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conferenceseries.com
Volume 7, Issue 9 (Suppl) Gynecol Obstet (Sunnyvale), an open access journal
ISSN: 2161-0932 Gynecologic Cancers 2017
August 29-30, 2017
2nd International Congress on
August 29-30, 2017 | London, UK
Contemporary Issues in
Women Cancers & Gynecologic Oncology
Gynecol Obstet (Sunnyvale) 2017, 7:9 (Suppl)
DOI: 10.4172/2161-0932-C1-019
How does ovarian cancer escape from the host immune system?
Marek Nowak
Polish Mother’s Memorial Hospital - Research Institute, Poland
The host response involves both innate and adoptive immune system, which closely cooperate. Generally, the innate
immunity is mainly responsible for early detection and elimination of malignant cells, while the adaptive immune system
rather controls the tumor progression. However, cancer cells developed variety of strategies to evade the host immune system.
They shed surface antigens and down-regulate the expression of molecules necessary for interaction with immune cells. They
also produce and release factors (cytokines, enzymes) that exert a modifying effect on the host-adaptive immune response or
induce the apoptosis of immune cells. These host-tumor interactions may or may not result in cancer elimination. When the
host mediated antitumor immunity is stronger, tumor cells are eliminated; otherwise, cancer cells undergo immune escape and
grow rapidly. Emphasizing the dynamic processes between cancer and host immune system, there developed the concept of
cancer immunoediting consisting of three phases: elimination, equilibrium, and escape. In the process of elimination nascent
transformed cells are recognized and eradicated by innate and adaptive immune system - if all neoplastic cells are eliminated,
cancer immunoediting is finished. If all transformed cells are not eliminated at the beginning, immunological pressure leads
to the selection of clones with decreased immunogenicity which successively become resistant to the immune system in the
equilibrium phase - tumors are usually still not detectable clinically. Developing tumor creates proinflammatory (e.g. IL-6, IL-
8) and immunosuppressive (e.g. IL-10, TGF-β) microenvironment leading to the impairment of the host immune function and
escape from immunosurveillance resulting in tumor growth and metastases.
Modulation of HeLa growth and proliferation by breast carcinoma secreted non-cellular
microenvironment
Nilesh Kumar Sharma, Himadri Patel and Devashree Jahagirdar
Dr. D Y Patil Biotechnology & Bioinformatics Institute, Pune, India
The tumor tissue microenvironment plays an important role in development and regulation of normal and tumor or
neoplastic cells and in essence support the cancer to be depicted as heterogenous complex diseases.Within the heterogenous
nature of tumor microenvironment, several cellular and non-cellular factors have been reported to drive cancer development,
invasion, metastasis and drug resistance debacles. Here, authors have attempted to understand the crosstalk between non-
cellular components from breast cancer cell MCF-7 towards cervical cancer cell HeLa growth and proliferation. In this paper,
authors have selected breast carcinoma cell MCF-7 and clinical tissue samples as a source of non-cellular microenvironment
factors. Further, these non-cellular components from breast cancer cells is evaluated for their growth and proliferation inhibitor
role upon HeLa using growth, viability and apoptosis assays. The current findings lead us to suggest that the microenvironment
secreted from MCF-7 and breast carcinoma tissue can play an interference role in growth and viability of HeLa during in vitro
assessment. Here, preliminary data strongly indicate that non-cellular secreted components are able to bring apoptosis induced
cell death of HeLa, which resulted into loss of cell viability. This observation is a novel of this kind, where cells and tissue
samples from one carcinoma such as breast carcinoma could be implicated in the modulation of another carcinoma cell line
HeLa for its growth and death process. However, this findings need to be tested in other cell lines and molecular mechanisms
and detection of non-cellular microenviroment components.