Personalized and Precision Medicine Journal

Abstract Cancer, the second foremost worldwide cause of mortality, affects individuals both physically and emotionally. Traditional therapies, including surgery, chemotherapy, and radiation, have detrimental consequences, necessitating the pursuit of more targeted methods. Precision medicine facilitates more tailored therapies. The introduction of next-generation sequencing technology, as well as the growing frequency of large-scale tumor molecular profiling programs throughout the world, have changed cancer diagnosis and treatment. With the increasing availability of comprehensive genetic tests in medical and scientific settings, healthcare practitioners face complex hurdles in understanding and translating data. The article encapsulates the existing and forthcoming strategies for the implementation of precision cancer therapy, emphasizing the obstacles and potential ways to enhance the understanding and optimize the therapeutic value of molecular profiling outcomes.

Abstract Cancer is a significant global cause of mortality, and enhancing therapy is essential to save lives and minimise adverse consequences. Aptamers, composed of DNA or RNA, have the potential for cancer treatment by precise targeting of certain molecules. Aptamers, unlike conventional therapies such as chemotherapy, have the specific objective of delivering medications directly to cancer cells, while reducing injury to healthy cells. This paper examines the process of aptamer development and utilisation in cancer treatment, with a specific emphasis on their capacity to enhance therapy and surmount drug resistance. Additionally, it explores the obstacles and potential advancements in using aptamers to transform cancer therapy.

Abstract In cancer treatment, anesthesia is commonly used during surgery to remove tumors, as well as for other procedures like biopsies, radiation therapy, and chemotherapy administration. Some research suggests that the choice of specific anesthetic drugs and nerve-sparing techniques can have a significant impact on cancer recurrence rates and overall patient survival. It is well-established that a patient's immune system plays a direct role in postoperative complications and long-term outcomes, highlighting the importance of optimizing anesthesia to minimize potential immune system suppression and improve immune function during cancer surgery. Recent studies have revealed a strong connection between the type of anesthesia used during surgery and the likelihood of cancer relapse and related mortality. Therefore, it is crucial to select the appropriate anesthesia technique for cancer resection, focusing on reversible effects, rapid recovery, and resistance to feedback. The specific anesthetic agents used during surgery have a significant impact on survival rates and the risk of cancer-related mortality. Genetic influences on anesthesia response are significant for improving patient care and achieving better results. Additionally, personalized medicine, which combines diagnostic testing and treatment, is now a clinical reality. Anesthesia's effects on depth, pain signals, vital signs, and the motor system are complex and not fully understood, and many researchers believe that anesthesia is regulated by multiple genes, although further research is needed to identify them and understand how they are regulated. The relationship between anesthesia and cancer is complex and evolving with implications for medical treatment. Limited evidence suggests that anesthesia and surgery-related factors can affect cancer biology and outcomes. Further research is needed to understand these interactions and develop strategies for improving cancer care during surgery. Better understanding can lead to safer and more effective cancer treatment, benefitting patients.

Abstract Lots of people are struggling with Kidney disease or cancer around the world. Chronic kidney disease (CKD) and renal cell carcinoma (RCC) are associated directionally and share risk factors. Because of the role of kidneys in detoxification, studying the relationship between cancer chemotherapy and kidney disorders is significant. This investigation fills the current gap between cancer occurrence and kidney problems.
CKD can induce RCC through a cystic disorder or oxidative stress. RCC also promotes CKD due to the tumor interactions, physical removal of kidney mass, and perioperative acute renal disease. Kidney failure also leads to renal cancer-specific pathways. For example, renal progenitors are converted to tumor-initiating cells through HIF, Notch, mTOR, and Hippo pathways. Furthermore, progress in cancer treatment during recent years has increased the overall survival of patients with advanced malignancies faced with early and late adverse effects from therapeutics. There are conflicting findings about the dosing of typical chemotherapeutics because of loss of kidney function. Recommended doses are usually according to expert opinion, not scientific evidence. This investigation has evaluated issues in cancer patients with kidney problems that can help patients by informing physicians about GFR loss and its effect on chemotherapy.
Keywords: kidney diseases, cancer, chemotherapy, CKD, AKI

Abstract Physicians are enthusiastic about using a novel approach known as cancer immunotherapy to address various forms of cancer. However, there are occasions when novel therapies that demonstrate efficacy in laboratory settings may not provide the same level of effectiveness when applied to actual patients. To address this issue, scientists are using miniature replicas known as microfluidic models. These models provide the examination of the interaction between cancer and immune cells in a manner that closely resembles the physiological conditions inside the human body. This review examines the role of microfluidic models in advancing the development of more effective cancer therapies. Let's begin by discussing the current state of affairs in cancer immunotherapy. Next, we explore the use of microfluidic models by scientists to gain insights into the mechanisms via which the immune system combats cancer and to evaluate the efficacy of novel therapeutic interventions. Additionally, we discuss the first measures used to demonstrate the efficacy of these models in predicting the effectiveness of therapies in human subjects. Lastly, we will discuss the advantages of using microfluidic models and the necessary steps to enhance their efficacy in the development of novel cancer therapies.
 

Abstract Recent research has pinpointed cancer as the primary cause of death on a global scale. Various traditional medications and cytotoxic immunotherapies have been established and are now accessible on the market. Given the intricate nature of tumor activity and the multitude of genetic and cellular elements implicated in the development and spread of cancers, it is imperative to create a highly effective immunotherapy that can specifically target tumors at both the cellular and genetic levels. In the clinical context, cancer immunotherapy is growing more and more significant, particularly for tumors that are resistant to traditional chemotherapy and targeted treatments. Chimeric antigen receptor (CAR) T cell therapy is a new method of modifying T cells taken from a patient's blood in a laboratory setting. These modified T cells are created to express artificial receptors that specifically target a particular tumor antigen. These specifically recognize the tumor antigen without the participation of the major histocompatibility complex. The use of CAR therapy has the promise of providing a prompt and more secure treatment regimen for both non-solid and solid malignancies. This study provides a comprehensive analysis of the benefits and progress made in CAR immunotherapy.

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 Platelets are tiny (2-4 m), anucleate, hematopoietic cells that are discharged into the circulation by bone marrow megakaryocytes. Platelets were formerly thought to be the main agents of hemostasis and thrombosis. Armand Trousseau established a strong link between thrombosis and cancer in 1865. The hypothesis that platelets play many roles in the development of malignancies and in cancer-associated thrombosis is thus supported by a wealth of clinical and experimental data.The functions of tumor-educated platelets (TEPs) in the development of cancer, from primary tumors to subsequent metastatic breakouts, will be covered in this study

Abstract Cancer is largely a disease of older people; the median age for cancer diagnosis in industrialised countries is approaching 70 years of age and is expected to increase. The morbidity and mortality rates of various tumors increase with age, and thus, malignant tumors are generally defined as aging diseases. The immune system has an ambiguous role in cancer, as it plays an important immune surveillance role in the antitumor response but is also closely associated with the initiation and progression of tumors. With aging we assist to the erosion of the immune response called immunosenescence. This deregulation particularly affects the T cell compartment of the adaptive immune response. In addition to the accumulation of genetic mutations, many researchers believe that immunosenescence may also play an important role in
the tumoral process. In the future, targeting immune senescent cells may be a novel interventional opportunity in cancer patients.

Abstract Humans are continuously exposed to a wide of carcinogenic and mutagenic stimuli, including environmental toxins, radiation and viruses as well as other infections. Tumor metastasis is responsible for approximately 9% of all cancer related deaths. The tumor microenvironment (TME) contains many distinct cell types, including endothelial cells and their precursors, pericytes, smooth muscle cells, fibroblasts, carcinoma-associated fibroblasts, myofibroblasts, neutrophils, eosinophils, basophils, mast cells, T and B lymphocytes, natural killer cells and antigen presenting cells (APC) such as macrophages and dendritic cells. Recent evidence has shown that stromal tissue is much more than a passive bystander in the development and progression of cancers. None the lese,the clinical therapy for many types of human cancers has mainly focused on the malignant cancer cell itself, and have made great achievements, yet cancer therapy still remains a great challenge. This review highlights the evidence for the crucial role of the tumor microenvironment in tumor progression and metastasis.

Abstract Mitochondria are the extra-nuclear source of DNA in cells and play an important role in cell death susceptibility,  oxidative stress regulation, metabolism, and signaling in normal cells. Because of this, its dysfunction can contribute to the progression of cancer and metastasis. Also, mtDNA mutations have been reported in many cancers, followed by altered mitochondrial activity and cellular signaling . This increase in mtDNA mutation is due to the proximity of the genome to the OXPHOS system which are thought to be more in extent than mutation nuclear. These mutations do not inactivate energy metabolism but change its state. Therefore, it is not surprising that the function of mitochondria is vital for cancer cells, in addition to understanding the mechanisms of mitochondrial function in the process of tumor formation and cancer progression is essential for cancer treatments.

Abstract The increasing literature exploring the role of circulating miR-210 has clarified its potential as a promising biomarker for early detection, diagnosis and prognosis. Measuring circulating miR-210 levels could be a non-invasive method for early cancer detection. Even if, to date, most studies appear to be preliminary it seems that miR-210 will be a good target for drug development. In this study, we had detected the difference of serum miR-210 expression between health and breast cancer patients. total of 15 breast cancer patients were selected for the breast cancer (BC) group and 15 healthy people. The results showed The expression level of miR-210 in the serum of breast cancer patients was significantly higher compared with that in healthy individuals. Patients with breast cancer present increased levels of circulating miR-210; thus, circulating miR-210 may be a potential biomarker of tumor presence and therapeutic response in breast cancer

Abstract Chemotherapy and radiotherapy adversely affect spermatogenesis, a consequence that is particularly relevant to young men who have yet to establish families. The harmful effects of chemotherapy on spermatogenesis are variable, depending on the type and dosage of chemotherapeutic agents used. The current study assessed the effect of cancer therapy on sperm DNA fragmentation by Comet assay. Sperm DNA fragmentation was evaluated in cured cancer patients. The results showed a significant relationship between chemotherapy and double-stranded and single-stranded sperm DNA fragmentation.
 
 

Abstract Spermatogenesis is a very complex process that can be affected by a number of factors which may lead to reduced fertility or infertility. Busulfan kills spermatogonia stem cells and disrupts the connections between Sertoli and spermatogonia cells at base layers. Moreover, vitamin D is very important in the reproductive system of men. In this study, the effect of vitamin D on biosulfur-induced azoospermia in mice was investigated. The results showed an increase in the quality of sperm parameters in the group treated with vitamin D.

Abstract One of the most well-known side effects of anticancer drugs is the disruption of spermatogenesis. One of the most important causes of infertility in men is impaired spermatogenesis. Busulfan is a cytotoxic alkylating agent and belongs to the alkyl sulfonate group. This agent causes DNA damage by cross-linking with DNA. It kills spermatogonial stem cells. The use of healthy antioxidants can reduce the side effects of alkylating agents. In this study, we measured the protective effect of curcumin on testicular tissue of mice treated with busulfan by measuring BAX expression as an apoptotic inducer and Bcl2 as an apoptotic inhibitor. The expression levels of the two apoptotic regulatory genes Bax and Bcl-2 were evaluated by realtime PCR in four groups of mice (control, treatment with busulfan, treatment with curcumin, and treatment with busulfan + curcumin). It was observed in the busulfan group that bcl2 expression decreased, and Bax increased significantly, and the busulfan + curcumin group showed the opposite effect. Curcumin can be beneficial as a dietary supplement in cancer patients treated with drugs such as busulfan.

Abstract In recent decades, there has been an increase in the incidence of cancer in the affected communities. However, the growth of therapeutic strategies has been very slow. Conventional diagnosis and subsequent treatment in medical centers originated from pathological based examinations, symptoms, and medications.