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Purpose: The immunosuppressive function of myeloid-derived suppressor cells (MDSCs) has been implicated in the regulation of immune responses against cancer and is associated with poor prognosis. Radiation treatment is known to alter immune cell populations within the tumor; however, whether this results in the recruitment of immunosuppressive MDSC populations is not well understood. Here we evaluate the response of circulating MDSC populations in patients treated per standard-of-care cisplatin chemoradiation therapy (CRT) for locally invasive cervical cancer. Methods and Materials: Newly diagnosed, treatment-naïve patients with locally advanced cervical cancer were enrolled. Blood samples were collected from patients prior to starting CRT (T0), after external beam radiation therapy (T1), and after high-dose-rate brachytherapy (T2). Samples from each time point were processed, and the prevalence of MDSC subsets was determined using flow cytometry. MDSC populations were identified using Live/Dead-CD11b+CD33+HLA-DR- staining. MDSC subsets were further subdivided into granulocytic (g-, CD15+CD14-), monocytic (m-, CD15-CD14+), or early-MDSCs (e-, CD15-CD14-). Results: Most patients in our study were Caucasian nonsmokers with human papillomavirus-associated squamous cell carcinoma of the cervix. We saw a trend for increased MDSC frequency in patients with more advanced-stage disease at the time of initiating treatment. MDSCs increase in response to CRT and peak after brachytherapy (T2). In particular, the g-MDSC subset increases by 6.44 times relative to the baseline. There was no correlation between MDSC expansion and response to therapy. Conclusion: Our study confirms other reports that circulating MDSCs in patients with cervical cancer increase in response to CRT and are associated with more advanced stages. Additionally, we show that MDSC expansion is driven by the g-MDSC subset. We did not see any correlation between MDSC expansion and treatment response, though this may be because of the limited sample size for this study.

The objective of this study was to determine the rate of germline high risk ovarian cancer susceptibility pathogenic variants in Somali patients with ovarian carcinoma treated at a single institution between 2015 and 2022. Out of eight identified patients, five underwent germline and/or somatic testing, revealing a high prevalence (3 of 5, 60 %) of a BRIP1 splice site mutation (c.1936 + 1G > A). Additionally, one patient had a BRCA2 pathogenic variant, and two had the same MLH1 variant of uncertain significance. The high prevalence of BRIP1 pathogenic variants warrants further study into a possible founder effect within the Somali population, emphasizing the need for targeted genetic screening and counseling. The study also highlights significant barriers to genetic testing, pointing to the critical role of healthcare disparities and social determinants of health (SDoH) in cancer outcomes. Comprehensive genomic profiling and community-based research are essential to address these disparities and improve cancer care for this underserved population. Larger studies are needed to validate these findings and to develop tailored interventions that enhance the prevention, diagnosis, treatment, and prognosis of ovarian cancer in Somali women.

The uterine cervix is an uncommon site of metastatic cancer. Specifically, pancreatic adenocarcinoma metastatic to the cervix is an exceptionally rarely reported phenomenon. We encountered a case of recurrent pancreatic adenocarcinoma presenting as a solitary metastasis to the cervix. To our knowledge, this is the only report describing an isolated recurrence of pancreatic adenocarcinoma to the cervix. When diagnosing metastatic disease to the cervix, it is also imperative for the clinician and pathologist to consider histologic mimics, such as the newly described gastric-type mucinous endocervical adenocarcinoma. Metastatic disease to the cervix may benefit from surgical resection. Keywords: Uterus, Cervix, Pancreatic adenocarcinoma, Metastasis, Gastric-type endocervical adenocarcinoma