If indeed ovarian cancer can originate from various types of transformed

cells from multiple sites in the female reproductive tract, then each type of ovarian cancer would have its own set of distinctive markers. Identification of these extra-ovarian progenitors of ovarian cancer is a first step in the recognition of possible markers for early detection. Figure 5 Attachment of CD44-positive ovarian cancer cells to the mouse ovary. A MULTI-TARGET APPROACH TO TREATING OVARIAN CANCER As previously mentioned, chemotherapy is standard for women with ovarian cancer. In most cases, the cancer responds to the Inhibitors,research,lifescience,medical chemotherapy, cancer markers substantially decrease, and a state of remission is achieved. However, for the majority of the women with ovarian cancer, a short period of remission is followed by a relapse, in which the tumor is chemo-resistant to both taxol and carboplatin. To address the question of recurrence and chemo-resistance we evaluated the phenotype of cells that survive chemotherapy and found that these cells possess Inhibitors,research,lifescience,medical the markers that distinguish the type I cells or tumor-initiating cancer cells. CD44-positive cells did not respond to chemotherapy and instead grew steadily even in the presence of these drugs. These results further support the current consensus that CD44-positive cells represent the chemo-resistant phenotype.19,21,22,27–29 On-going studies using an in-vivo recurrence

model of ovarian Inhibitors,research,lifescience,medical cancer also showed that tumors initially respond to chemotherapy and shrink considerably. However, after a short remission period the Inhibitors,research,lifescience,medical tumor grows back, and at this stage it is totally non-responsive to chemotherapy treatment that was previously successful. Moreover, the cellular composition of the recurring tumor differs significantly from the primary tumor. These studies clearly indicate that the two distinct subtypes of ovarian cancer cells must be treated differently. If only one type of treatment is given, recurrence and disease progression Inhibitors,research,lifescience,medical will be delayed but not prevented.

Subsequent tumors will be comprised of a different cell type that will only respond to an entirely different agent. CONCLUSION There are multiple forms of epithelial ovarian cancer due to the diversity of the cells that form the primary Selleck Perifosine lesion. Therefore, a wider range of early detection markers should be GBA3 used to screen for early detection of the disease. In addition, treatment for ovarian cancer should take into account the clonal diversity that is persistently found in the ovarian tumor. The future treatment for patients with ovarian cancer will include multiple steps: Once a tumor is detected, a biopsy should be taken and the cell type and origin should be determined. A personalized tailor-made chemotherapeutic regimen should be provided based on the tumor’s unique cellular make-up (Figure 6). Maintenance should be done by targeting the surviving cancer stem cells, consequently preventing relapse.