Tarim Mahmood* and Bhaskar Chakraborty
DOI: 10.37421/ 2576-3857.2022.7.002
Seeram Ramakrishna
A core of several tetraspanin proteins organizes other membrane proteins like growth factor receptors, integrins, and Human Leukocyte Antigen (HLA) antigens in these complexes. Albeit most tetraspanin proteins have been concentrated separately, tetraspanin proteins and their edifices can affect cell grip and motility, associations with stroma or influence announcing development factors, and for the greater part of them no ligand has been distinguished. Although they are found in all cell types, these proteins have primarily been studied functionally in lymphoid cells. Tetraspanins have been identified as metastasis suppressors in some tumors, but their significance is still unclear. Data are also available for these tumors. They are outlined, along with some of their implications for tumor biology and areas that require additional research. The biological properties of tumor cells, particularly those pertaining to tumor adhesion and dissemination, can be significantly affected by membrane proteins that are involved in cellular interactions with other cells or the stroma as well as signaling pathways. The tetraspanins, a brand-new class of membrane proteins, are beginning to gain importance in cell biology but have received very little attention in the context of cancer biology up until this point.
Wenbin Lin
Heterochromatin Protein 1α (HP1α) is a critical player in chromatin organization and gene regulation, and its dysregulation has been implicated in various cellular processes, including cell proliferation and cancer development. This review focuses on the role of HP1α as a characteristic of cell proliferation that is pertinent to clinical oncology. Extensive research has demonstrated that HP1α plays a dual role in regulating cell proliferation. On one hand, it functions as a transcriptional repressor, modulating the expression of genes involved in cell cycle control and DNA replication. On the other hand, HP1α has also been found to interact with numerous signaling pathways and transcription factors, thereby promoting cell proliferation under certain conditions. Aberrant expression and localization of HP1α have been observed in various types of cancer, including breast, prostate, lung, and colorectal cancer. Furthermore, studies have shown that altered HP1α expression is associated with poor prognosis and resistance to conventional therapies in cancer patients. Understanding the molecular mechanisms underlying HP1α's involvement in cell proliferation is of significant interest in clinical oncology. Targeting HP1α and its associated pathways may offer promising therapeutic opportunities for cancer treatment. In addition, HP1α expression levels and subcellular localization can potentially serve as diagnostic and prognostic biomarkers in clinical practice.
Cancer Biology
Overall Survival (OS) is regarded as the most trustworthy and preferred endpoint in oncology trials to evaluate drug treatment benefits. In order to speed up and streamline the development of clinical oncology drugs, it is critical to identify the dynamic effects and connections between the various variables collected from patients for a given drug and its indication. Due to temporal differences, drug-induced effects and causal relationships can be difficult to interpret. Parametric time-to-event models and population pharmacokinetic– pharmacodynamic modeling are increasingly being used to address this issue.
Journal of Oncology Medicine & Practice received 142 citations as per Google Scholar report
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