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The Accelerate Cancer Education (ACE) summer research program at The University of Kansas Cancer Center (KUCC) is a six-week, cancer-focused, summer research experience for high school students from historically marginalized populations in the Kansas City metropolitan area. Cancer affects all populations and continues to be the second leading cause of death in the United States, and a large number of disparities impact racial and ethnic minorities, including increased cancer incidence and mortality. Critically, strategies to bolster diversity, equity, inclusion, and accessibility are needed to address persistent cancer disparities. The ACE program offers an educational opportunity for a population of students who otherwise would not have easy access onto a medical center campus to make connections with cancer physicians and researchers and provides a vital response to the need for a more diverse and expansive oncology workforce. Students grow their technical, social, and professional skills and develop self-efficacy and long-lasting connections that help them matriculate and persist through post-secondary education. Developed in 2018, the ACE program has trained 37 high school junior and senior students. This article describes the need for and how we successfully developed and implemented the ACE program.

An increasingly diversified demographic landscape in rural and urban America warrants the attention of The University of Kansas Cancer Center (KU Cancer Center) researchers, clinicians, outreach staff and administrators as the institution assesses ways to reach its expansive, bi-state catchment area. Within the counties of the KU Cancer Center catchment area, patient level and public health data are available and categorized by varying geographic regional boundaries. Multiple data sources and different data collection processes complicate summarizing catchment area data. A curated data warehouse that retrieves and structures the data, with a common denominator, can support meaningful use of the data in a standard and consistent format. The KU Cancer Center built a data warehouse to Organize and Prioritize Trends to Inform KU Cancer Center (OPTIK), which functions to streamline the process of synthesizing data regarding Kansas and Missouri demographics, cancer risk factors and incidence and mortality rates. OPTIK standardizes these diverse data sources to enable analyses of the cancer burden at local, regional and national levels while upholding a strict standard of patient privacy. The OPTIK database enables researchers to use available data and create heat maps and other visualizations to aid in funding proposals, presentations and research activities. Furthermore, using knowledge provided by OPTIK, the KU Cancer Center is able to prioritize action items for research and outreach and more effectively communicate the impact of those efforts., (© The Author(s) 2020. Published by Oxford University Press.)

BRCA1 (breast cancer 1, early onset), a well-known breast cancer susceptibility gene, is a highly alternatively spliced gene. BRCA1 alternative splicing may serve as an alternative regulatory mechanism for the inactivation of the BRCA1 gene in both hereditary and sporadic breast cancers, and other BRCA1 -associated cancers. The alternative transcripts of BRCA1 can mimic known functions, possess unique functions compared with the full-length BRCA1 transcript, and in some cases, appear to function in opposition to full-length BRCA1 In this review, we will summarize the functional "naturally occurring" alternative splicing transcripts of BRCA1 and then discuss the latest next-generation sequencing-based detection methods and techniques to detect alternative BRCA1 splicing patterns and their potential use in cancer diagnosis, prognosis, and therapy., (©2019 American Association for Cancer Research.)

The familial aggregation of prostate cancer and breast cancer has been observed for almost half a century and about 85% of the inherited breast cancer can be linked to germ-line mutations of BRCA1 (breast cancer 1, early onset) and BRCA2. In this review, we are mainly focusing on the contribution of BRCA1/2 sequence variations to prostate cancer risk and disease progression. We will discuss the biological functions of BRCA1/2 and BRCA1/2-related signaling pathways in prostate cancer biology. The majority of studies supporting the link between BRCA1/2 mutations and prostate cancer are from populations with a high frequency of mutations, such as Ashkenazi Jewish, Icelandic, and U.K. population. BRCA1 can directly interact with the androgen receptor (AR) and Janus kinase (JAK), and can differentially regulate insulin-like growth factor 1 receptor (IGF-IR) expression in an AR-dependent manner. BRCA2 homeostasis in prostate cancer cells has been found to be critical in determining cell fates during prostate cancer progression. This review may be helpful for medical professionals and prostate cancer patients when discussing prostate cancer risks, treatment and prognosis.

Expression of functional breast cancer susceptibility gene 1 (BRCA1) in human breast and ovarian cancers is associated with resistance to platinum-based chemotherapeutics and poly(ADP ribose) polymerase (PARP) inhibitors. BRCA1 is a nuclear tumor suppressor that is critical for resolving double-strand DNA breaks (DSBs) and interstrand crosslinks (ICLs) by homologous recombination (HR). In vitro, animal and human clinical data have demonstrated that BRCA1-deficient cancers are highly sensitive to ICL-inducing chemotherapeutic agents, are amenable to synthetic lethal approaches that exploit defects in DSB/ICL repair, and may be associated with improved survival. Conversely, high or restored expression of BRCA1 in breast and ovarian cancer is associated with therapeutic resistance and poor prognosis. There has been much interest in identifying agents that interfere with BRCA1-dependent DSB/ICL repair to restore or enhance sensitivity to cancer therapeutics. We demonstrate that the heat-shock protein 90 (HSP90) inhibitor 17-allylamino-17-demethoxygeldanamycin [17-AAG (Tanespimycin)], currently in Phase II/III clinical evaluation for several cancers, induces BRCA1 ubiquitination and proteasomal degradation, resulting in compromised repair of ionizing radiation- and platinum-induced DNA damage. We show that loss of HSP90 function abolishes BRCA1-dependent DSB repair and that BRCA1-deficient cells are hypersensitive to 17-AAG due to impaired Gap 2/Mitosis (G2/M) checkpoint activation and resultant mitotic catastrophe. In summary, we document an upstream HSP90-dependent regulatory point in the Fanconi anemia/BRCA DSB/ICL repair pathway, illuminate the role of BRCA1 in regulating damage-associated checkpoint and repair responses to HSP90 inhibitors, and identify BRCA1 as a clinically relevant target for enhancing sensitivity in refractory and/or resistant malignancies.