Personalized and Precision Medicine Journal

Abstract Breast cancer is responsible for more than 2.3 million newly diagnosed cases each year, according to the statistics. A hormonal imbalance, which is defined by unregulated activity of estrogen and progesterone, is often the cause of this type of cancer. It has become easier to handle patients who have HR+ breast cancer, particularly in women who have both advanced and early-stage disease, as a result of the deployment of estrogen-blocking hormone treatment. The permissiveness of tamoxifen, which was the first selective estrogen receptor modulator (SERM) to be commercialized, made it possible for more hormonal therapies to be developed. The cornerstone of breast cancer treatment is comprised of aromatase inhibitors (AIs), selective estrogen receptor degraders (SERDs), and cyclin-dependent kinase inhibitors (CDK) 4/6. These three types of drugs ultimately lead to improved patient outcomes. On the other hand, the inherent or acquired resistance of cancers to hormone therapy continues to be a serious cause for concern. Alterations in the genetic makeup of the tumor, as well as the activation of alternate pathways, make this situation even worse. The increasing development of molecular biology, precision medicine, and targeted therapies, on the other hand, is pointing to a new strategy for dealing with these problems. The purpose of this study is to investigate prospective treatment options and to shed light on the significant role that hormone therapy plays in the management of HR-positive breast cancer.

Abstract Drug resistance in cancer is a major challenge to properly treating malignancy. Therapies aimed at proteins involved in cancer development may become less effective due to acquired resistance to medications, often resulting from mutations as well as heightened expression of the targeted proteins. Posttranslational modifications (PTMs) like as phosphorylation, methylation, ubiquitination, and acetylation are crucial for regulating protein expression levels. PROTACs are engineered to selectively degrade a specific protein of interest (POI) by ubiquitination, resulting in a regulated decrease in the POI’s expression. PROTACs show great potential in targeting hitherto untargetable proteins, such as various transcription factors. PROTACs enhance antitumor immune therapy by specifically modifying certain proteins. Although molecular therapies have advanced, lung cancer remains a major contributor to cancer-related mortality. The management of those with lung cancer is now limited by a lack of targeted therapy choices and the development of acquired drug resistance. Using the intracellular ubiquitin-proteasome system for directed protein breakdown might enhance individualized treatment for lung cancer patients. This study explores the rationale for using PROTAC therapy as an innovative specific therapy and the current advancements in PROTAC development for lung tumors.

Abstract Exposure to low-frequency electromagnetic fields (LF-EMF) has been considered a global concern because of its harmful effects on human health (cancer, neurodegenerative disorders, etc.). According to the International Agency for Research on Cancer, EMF has been classified as a possible cancerous element for human health. Antioxidants such as vitamin C improve the damage caused by EMF by reducing oxidative stress. To evaluate the effects of EMF on the serum total protein, blood sugar, albumin and triglyceride, and the inhibitory role of vitamin C, 40 male BALB/c mice were recruited. Participants were randomly distributed into four groups 1- exposure to LF-EMF, 2- exposure to LF-EMF which received vitamin C (50 mg/kg), 3- exposure to LF-EMF which received vitamin C (100 mg/kg), and 4- control group (no exposure). The experimental groups (1-3) received LF-EMF (50 Hz, 4 mT, 4 hours/day, and 1 month) while both groups 2 and 3 had intraperitoneally injected vitamin C (50 mg/kg, 100 mg/kg) every other day basis respectively. The obtained results demonstrated higher triglyceride and total protein levels and lower albumin and blood sugar levels in the LF-EMF group compared to controls while vitamin C restricts their alterations (p<0.05). To sum it up, our data show that intraperitoneal injection of vitamin C restricts the effects of LF-EMF exposure on the biochemical parameters in mice. However, the antioxidant characteristics of vitamin C may be probably involved in the LF-EMF effects of biochemical parameters in mice.

Abstract Objectives: Diabetes mellitus type 1 (T1DM), which is also an autoimmune disorder, can coexist alongside other types of autoimmune diseases. This study aimed to investigate the possibility of a subclinical association between diabetes disease and autoimmune thyroid dysfunction. The clinical condition of the patient and their approach to managing their diabetes were specifically considered when deciding whether or not the patient had autoantibodies.
Methods: This study included sixty individuals who were diagnosed with diabetes type 1. (thirty males and thirty women, with a mean age of 21.04 years) and 30 healthy controls (12 males and 18 females).
Results: Diabetics had considerably greater serum IL-10, IL-6, and TNF-α levels than healthy controls. Stepwise regression indicated significant positive correlations between IL-10, IL-6, and TNF-α with these antibodies and strong inversed relationships between IL-6 and Anti-TPO, Anti-TG, antibodies.
. No matter if the antibodies were present or how severe they were, this held true. The study's findings lend credence to the idea that people with type 1 diabetes should have their thyroid antibodies and function checked.
Conclusions: Thyroid antibodies were most common among type 1 diabetics aged 21–35, according to our study (Anti-TPO and Anti-TG). IL-10, IL-6, and TNF-α levels in diabetic patients and controls were significantly different (P<0.01). IL-10, TNF-α, HbA1C, and body mass index positively correlated with thyroid antibodies, except for IL-6. Thyroid antibodies and functional abnormalities should be tested often in type 1 diabetics due to the high occurrence of thyroid autoimmune illnesses.