ in human melanoma by immunization with synthetic peptide-pulsed autologous antigen presenting cells.
Human melanoma cells can process the MAGE-1 gene product and present the processed nonapeptide EADPTGHSY on their major histocompatibility complex class I molecules, HLA-A1, as a determinant for cytolytic T lymphocytes (CTLs). Considering that autologous antigen presenting cells (APCs) pulsed with the synthetic nonapeptide might, therefore, be immunogenic, melanoma patients whose tumor cells ex...
متن کاملImmunogenicity of oncolytic vaccinia viruses JX-GFP and TG6002 in a human melanoma in vitro model: studying immunogenic cell death, dendritic cell maturation and interaction with cytotoxic T lymphocytes
Oncolytic virotherapy is an emerging immunotherapeutic modality for cancer treatment. Oncolytic viruses with genetic modifications can further enhance the oncolytic effects on tumor cells and stimulate antitumor immunity. The oncolytic vaccinia viruses JX-594-GFP+/hGM-CSF (JX-GFP) and TG6002 are genetically modified by secreting granulocyte-macrophage colony-stimulating factor (GM-CSF) or trans...
متن کاملPersistence of immunogenic pulmonary metastases in the presence of protective anti-melanoma immunity.
We have developed a murine melanoma model that allows us to investigate the mechanisms by which spontaneous, immunogenic melanoma metastases escape immunological destruction in syngeneic mice. In the current study, we tested the hypothesis that loss of immunogenicity is an obligatory step in the persistence of pulmonary metastases. Fragments of syngeneic K1735-M2 tumor were implanted in the out...
متن کاملA comparative study of estrogen receptor beta expression in melanoma and benign melanocytic lesions
Background: Malignant melanoma is the most aggressive form of skin cancer. In contrast to other tumors, the role of estrogen in the initiation and progression of melanoma remains unclear. The aim of this study was to evaluate estrogen receptor beta protein expression in human melanoma tissues and in the benign melanocytic lesions. Method: Twenty-one patients, 11 with cutaneous melanoma and 10 w...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Cancer research
دوره 46 7 شماره
صفحات -
تاریخ انتشار 1986