TY - JOUR
T1 - Immunopathogenesis of ovarian cancer
AU - Torres, M. P.
AU - Ponnusamy, M. P.
AU - Lakshmanan, I.
AU - Batra, Surinder K.
PY - 2009/10
Y1 - 2009/10
N2 - Ovarian cancer, the most aggressive gynecologic cancer, is the foremost cause of death from gynecologic malignancies in the developed world. Over 90% of ovarian cancers arise from the surface epithelium, which are classified as epithelial ovarian cancer (EOC). EOCs can be categorized as serous, mucinous, endometrioid, clear cell, and transitional cell types. The molecular pathology of ovarian carcinomas is heterogeneous and involves various putative precursor lesions and multiple pathways of development. Furthermore, in another aspect, immune deficiencies that are present in the ovarian tumor environment enhance the progression of the tumor in the host. The presence of regulatory T cells, the inhibition of natural killer cytotoxic responses, the accumulation of myeloid suppressor cells in the tumor, deficiencies on interferon signaling, the secretion of cytokines that enhance tumor growth (i.e., IL-6, IL-10, CSF-1, TGF-β, TNF), and the expression of surface molecules (i.e., HLA-G, B7-H1, B7-H4, CD40, CD80) that have a role on immune suppression, are discussed in detail. The aim of this review is to provide insight of the evidence that supports the role of immunodeficiency in the progression of ovarian cancer and future directions for ovarian cancer therapies. It also discusses the genetic alterations in the subtypes of ovarian cancers.
AB - Ovarian cancer, the most aggressive gynecologic cancer, is the foremost cause of death from gynecologic malignancies in the developed world. Over 90% of ovarian cancers arise from the surface epithelium, which are classified as epithelial ovarian cancer (EOC). EOCs can be categorized as serous, mucinous, endometrioid, clear cell, and transitional cell types. The molecular pathology of ovarian carcinomas is heterogeneous and involves various putative precursor lesions and multiple pathways of development. Furthermore, in another aspect, immune deficiencies that are present in the ovarian tumor environment enhance the progression of the tumor in the host. The presence of regulatory T cells, the inhibition of natural killer cytotoxic responses, the accumulation of myeloid suppressor cells in the tumor, deficiencies on interferon signaling, the secretion of cytokines that enhance tumor growth (i.e., IL-6, IL-10, CSF-1, TGF-β, TNF), and the expression of surface molecules (i.e., HLA-G, B7-H1, B7-H4, CD40, CD80) that have a role on immune suppression, are discussed in detail. The aim of this review is to provide insight of the evidence that supports the role of immunodeficiency in the progression of ovarian cancer and future directions for ovarian cancer therapies. It also discusses the genetic alterations in the subtypes of ovarian cancers.
KW - Immune diseases
KW - Mutation
KW - Ovarian neoplasms
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M3 - Review article
C2 - 19910891
AN - SCOPUS:77949534749
SN - 0026-4806
VL - 100
SP - 385
EP - 400
JO - Minerva Medica
JF - Minerva Medica
IS - 5
ER -