Essay On Glioblastoma

Glioblastoma is the most common and aggressive form of malignant brain cancer in adults. On average, 8 of every 100,000 people in the U.S. are diagnosed with glioblastoma every year – representing approximately 2% of all cancers diagnosed [1]. Glioblastoma tumors form when astrocytes, star-shaped cells which support and protect the brain, re-enter the cell cycle and start to rapidly divide. Because the brain is supported by a large network of blood vessels, tumors grow quickly and are difficult to remove surgically. Present treatments for glioblastoma are limited to surgery, radiation therapy, and chemotherapy; however, despite these interventions tumors are likely to regrow. Consequently, typical survival time following glioblastoma diagnosis is less than 2 years.

Glioma is a tumor that is a type of brain cancer. Glioma tumors are made up by cells called glial cells. Glial cells normally provide nutrition, oxygen, and structural support to the brain. Three types of glial cells can produce tumors. Gliomas are named after the type of glial cell that is involved in the tumor. A tumor is formed when the glial cells grow into an abnormal mass of tissue. Gliomas are one of the most common types of brain tumors that occur in adults.

CNS tumors represent the second most frequent tumor of childhood and the most common pediatric solid tumor; approximately 2,200 patients under the age of 20 are diagnosed each year with invasive CNS tumors, and CNS tumors are the number one cause of death from childhood cancer. [1] Therapeutic strategies generally involve surgery as a primary intervention, but complete resection is often not possible due to tumor location. In such cases, adjunct therapies, including chemotherapy and radiation therapy, may be required based on the tumor histology and presence of residual tumor. [2]

Current investigations indicate that Central neurocytoma could be of astrocytic origin or mixed lineages. Immunohistochemical tests shows multiple positive markers of neural cell that includes synaptophysin, neuron specific enolase, neuronal specific nuclear protein , and neuron specific class III beta tubulin. In addition to dense core vesicles and parallel microtubules are present in pathology. The tumor also shows positive neurofilament (NF) staining but some of the Central Neurocytoma fails to show consistent pathology. Unfortunately, the Immunohistochemical studies are not specific to draw a concrete conclusion to the origin of neurocytoma. Von Deimling et al. investigation indicated that Central neurocytoma shows glial fibrillary acidic protein (GFAP) and Syn, which is related to reactive astrocytes. Other studies were unable to attain the same results. In vitro, the tumor cells tend to become glial cells regardless of the medium of the culture. In vivo, the origin of the cells is not clear. Some researches hypothesize that CN arise from neural stem cells surrounding the ventricle zones. This hypothesize was based on high levels of choline, cholinergic receptors, gamma-aminobutyric acid, and normal or low levels of glutamate and catecholamines. Kim et al also showed the presence of Musashi-1, and the neuroep- ithelial enhancer gene nestin. These results point towards possible genetic properties to

Glioblastoma (pronounced like gleO blastoma) is an incurable brain cancer,Survival rate is usually measured in months.This became a word that was instantly defined, researched, dissected, feared, and tried to comprehend and understand by family,friends and acquaintances of Larry McKee (McKee)who was personally affected from this single word, it was quickly added to their vocabulary, because of the of the events that transpired on October 22, 2011 that forever changed lives “Glioblastomas are tumors that arise from the astrocytes- the star-shaped cells that make up the “glue-like,” or supportive tissue of the brain. These tumors are usually highly malignant (cancerous) because the cells reproduce quickly and they are supported by a large network of blood vessels.”(A.B.T A..) He was diagnosed with stage four.

Dysregulation of gene expression within the neurons could also result in uncontrolled cell growth leading to formation of tumors. This was facilitated by expressing the targets of miR-10b—BCL2L11/Bim, TFAP2C/AP-2γ, CDKN1A/p21, and CDKN2A/p16 that regulated controlled cell growth. MiR-10b was therefore responsible for uncontrolled cellular growth by downregulating proapoptotic genes. These miRNAs have been validated to negatively regulate the protein tyrosine phosphatase μ (PTPμ) gene that has been observed to be down regulated in these tumor cells. Inhibition of miR-10b decreased growth of the tumor by retraction from the cell cycle and encouraging programmed cell death. Decreased survival of glioblastoma

Common malignant brain cancers increase significantly according to statistical data collected by the National Cancer Institute. In 1984, the annual incidence rates of primary brain tumor and primary brain lymphoma also increased notably, the rate of lymphoma almost tripling,

Another major breakthrough that occurred in the early 1970’s was the discovery of the first promising chemotherapy for glioma. A glioma is a malignant tumor that begins in the glial cells which surround the nervous system. Gliomas can be found in the brain and spinal cord. Researchers studied a chemotherapy drug called carmustine (BCNU) and

The purpose of the study Single-Cell RNA-Seq Highlights Intratumoral Heterogeneity in Primary Glioblastoma was to determine the composition of a glioblastoma tumor to better understand how the heterogeneity in the regulatory programs of the cell are important to prognosis and therapy. The authors took 5 glioblastomas and used SMART-Seq to profile them. They isolated the individual cells from the 5 glioblastomas and created single-cell full-length transcriptomes to then determine the intratuormal heterogeneity. From this, the authors were able to find that the tumors were variable in their expression when it came to the different transcriptional programs within the cell. When the authors determined the characteristics of the tumors that

If the hypothesis that CCND1 is a potent oncogene in glioblastoma becomes validated, the next step would be to exploit this oncogene as a therapeutic target. Despite outstanding developments in cancer research and current advances in multimodality therapies, no significant progression has been made in the treatment of glioblastoma over the past decade and the disease remains fatal.

Neuroblastoma is the most common solid extracranial cancer in children under the age of five. Mainly a neuroendocrine cancer, neuroblastoma is prevalently found in neuronal tissue of the adrenal glands as well as the ganglia in the spine. It is believed that neuroblastoma arises from neuronal crest cells; immature cells that branch off the neural tube in embryonic development (Roberts et al., 1998). Though 98% of all neuroblastoma cases are sporadic, there is a small percentage of the cancer that is inheritable. One of the genes believed to contribute to familial neuroblastoma is MYCN. MYCN, which encodes a transcription factor, is observed to be duplicated multiple times through out the genome of neuroblastoma cells, both familial and sporadic.

The brain is made up of millions upon millions of cells. These cells are formed from before birth, up until about 7 years old. Once these brain cells stop dividing, they are never meant to divide again. You can see that the division of brain cells is under strict regulation and control. When this control is lost in a single cell, then it starts dividing in an uncontrolled manner. All of the data obtained through research on cancer shows that this disease is caused by a rapidly dividing cell, with no regulators to stop it from dividing. As the cell makes more and more copies of itself, it grows to form a tumor. This is known as cancer.

The fundamental basis to the cancer stem cell hypothesis is the belief that all cancers have cancer stem cells that are responsible for the resistance and recurrence of cancers, even after conventional treatment methods (Tao & Kiera, 2015, p.1). If these specialized cells are not destroyed

A major player in neuroblastoma biology is MYC, it is normally contained within our cells and is a large protein that functions as a transcription factor. MYC is known to be a proto-oncogene which normally activates gene expression, it can also repress it depending on what gene it sits on.

Ngns (class II bHLH transcription factors) are known as pro-neural factors as they are necessary to initiate differentiation of NSPCs and are important to specify a neuronal subtype[3]. Ngns activate downstream several pro-neural factors for the formation of neurons from NSPCs. Earlier studies showed that development of neurogenic machinery is mediated by cascade of transcriptional activation which begins by activation of Ngn1 and Ngn2. This then activates NeuroD1 and NeuroD6 (other bHLH factors). In turn NeuroD1 and NeuroD6 activates Nsc1 which then activated terminal transcription factors and triggers neurogenesis[4]. Thoma et al observed that Ngn2 alone is sufficient to induce neuronal differentiation in embryonic stem cells. In this study they used murine embryonic stem cells and transfected with Ngn2 expression and after five days post transfection they observed that cells expressed Tuj1 and MAP2 (both are neuronal markers). This indicates that presence of a single pro-neural factor as well could promote neurogenesis. Ectopic expression of Ngn2 was sufficient to form mature neurons from embryonic stem cells[5]. Ngn2 was also seen to have a vital role in the development of dentate gyrus (DG). Galichet et al observed that in Ngn2 knockout mice there was a strong reduction in the size of DG. They also showed a marked reduction in the number of neural stem progenitors in DG. These Ngn2 mutant