Summer Cancer Research Experience for High School Students from Historically Marginalized Populations in Kansas City.

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.

A community engagement training program for basic and translational cancer researchers.

Purpose: There is an increasing awareness of the importance of patient engagement in cancer research, but many basic and translational researchers have never been trained to do so. To address this unmet need, a 1-year patient engagement training program for researchers was developed.

Methods: Eleven researchers and eleven paired research advocates participated.

Evaluating Work Impairment as a Source of Financial Toxicity in Cancer Healthcare and Negative Impacts on Health Status.

Unlabelled: How the socioeconomic factors intersect for a particular patient can determine their susceptibility to financial toxicity, what costs they will encounter during treatment, the type and quality of their care, and the potential work impairments they face. The primary goal of this study was to evaluate financial factors leading to worsening health outcomes by the cancer subtype. A logistic model predicting worsening health outcomes while assessing the most influential economic factors was constructed by the University of Michigan Health and Retirement Study.

Functional inhibition of the RNA-binding protein HuR sensitizes triple-negative breast cancer to chemotherapy.

Chemotherapy remains the standard treatment for triple-negative breast cancer (TNBC); however, chemoresistance compromises its efficacy. The RNA-binding protein Hu antigen R (HuR) could be a potential therapeutic target to enhance the chemotherapy efficacy. HuR is known to mainly stabilize its target mRNAs, and/or promote the translation of encoded proteins, which are implicated in multiple cancer hallmarks, including chemoresistance.

Career disruption and limitation of financial earnings due to cancer.

Purpose: This study investigated how cancer diagnosis and treatment lead to career disruption and, consequently, loss of income and depletion of savings.

Design: This study followed a qualitative descriptive design that allowed us to understand the characteristics and trends of the participants.

Method: Patients recruited (n = 20) for this study were part of the University of Kansas Cancer Center patient advocacy research group (Patient and Investigator Voices Organizing Together).

Generating Mitochondrial-Nuclear Exchange (MNX) Mice to Identify Mitochondrial Determinants of Cancer Metastasis.

Understanding the contributions of mitochondrial genetics to disease pathogenesis is facilitated by a new and unique model-the mitochondrial-nuclear exchange mouse. Here we report the rationale for their development, the methods used to create them, and a brief summary of how MNX mice have been used to understand the contributions of mitochondrial DNA in multiple diseases, focusing on cancer metastasis. Polymorphisms in mtDNA which distinguish mouse strains exert intrinsic and extrinsic effects on metastasis efficiency by altering epigenetic marks in the nuclear genome, changing production of reactive oxygen species, altering the microbiota, and influencing immune responses to cancer cells.

Comparison of the marginal microleakage of a bioactive composite resin and traditional dental restorative materials.

The primary objective of this study was to evaluate the marginal microleakage of Activa Kids BioActive-Restorative used with an adhesive bonding agent (AB+) and compare it with the microleakage of a traditional composite resin (CR), a resin-modified glass ionomer cement (RMGIC), and Activa Kids BioActive-Restorative placed without the use of an adhesive bonding agent (AB-). Standard Class I cavities were prepared in 200 extracted, caries-free permanent molars, which were then restored with 1 of the 4 restorative materials (n = 50 each). The restored teeth were thermocycled for 500 cycles, alternating between 5°C and 55°C with a dwell time of 25 seconds; stained with basic fuchsin dye with a soak time of 24 hours; and sectioned buccolingually.

KISS1 metastasis suppressor in tumor dormancy: a potential therapeutic target for metastatic cancers?

Present therapeutic approaches do not effectively target metastatic cancers, often limited by their inability to eliminate already-seeded non-proliferative, growth-arrested, or therapy-resistant tumor cells. Devising effective approaches targeting dormant tumor cells has been a focus of cancer clinicians for decades. However, progress has been limited due to limited understanding of the tumor dormancy process.

Roles of mitochondrial genetics in cancer metastasis.

The contributions of mitochondria to cancer have been recognized for decades. However, the focus on the metabolic role of mitochondria and the diminutive size of the mitochondrial genome compared to the nuclear genome have hindered discovery of the roles of mitochondrial genetics in cancer. This review summarizes recent data demonstrating the contributions of mitochondrial DNA (mtDNA) copy-number variants (CNVs), somatic mutations, and germline polymorphisms to cancer initiation, progression, and metastasis.

Questions to guide cancer evolution as a framework for furthering progress in cancer research and sustainable patient outcomes.

We appear to be faced with 'two truths' in cancer-one of major advances and successes and another one of remaining short-comings and significant challenges. Despite decades of research and substantial progress in treating cancer, most patients with metastatic cancer still experience great suffering and poor outcomes. Metastatic cancer, for the vast majority of patients, remains incurable.

Synergistic anti-proliferative activity of JQ1 and GSK2801 in triple-negative breast cancer.

Background: Triple-negative breast cancer (TNBC) constitutes 10-20% of breast cancers and is challenging to treat due to a lack of effective targeted therapies. Previous studies in TNBC cell lines showed in vitro growth inhibition when JQ1 or GSK2801 were administered alone, and enhanced activity when co-administered. Given their respective mechanisms of actions, we hypothesized the combinatorial effect could be due to the target genes affected.

Functional characterization of NPM1-TYK2 fusion oncogene.

Gene fusions are known to drive many human cancers. Therefore, the functional characterization of newly discovered fusions is critical to understanding the oncobiology of these tumors and to enable therapeutic development. NPM1-TYK2 is a novel fusion identified in CD30 + lymphoproliferative disorders, and here we present the functional evaluation of this fusion gene as an oncogene.

Perturbation of BRMS1 interactome reveals pathways that impact metastasis.

Breast Cancer Metastasis Suppressor 1 (BRMS1) expression is associated with longer patient survival in multiple cancer types. Understanding BRMS1 functionality will provide insights into both mechanism of action and will enhance potential therapeutic development. In this study, we confirmed that the C-terminus of BRMS1 is critical for metastasis suppression and hypothesized that critical protein interactions in this region would explain its function.

DCLK1 isoforms and aberrant Notch signaling in the regulation of human and murine colitis.

Alternative promoter usage generates long and short isoforms (DCLK1-L and DCLK1-S) of doublecortin-like kinase-1 (DCLK1). Tight control of Notch signaling is important to prevent and restitute inflammation in the intestine. Our aim was to investigate whether Notch1-DCLK1 axis regulates the mucosal immune responses to infection and whether this is phenocopied in human models of colitis.

Mechanisms of breast cancer metastasis.

Invasive breast cancer tends to metastasize to lymph nodes and systemic sites. The management of metastasis has evolved by focusing on controlling the growth of the disease in the breast/chest wall, and at metastatic sites, initially by surgery alone, then by a combination of surgery with radiation, and later by adding systemic treatments in the form of chemotherapy, hormone manipulation, targeted therapy, immunotherapy and other treatments aimed at inhibiting the proliferation of cancer cells. It would be valuable for us to know how breast cancer metastasizes; such knowledge would likely encourage the development of therapies that focus on mechanisms of metastasis and might even allow us to avoid toxic therapies that are currently used for this disease.

Preclinical Evaluation of Gilteritinib on NPM1-ALK-Driven Anaplastic Large Cell Lymphoma Cells.

Anaplastic large cell lymphoma (ALCL) is an aggressive type of non-Hodgkin lymphoma. More than three-fourths of anaplastic lymphoma kinase (ALK)-positive ALCL cases express the () fusion gene as a result of t(2;5) chromosomal translocation. The homodimerization of NPM1-ALK fusion protein mediates constitutive activation of the chimeric tyrosine kinase activity and downstream signaling pathways responsible for lymphoma cell proliferation and survival.

Roles of mitochondria in the hallmarks of metastasis.

Although mitochondrial contributions to cancer have been recognised for approximately a century, given that mitochondrial DNA (mtDNA) is dwarfed by the size of the nuclear genome (nDNA), nuclear genetics has represented a focal point in cancer biology, often at the expense of mtDNA and mitochondria. However, genomic sequencing and advances in in vivo models underscore the importance of mtDNA and mitochondria in cancer and metastasis. In this review, we explore the roles of mitochondria in the four defined 'hallmarks of metastasis': motility and invasion, microenvironment modulation, plasticity and colonisation.

Suppression of pancreatic cancer liver metastasis by secretion-deficient ITIH5.

Background: Previously, we identified ITIH5 as a suppressor of pancreatic ductal adenocarcinoma (PDAC) metastasis in experimental models. Expression of ITIH5 correlated with decreased cell motility, invasion and metastasis without significant inhibition of primary tumour growth. Here, we tested whether secretion of ITIH5 is required to suppress liver metastasis and sought to understand the role of ITIH5 in human PDAC.