Journal of Neoplasm

Description

The term tumor heterogeneity refers to the fact that distinct tumor cells can exhibit distinct morphological and phenotypic profiles, such as cellular morphology, gene expression, metabolism, motility, proliferation, and metastatic potential. This phenomenon occurs both within tumors and between tumors, which is referred to as inter tumor heterogeneity. The flawed replication of DNA simply results in a small amount of intra tumor heterogeneity: A few mutations are acquired whenever a normal or cancerous cell divides, resulting in a diverse population of cancer cells. The heterogeneity of cancer cells presents significant obstacles to the development of effective treatment strategies. However, understanding and characterizing heterogeneity can facilitate a deeper comprehension of diseases origins and progression. This, in turn, has the potential to direct the development of more refined treatment plans that take into account heterogeneity to increase efficacy.

Malignant Tumor

However, it is still up for debate whether CSCs exist. This is due, in part, to the difficulty of reproducing CSC markers across multiple tumors. Furthermore, xenograft models are utilized in methods for assessing the possibility of tumorigenesis. The inherent limitations of these methods include the need to control the transplant animal’s immune response and the significant difference in environmental conditions between the primary tumor site and the xenograft site such as the absence of necessary exogenous molecules or cofactors. As a result, the accuracy of CSC results and the conclusions regarding which cells have the potential to become tumors has been questioned. According to the cancer stem cell model, there are only a small number of cells that are tumorigenic capable of forming tumors in a population of tumor cells. Cancer Stem Cells (CSCs) are characterized by their capacity for self-renewal and differentiation into progeny that are not tumor causing. According to the CSC model, differences in the stem cells from which tumor cells originate account for the observed heterogeneity. Changes in epigenetics frequently cause variability in stem cells. The most common malignant brain tumor that arises from glial tissue is a glioma. According to a number of studies, Glioma Cancer Stem Cells (GCSCs) play a significant role in the characteristics of malignant gliomas that lead to the formation of tumors. A small population of GCSCs in the brain plays a crucial role in glioma cell metastasis to other organs. The accumulation of evidence demonstrated that GCSC growth, proliferation, migration, and invasion were mediated by a number of signaling pathways, including Notch, TGF-, STAT3, and EGFR. In addition, it has been discovered that non coding RNAs, such as miRNAs, circular control GCSC pathogenesis and drug resistance. As a result, glioma treatment could expand by targeting these pathways. We summarized important signaling pathways that are involved in the stimulation or inhibition of GCSC tumorigenesis. Adult gliomas are the most common primary malignant brain tumor. They can occur anywhere in the Central Nervous System (CNS), but their development in the glial tissue of the brain is where they are most common. With 81% of malignant brain tumors, gliomas are the most common primary intracranial tumor. Low grade gliomas have a low proliferative capacity, while high grade gliomas have a high proliferative rate, a poor prognosis, and an aggressive phenotype. Glioblastoma, also known as grade glioma, is an aggressive and diverse CNS tumor. Astrocytes and oligodendrocytes are the sources of this malignant tumor. Primary isocitrate dehydrogenase wild type and secondary GBM are the two subtypes. Tumor maximum surgical resection and concurrent postoperative chemo radiotherapy or adjuvant chemotherapy are currently the standard treatment options for glioma. Similar to other types of cancer cells, Glioma Cancer Stem Cells (GCSCs) have been identified and isolated in a number of studies. These GCSCs contain tumor initiating characteristics in malignant gliomas. It was reported that GCSCs induced therapeutic responses, metastasis, and angiogenesis. Through its effects on the pathway and Wnt signaling, our findings demonstrate that rictor is responsible for miR-34a tumor suppressive function in glioblastoma. Glioma malignancy is profoundly affected by these pathways.

Stem Cells

The most prevalent tumor of the Central Nervous System (CNS) is glioma. Glioblastoma multiforme, which is categorized as grade glioma by the World Health Organization (WHO), is the most aggressive, infiltrative, and vascularized type of glioma. Patients with GBM have a median survival time of one year. The location of the disease and the high level of inter and intra tumoral heterogeneity, which results in the accumulation of multiple genetic changes over time, poses significant obstacles to GBM therapy. The existence of a hierarchy between tumorigenic and non-tumorigenic subpopulations of cancer stem cells may have contributed to the heterogeneity. Glioma Stem Cells (GSCs), also known as Glioma Initiating Cells (GICs), are thought to be the cell of origin for gliomas. These cells have a tendency to differentiate into Glioma Stem Cells (GSCs). A variety of abnormal events at the genetic and epigenetic levels, including modifications to the microRNA class of non-coding RNAs, are involved in this transformation into a glioma stem cell state. Glioblastoma is a difficult CNS tumor to treat due to its heterogeneity within the tumor, its deep seated location in the brain, aggressive nature, and angiogenic behavior. GBM prognosis remains challenging despite the fact that multimodal therapies improve patient survival. The presence of a small tumor initiating cell population that propels the tumor is thought to be the source of the tumors phenotypic and functional heterogeneity. Upregulated expression of a number of miRNAs has been found to regulate GCSC oncogenic characteristics like cell proliferation, migration, invasion, and so on. High grade glioma is characterized by invasion, as evidenced by the aggressive mesenchymal GBM phenotype. One of the anti-invasive microRNAs and there is a positive correlation between miR-21 and miR-10b and glioma invasion in recent years. The growth and recurrence of glioma tumors are significantly influenced by glioma stem cells. Glioma can be cured by focusing on signaling pathways linked to drug resistance and stemness properties of these cells. As a result, glioma stem cell self-renewal and invasion can be effectively controlled with the help of miRNAs.