Neuroblastoma Biology Essay

When cancer forms, your body has ways of trying to stop it from further developing. The four regulators are known as proto-oncogenes (which when mutated are known as oncogenes), tumor suppressor genes, apoptosis, and telomerase genes. When there is a mutation in each of the genes, cancer can develop. Once cancer develops it continues to grow and divide and turn into a tumor. For a tumor to develop it essentially needs something supplying it with blood and nutrients so that it can continue to grow. One player in the game of supplying the tumor with blood is a protein kinase known as Protein kinase C. A protein kinase is simply a molecule that regulates numerous cellular responses including gene expression, protein secretion, cell proliferation, and the inflammatory response. According to researchers at Harvard University, EBC-46 has the ability to target protein kinase C and inhibit it, which in turn causes the tumor to die because it is no longer has the ability to synthesize proteins it needs to survive. According to the Queensland Institute, the inhibition of  protein kinase C helps destroy the blood vessels that supply the tumor with the oxygen and the nutrients it would need for survival. Pretty exciting stuff

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.

Its locus is particularly amplified in these noted tumours leading to the progression of these cancers, it can be suppressed by p53 (tumour/ proliferation suppressor) which represses the EZH2 promoter, resulting inhibition of cell proliferation and invasion (Bracken, 2003; Xiao, 2011).

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.

Tumors can be classified into three types: 1) benign 2) pre malignant 3) malignant tumor. Benign tumors are those which are incapable of abrupt expanding and affecting the other healthy brain tissues. Premalignant tumor is a pre cancerous stage, if not treated properly it may lead to cancers. It is often considered as a disease. Malignant tumor grows rapidly with time an ultimately leads to death of patient. Malignant is a medical term describing a sever growth of a disease. The most common primary brain Tumors are gliomas, wherein 70% are in the group of malignant gliomas, glioblastoma multiform (GBM).The GBM is one of the highest malignant human

This year it is estimated that roughly 24,000 adults in the United States alone will be diagnosed with primary cancerous tumors of the brain or spinal cord (Brain Tumor: Statistics) . Brain related cancers are the 2nd leading cause of death for men up to age 39 and women up to age 20 (Brain Tumor Primer) . There are two types of tumors, benign and malignant. Each tumor has a different possible treatment method. Malignant tumors may require surgery, chemotherapy and radiation therapy, while benign tumors may only require surgery. There are also various clinical trials for malignant tumors, one of which involves combining the chemotherapy medication temozolomide with radiation therapy to treat the tumor, or at the very least slow the growth

Glioblastoma(GB) is the most common primary malignant solid brain tumor in adults1. Known for its aggressive characteristics and poor prognosis, the median survival rates of GB patients remain less than 18 months2,3. Tumor relapse owing to chemotherapeutic resistance is almost universal and GB is no exception, thus reflecting in high mortality and morbidity rates4. The WHO 2016 classification of brain tumors identifies GB tumors based on histology, molecular and genetic characterization into defined transcription profiles such as classical, neural, pro-neural and mesenchymal types5. Additionally, the commonly occurring genetic aberrations of primary GB are amplifications/mutations of EGFR, PDGFRA, PTEN, and of secondary GB are IDH1, MDM2

Neuroblastoma is a type of cancer where neuroblasts, which are a type of nerve cell, fail to mature and become Neuroblastomas, which can be cancerous. Susceptibility to Neuroblastoma can be inherited through your parents and through the PHOX2B gene. Although, there are suspicions that the ALK gene might contribute to the disorder as well as the PHOX2B gene, but scientists are still not sure.

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

Gliomas are broad category of brain tumors arising from glial cells. They are the most common primary malignant neoplasms of the central nervous system. They are classified into low-grade (WHO grades I and II) and high-grade (WHO grade III and IV) tumors. Almost 80% of gliomas are astrocytic tumors including Glioblastoma multiforme (GBM). Diagnosis of glioma includes a CT scan/MRI scan and biopsy. These tumors are highly resistant to current treatment modalities including surgery, radiation therapy, chemotherapy, corticosteroids, antiangiogenic therapy, and experimental approaches such as gene transfer, their prognosis is dismal.Malignant gliomas results from a multistep process which involves genetic alterations arised from innate and environmental

Glioblastoma Multiforme accounts for about 17 percent of all tumors of the brain. These tumors

Neuroblastoma can either be benign, which means the tumor is not cancerous and it just needs to be removed, or it can malignant, which means the tumor is

(2000) reported that 90% of IBC tumours displayed an over expression of RhoC GTPase, an oncogene that contributes to the invasive nature of IBC. Rho protein activation causes the actin-myosin contractile filaments and focal adhesion complexes to assemble, leading to the formation of lamellipodia. Lamellipodia form at the edge of cells and drive cell migration and motility, furthering metastasis in IBC (Machesky 2008).

Glioblastoma multifore (GBM) or simply glioblastoma is the most malignant type of brain tumors that is characterized by a strong infiltrative growth. Although the exact etiology of this malignancy is not fully understood, several concepts are contributed to support the aggressiveness and tumor re-initiation behaviors. Among these concepts, is the Cancer Stem Cell (CSC), a sub-population of tumor cells that featured by stemness capability, oncogenic potential and chemo-/radiotherapeutic resistance.

Tumor suppressor genes in normal cells act as braking signals during phase G1 of the cell cycle, or to stop or slow the cell cycle before S phase. If tumor-suppressor genes are mutated, the normal brake mechanism will be disabled, resulting in uncontrolled growth. Mutations in tumor-suppressor genes cause loss-of-function. Loss-of-function mutations generally only show up when both copies of the gene are mutated. In other words, if a pair of tumor suppressor genes are lost or mutated, their functional absence might allow cancer to develop. For instance, a growth factor receptor may send signals even when