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Immunotherapy in Head and Neck Cancers
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Oncogenes are mutated versions of normal cellular genes (called proto-oncogenes) encoding proteins that control cell proliferation, survival, and spread. Abnormalities in proto-oncogenes cause uncontrolled cell division, enhanced cell survival, and dissemination. A single mutated copy can promote cancer. Oncogenes are activated in three ways to cause cancer: mutation, amplification, and translocation.
Cancer Biology and Genetics for Non-Biologists
Published in Trevor F. Cox, Medical Statistics for Cancer Studies, 2022
There are three special types of gene, proto-oncogenes, tumour suppressor genes and DNA repair genes. Their functions are: DNA repair genes do the job of repairing genes.Proto-oncogenes make proteins that stimulate cell division, inhibit cell differentiation (stop a cell changing) and preventing apoptosis. If a proto-oncogene mutates, it can become an oncogene that does the opposite to what it should be doing, and it can make a cell divide uncontrollably.Tumour suppressor genes slow down cell division, repair DNA and send signals to cells to die. When these mutate, they no longer suppress the tumour.
The Fight Against Cancer
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
An individual may have a genetic predisposition for a certain cancer. Defective genes can be inherited, increasing the risk of cancer in subsequent generations. There are numerous possible genetic faults that can lead to cancer. Proto-oncogenes are genes that normally code for proteins that are involved in the control of cell division and differentiation. If they become mutated into an oncogene, this may disrupt the normal function of the gene and without control mechanisms in place, the cell could become cancerous. For example, the Ras protein is involved in the signalling pathway leading to cells division, during the processes of mitosis and meiosis. In normal cells, this protein has the self-regulating ability to switch itself off. In the mutated gene, Ras loses this ability, and is continually active leading to uncontrolled cell division. This mutation is found to be present in around one-fifth of human cancers.
Gene expression analysis and the risk of relapse in favorable histology Wilms’ tumor
Published in Arab Journal of Urology, 2023
Mariam M. Abdel-Monem, Omali Y. El-Khawaga, Amira A. Awadalla, Ashraf T. Hafez, Asmaa E. Ahmed, Mohamed Abdelhameed, Ahmed Abdelhalim
Normal cellular growth requires a delicate balance between growth promoting genes, known as proto-oncogenes, and tumor suppressor genes. Tumors are characterized by uncontrolled cellular division and occur when this balance is disturbed. Perturbations causing inappropriate activation or enhanced expression of proto-oncogene, or loss of tumor suppressor gene function can lead to oncogenesis. Extensive research addressing WT tumorigenesis has resulted in the recognition of mutations affecting WT1, CTNNB1, WTX, TP53 and 11p15. Yet, about 25% of WT do not have abnormalities in any of these five genetic regions, suggesting other possible underlying genetic abnormalities that are worthy of research [7]. Identifying the genes controlling cellular growth and their products can have several potential clinical implications. First, these genes or their metabolic products can serve as tumor markers used for diagnosis, follow-up and relapse detection before it is clinically evident. Secondly, these cellular markers can indicate tumor aggressiveness and, hence, stratify patients for treatment and predict relapse risk. Importantly, these genes and the resulting metabolic pathways can be used as therapeutic targets for cancer treatment. To date, there are no reliable biological markers for WT. LOH for 1p and 16q are the only genetic markers currently used in clinical practice to stratify WT patients for treatment. In this study, we examined several biological markers in WT patients and demonstrated significant associations with tumor relapse.
Enhancing anti-tumor efficacy and immune memory by combining 3p-GPC-3 siRNA treatment with PD-1 blockade in hepatocellular carcinoma
Published in OncoImmunology, 2022
Liwei Shao, Xin Yu, Qiuju Han, Xinke Zhang, Nan Lu, Cai Zhang
Immunotherapy for HCC is a rapidly evolving field, which in this past decade has transformed the oncology treatment landscape. A variety of strategies, such as cytokine administration, cancer vaccines, adoptive cellular therapy, and immune checkpoint blockade have been explored.30–32 These strategies rely on the characteristics of the TME. Firstly, some proto-oncogenes promote tumor cell proliferation and inhibit tumor cell apoptosis, which are the main reasons for tumorigenesis.33,34 Secondly, immunosuppressive TMEs created by the presence of immunosuppressive cytokines, immunosuppressive cells (such as Tregs, MDSCs, and tumor stromal cells), and inhibitory molecules may cause immune cell dysfunction.35–39 Once dysfunctional, these immune cells are unable to recognize and eliminate liver cancer cells. Therefore, combination therapy designed to inhibit oncogene expression, stimulate anti-tumor immune responses, and reverse the immunosuppressive TME state, represents a novel promising treatment strategy.40 In our study, we synthesized a short 5ʹ-triphosphate (3p) RNA targeting GPC-3, 3p-GPC-3 siRNA, and showed that it exerted a therapeutic effect on HCC, which could be further improved when used in combination with PD-1 blockade.
Bromodomain protein BRD4 is an epigenetic activator of B7-H6 expression in acute myeloid leukemia
Published in OncoImmunology, 2021
Aroa Baragaño Raneros, Ramon M Rodriguez, Aida Bernardo Flórez, Pilar Palomo, Enrique Colado, Alfredo Minguela, Beatriz Suarez-Alvarez, Carlos López-Larrea
The development of diverse BET protein inhibitors, such as JQ1 and I-BETs, had revealed the involvement of BRD4 in tumorigenesis and their great therapeutic potential. BRD4 is deregulated in several human cancers, promoting the progression of cellular cycle, invasion, inflammation, and metastatic phenotype of cancer cells.25 In fact, the MYC proto-oncogene is one of the most important targets of BRD4.26 In AML, BRD4 suppression with the JQ1 inhibitor reduces the cellular proliferation and improves the survival in murine models, suggesting that BRD4 has an essential role in the pathogenesis of the disease.27 Moreover, JQ1 induces apoptosis of leukemic stem and progenitor cells in AML patients so that cellular growth is inhibited.28 Some phase I clinical trials with BET inhibitors are completed in AML indicating that BET inhibition therapy, alone or in combination with standard therapy in AML, is acceptable although it induces some toxic effects (fatigue, diarrhea, raised bilirubin concentration, etc.) and has antitumor activity.29–31 Another clinical trial in AML using the BET inhibitor, MK-8628 (NCT02698189), is currently underway. However, the role of BRD4 in regulating molecules involved in the immune recognition is less clear.