Despite the advances in research and treatment of human breast cancer, its incidence rate continues to increase by 0.5% per year, and the discovery of novel therapeutic strategies for specific subtypes of human breast cancer remains challenging. Traditional laboratory mouse models have contributed tremendously to human breast cancer research. However, mice do not develop tumors spontaneously; consequently, genetically engineered mouse models or patient-derived xenograft models are often relied upon for more sophisticated human breast cancer studies. Since human breast cancer develops spontaneously, there is a need for alternative, yet complementary, models that can better recapitulate the features of human breast cancer to better understand the molecular and clinical complexities of the disease in developing new therapeutic strategies. Canine mammary tumors are one such alternative model that share features with human breast cancer, including prevalence rate, subtype classification, treatment, and mutational profiles, all of which are described in this review.

Glioblastoma multiforme (GBM) is the most common primary brain cancer. Even with aggressive combination therapy, the median life expectancy for patients with GBM remains approximately 14 months. In order to improve the outcomes of patients with GBM, the development of newer treatments is critical. The concept of using the immune system as a therapeutic option has been suggested for several decades; by harnessing the body's adaptive immune mechanisms, immunotherapy could provide a durable and targeted treatment against cancer. However, many cancers, including GBM, have developed mechanisms that protect tumor cells from being recognized and eliminated by the immune system. For new immunotherapeutic regimens to be successful, overcoming immunosuppression via immune checkpoint signaling should be taken into consideration.
Brain Neoplasms ; Glioblastoma* ; Humans ; Immune System ; Immunosuppression ; Immunotherapy ; Life Expectancy ; Radiosurgery

Non-transfused β-thalassaemia patients develop complications related to unsuppressed ineffective erythropoiesis (IE). Serum markers of IE would be useful for risk stratification and monitoring treatment. We studied βthalassaemia trait (β-TT) and non-transfusion-dependent βthalassaemia (β-NTDT) patients. Serum erythropoietin (EPO) and soluble transferrin receptor (sTfR) were correlated against markers of clinical severity (haemoglobin, LDH, retics, bilirubin, spleen size) and iron overload (ferritin, hepcidin, and MRI-T2* in NTDT patients). Eleven β-NTDT and nine β-TT subjects were studied. βNTDT patients had significantly higher markers of haemolysis and iron overload. In β-NTDT, liver iron ranged from mild to severe, but no cardiac loading was seen. EPO and sTfR were higher in patients with β-NTDT than β-TT, and correlated significantly with each other (ρ=0.630, p=0.003). Both markers were negatively correlated with haemoglobin (sTfR ρ=-0.540, p=0.014; EPO ρ=-0.807, p<0.001, and positively correlated with spleen size (sTfR ρ=0.783, p<0.001; EPO ρ=0.654, p=0.002) and markers of iron overload. There was a strong correlation between ferritin and hepcidin (ρ=0.720, p<0.001), and a relatively lower increment of hepcidin for the degree of iron overload in βNTDT compared to β-TT. EPO and sTfR appear to be reliable markers of erythropoiesis in non-transfused β-thalassaemia and correlate well with markers of disease severity. Their role in managing patients, predicting complications, and monitoring response to treatments aimed at reducing IE should be explored.

Despite advances in the field of male reproductive health, idiopathic male infertility, in which a man has altered semen characteristics without an identifiable cause and there is no female factor infertility, remains a challenging condition to diagnose and manage. Increasing evidence suggests that oxidative stress (OS) plays an independent role in the etiology of male infertility, with 30% to 80% of infertile men having elevated seminal reactive oxygen species levels. OS can negatively affect fertility via a number of pathways, including interference with capacitation and possible damage to sperm membrane and DNA, which may impair the sperm's potential to fertilize an egg and develop into a healthy embryo. Adequate evaluation of male reproductive potential should therefore include an assessment of sperm OS. We propose the term Male Oxidative Stress Infertility, or MOSI, as a novel descriptor for infertile men with abnormal semen characteristics and OS, including many patients who were previously classified as having idiopathic male infertility. Oxidation-reduction potential (ORP) can be a useful clinical biomarker for the classification of MOSI, as it takes into account the levels of both oxidants and reductants (antioxidants). Current treatment protocols for OS, including the use of antioxidants, are not evidence-based and have the potential for complications and increased healthcare-related expenditures. Utilizing an easy, reproducible, and cost-effective test to measure ORP may provide a more targeted, reliable approach for administering antioxidant therapy while minimizing the risk of antioxidant overdose. With the increasing awareness and understanding of MOSI as a distinct male infertility diagnosis, future research endeavors can facilitate the development of evidence-based treatments that target its underlying cause.
Antioxidants ; Classification ; Clinical Protocols ; Diagnosis ; DNA ; Embryonic Structures ; Female ; Fertility ; Health Expenditures ; Humans ; Infertility ; Infertility, Male ; Male ; Membranes ; Ovum ; Oxidants ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species ; Reducing Agents ; Reproductive Health ; Semen ; Spermatozoa ; Subject Headings