Setsuko Chambers


Our long term goal is to develop and clinically evaluate a novel strategy for inhibition of CSF-1 and/or c-fms function that will inhibit the invasive, metastatic phenotype in ovarian cancer patients.  Epithelial ovarian cancer typically presents with widespread disease within the peritoneal cavity, with a 10-year patient survival of 15%. With the growing recognition of the impact of post-transcriptional gene regulation on cancer-related biological processes, we apply our multi-factorial expertise to the ovarian cancer problem, with a focus on RNA binding proteins and miRNAs.






Our long-term goal is to decrease bone metastasis from breast cancer and help alleviate bone pain, to improve quality of life of patients with metastatic breast cancer. Bone metastases are common in women with metastatic breast cancer, resulting in bone destruction and rendering the patient largely incurable. As opposed to the case with many other solid tumors which have spread, breast cancer patients with bone spread can live many years. Ultimately 70% of those patients will develop skeletal complications including fractures and bone pain, severely impacting their quality of life. To work towards our goal, we will build upon work from our laboratory on regulation of breast cancer metastasis by the c-fms proto-oncogene.

Lynch Syndrome Related Endometrial Cancer: Clinical Significance Beyond The Endometrium. Source: Journal Of Hematology & Oncology
March 25th, 2013 PMID: 23531335 Setsuko Chambers
Lynch syndrome (LS), an autosomal dominant inherited cancer susceptibility syndrome, also known as hereditary non-polyposis colon cancer (HNPCC), is caused by a germline mutation in one of several DNA mismatch repair (MMR) genes. LS is the most common presentation of hereditary colorectal cancer (CRC), accounting for about 2-5% of all CRC cases. More recently, it is found that a similar number of endometrial cancers is also due to one of the MMR gene mutations. There has been significant progress in LS-related CRC in terms of molecular pathogenesis, risks, genetic basis, and cancer prevention. In contrast, the advance about LS-related endometrial cancer (EC) is very much limited. In this commentary, we summarize the main clinicopathologic features of LS-related EC and propose universal screening for LS in individuals with endometrial cancer.<br /><br />
Tubal Origin Of 'Ovarian' Low Grade Serous Carcinoma. Source: Modern Pathology : An Official Journal Of The United States And Canadian Academy Of Pathology, Inc
June 24th, 2011 PMID: 21701538 Setsuko Chambers
Ovarian low-grade serous carcinomas are thought to evolve in a stepwise fashion from ovarian epithelial inclusions, cystadenomas, and borderline tumors. The current study was designed to gain insight into the origins of low-grade serous carcinomas (tubal versus ovarian) by comparatively evaluating the morphologic (secretory and ciliated cell distribution) and immunophenotypic (using antibodies to PAX8, tubulin, calretinin, and Ki67) attributes of its putative precursor lesions, the normal tubal epithelium, and the overt malignancy. A total of 226 adnexal tissues from 178 patients were studied, including 98 adnexae removed for non-neoplastic indications, 48 serous cystadenomas, 42 serous borderline tumors, and 38 low-grade serous carcinomas. Normal distal tubal epithelium comprised an admixture of PAX8+/tubulin- secretory cells and PAX8-/tubulin+ ciliated cells with a proliferative index of ∼3%. The vast majority of ovarian surface epithelia displayed a mesothelial phenotype (calretinin+/PAX8-/tubulin-) and low proliferative index (0% (12 per 1000)), although 4% of cases also displayed foci with tubal phenotype (calretinin-/PAX8+/tubulin+). In contrast, most (78%) of the ovarian epithelial inclusions displayed a tubal phenotype and had a significantly higher proliferative index (1%) than ovarian surface epithelium, indicating that in most cases, the ovarian surface epithelium and ovarian epithelial inclusions are of different lineages. There was a progressive decrease in the population of ciliated cells, as evidenced by increasing secretory/ciliated cell ratio, from ovarian epithelial inclusions/cystadenomas to borderline tumors to low-grade serous carcinoma, indicating that the latter is a clonal expansion of secretory cells. Overall, the findings make a strong argument that the ovarian epithelial inclusions with a tubal phenotype is likely derived from fallopian tube through an intraovarian endosalpingiosis rather than through Mullerian metaplasia from ovarian surface epithelium. Genetic and molecular studies are needed to further confirm this finding as tubal origination of ovarian serous cancers will have a significant impact on ovarian cancer prevention and management.<br /><br />
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