Glioblastoma Case Study

Once a person has been diagnosed with brain cancer, treatment should begin immediately. Treatment for brain tumors involves any combination of surgery, radiation, and chemotherapy. Some tumors require several different surgical procedures; some can be treated with radiation alone. Surgery is the best process to remove a brain tumor. Surgery attempts to remove most, if not all of the tumor. Once most of the tumor is removed, the rest of the tumor can be removed through a process called radiotherapy.

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.

Optimal management of NSCLC now requires that tumours be screened for a certain range of predictive and prognostic biomarkers that help to predict sensitivity to targeted therapy and estimate prognosis respectively . For NSCLC, much of the work in the past years has been focussed on mutations of the epidermal growth factor receptor (EGFR) and on the abnormal fusion of the anaplastic lymphoma kinase (ALK) being inhibited successfully with EGFR tyrosine kinase inhibitors (TKI) and crizotinib respectively. Targeted agents are now being rationally designed to inhibit particular mutations leading to a more streamlined clinical trial process. In this review, we will examine the major subtypes of driver mutations that have been identified in NSCLC and relevant targeted therapies available both now, and in the foreseeable future.

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.

Glioblastoma Multiforme is an extremely aggressive brain tumor that can drastically alter how the body moves, a person’s memory, vision, emotion, thought, etc (GBM Guide). Having something in your brain that has the potential to drastically

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 (NB) is a common type of cancer in the early stage of childhood life, more specifically; it is known to be a disease of infancy. It is closely associated with a defect in the neuroblast differentiation process, as it plays a role in developing tissues. One of the most challenging aspects of treating NB is the variation in response to therapy among patients. This is, in part, due to the heterogeneity of the disease, which presents phenotypic differences in patients ranging from spontaneous regression of NB with unnecessary therapy to successful therapy to a more aggressive form with unpredictable outcomes. Much of the focus on understanding reasons for treatment failure has been directed toward a subgroup within the aggressive

The EGFR is a strong biomarker candidate for multiple reasons. First, it is overexpressed in most of the NSCLC tumours. This overexpression, ultimately is causing increased proliferation or cell motility, and decreased apoptosis, leading to the progression of the tumour(27). Another appealing reason is the fact that new approved therapies for those cancers are targeting EGFR, based on the inhibition of its TK activity(12). In addition, it is known that a portion of the membrane receptor is shed into the bloodstream(28), thus making plasma or serum an

Cancer is the uncontrollable division and growth of abnormal cells resulting in formation of an aggressive tumour. In some forms of Breast cancer, the cells proliferate uncontrollably due to over-expression of the protein HER2 (Human Epidermal Growth Factor Receptor 2); a receptor embedded within the membrane of cells, allowing for the transfer of signals outside to inside the cell. Trastuzumab is a monoclonal antibody administered through intravenous infusion, to be taken on its own or in combination with one or more chemotherapy regimens. It reduces risk of the cancer reoccurring or spreading by inhibiting the effects of HER2, and enhancing the body’s immune system.

Many gene targets have been used in the antineoplastic therapy. Up to now, mainly chemical inhibitors have been used to inhibit growth of cancer cells. Chemical inhibitors, however, have the intrinsic disadvantage that they often evoke nonspecific side effects (19). The current antisense technologies provide an attractive alternative but usually can only inhibit the expression of gene transiently and partially. The key features of glioma are growth and opposing cell apoptosis. Interactions with the extracellular matrix (ECM) are likely to play an important role in regulation of glioma cell growth (20). Cyr61, a cysteine-rich, heparinbinding, protein that is secreted and associated with the cell surface and ECM (21). It has been proposed that Cyr61 proteins function primarily as matricellular proteins and bridge the functional separation between structural macromolecules in the ECM and effector molecules such as growth factors and cytokines (22). Given the central role of the ECM in cell homeostasis (23), Cyr61 proteins are able to influence cell function by their regulation of ECM production as well as by binding to specific ECM components. Therefore, we tried to determine the roles of Cyr61 by acting on integrin- ECM in the human glioma.

Liquid Biopsies in colorectal cancer patients can elucidate mechanisms of clonal evolution and resistance to EGFR blockade

David is a 49-year-old male diagnosed with stage IV malignant neoplasm of colon/rectum (C18.9), along with anemia. David was previously treated with Folfox, avastin, folfiri and a hemicolectomy but still experienced disease progression. David’s disease is aggressive and progressive. David’s testing identified a KRAS exon 2 mutations, TS is un-mutated, studies show that some colon cancer patients with this mutation do not have positive outcomes following treatment with anti-EGFR medications. Stivarga improves survival and delays cancer progression among patients with metastatic colorectal cancer that has worsened in spite of other treatments. Due to his advancing age and disease state, David is currently unable to tolerate IV chemotherapy.

Bevacizumab is an anti-VEGF recombinant humanized IgG¬1 monoclonal antibody (rhuMAb) angiogenesis inhibitor that is indicated as supplemental chemotherapy for metastatic cancers including colorectal carcinoma, breast cancer, and renal cell carcinoma, as well as advanced non-squamous non-small cell lung cancer.1,3,4 It has also been approved as a second-line single agent therapy for glioblastoma multiform.3,4 Characteristic to all IgG monoclonal antibodies is the presence of two fragment-antigen binding (Fab) domains that are covalently bound to a constant (Fc) region.2 Bevacizumab is available for intravenous administration after dilution with 0.9% Sodium Chloride Injection USP with recommended dosing regimens ranging from 5 mg/kg to 15 mg/kg every 2-3 weeks, depending on the type of malignancy.3,4

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

Imatinib mesylate is a protein tyrosine kinase (RTK) inhibitor that exhibits high specificity and potency for ABL, c-kit, and PDGF receptors, which often harbor activating mutations and are typically mutually exclusive of each other and within specific cancer types.2 The compound has been approved as a targeted chemotherapy for Philadelphia chromosome positive chronic and acute myeloid leukemia (Ph+ CML and AML), Ph+ acute lymphoblastic leukemia (ALL), platelet-derived growth factor receptor (PDGFR) aberrancy-related myelodysplastic or myeloproliferative pathologies, kit+ expressing advanced gastrointestinal stromal tumors (GIST), and for FIP1L1-PDGFRα gene fusion expressing hypereosinophilic syndrome (HES) or chronic eosinophilic leukemia (CEL).1 Imatinib is available in 100 mg and 400 mg tablets for case-dependent single agent or adjunct therapy1. Therapeutic doses range from 100 mg to 800 mg/day, depending on diagnosis, age, and hepatic function.1 The drug exhibits pH-dependent solubility in aqueous solutions (soluble at pH ≤ 5.5), varying solubility in polar protic solvents, and is immiscible in polar aprotic liquids.1