Oncogenisis and Tumor Markers
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Human cancer development, or oncogenesis, results from genetic changes in oncogenes and tumor suppressor genes. Oncogenes like Ras, Myc, and EGFR promote cancer when overexpressed, while tumor suppressors like p53 and Rb inhibit cancer when functioning normally. Genetic changes from carcinogens, radiation, viruses, or other sources can delete or mutate these genes, altering the control of mitosis and apoptosis and leading to uncontrolled cell growth and the multi-step development of tumors over time. Tumor markers in the blood can indicate the presence, severity, or progression of cancers and help guide treatment responses.
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Iron plays an important role in the body, being essential for hematopoiesis, energy production, and enzyme/hormone synthesis. It exists in protein-bound forms like heme and ferritin or insoluble hemosiderin. Iron levels are tightly regulated through dietary intake and absorption in the small intestine. Deficiency can lead to anemia and other issues, while excess free iron is toxic. The document discusses iron transport, absorption, dietary sources, and factors affecting absorption.
Chapter 19 Immune Basics
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Iron metabolism final
Iron is an essential nutrient that is important for many biological processes. It exists in hemoglobin, myoglobin, and various enzymes. Iron is absorbed in the diet as heme or non-heme iron and is transported by transferrin in the blood. Disorders can result from iron deficiency or overload. Iron deficiency is common and causes anemia, while iron overload disorders like hemochromatosis result from genetic mutations affecting iron regulation.
Tumour Markers
Tumour markers are substances that are produced by tumour cells or the body's response to tumours that can be detected and measured in blood, urine, or body tissues. They can be used for screening, diagnosis, staging, detecting recurrence, and monitoring treatment response. However, tumour markers have limitations as they are not always tumour-specific and levels can be elevated in benign conditions. The main uses of common tumour markers are monitoring disease in patients with known cancers like CEA for colorectal cancer, PSA for prostate cancer, and AFP and HCG for germ cell tumours.
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Carcinogenesis is a multistep process involving genetic mutations that cause cells to proliferate uncontrollably. There are four classes of regulatory genes involved: 1) growth promoters like proto-oncogenes that become activated oncogenes, 2) inhibitors like tumor suppressor genes, 3) genes regulating apoptosis, and 4) DNA repair genes. Genetic damage occurs through environmental and spontaneous mutations and fails to be repaired if the DNA damage response is defective. This can result in oncogene activation and tumor suppressor inactivation, leading to autonomous growth, evasion of growth inhibition, apoptosis resistance, limitless replication through telomerase expression, angiogenesis, invasion and metastasis. Cancer progression involves the accumulation of additional mutations that
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Cancer is the second leading cause of death worldwide after cardiovascular disease. In India, an estimated 2.25 million people are living with cancer, with over 11 lakh new cases registered annually. Some key statistics for India include one woman dying of cervical cancer every 8 minutes and two women dying of breast cancer for every one diagnosed. Tumor markers are substances produced by cancerous tissues or the body in response to cancer that can help detect or monitor cancer. Some common tumor markers are CEA, AFP, CA125, and PSA. Tumor markers can be used for screening, diagnosis, staging, prognosis, and monitoring treatment effectiveness and recurrence. Characteristics of ideal tumor markers include cancer specificity, high sensitivity and specificity for detection
Cancer biology
Cancer biochemistry involves biochemical alterations in cancer cells. Specific objectives include listing protooncogenes and tumor suppressor genes, and explaining their roles and mechanisms of action. Protooncogenes become oncogenes through activation mechanisms like mutations. Tumor suppressor genes like p53 regulate cell proliferation and their mutation leads to cancer. Cyclins and cell cycle phases are also discussed. Standard cancer treatments include surgery, radiotherapy, and chemotherapy using antimetabolite drugs. Tumor markers can be used for cancer diagnosis, prognosis, localization, and treatment monitoring and are classified based on their type.
Tumour markers with Recent Advances
Tumor markers are biological substances that are produced by cancer cells or the body's response to cancer. Ideal tumor markers should be highly specific, sensitive, correlate with tumor stage/mass, and predict prognosis. Recent advances include new genetic and viral biomarkers. Tumor markers can be classified as hormones, oncofetal antigens, enzymes, tumor-associated proteins, receptors, and genetic markers. Oncogenes like RAS and C-myc can also serve as markers when mutated or translocated. Establishing biomarkers requires understanding how small molecular changes disrupt cellular functions and cancer initiation.
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This document discusses chemical carcinogenesis and the initiation and promotion stages. Initiation results from exposure to a carcinogenic agent and causes permanent DNA damage (mutations). Promotion alone cannot cause tumors, but can induce tumors in initiated cells by causing proliferation and clonal expansion of initiated cells. The document also discusses various carcinogens like radiation, viruses, and bacteria that can cause cancer through direct DNA damage or indirect mechanisms like chronic inflammation. It also summarizes tumor immunity, how tumors evade the immune system, and some clinical aspects of cancer like paraneoplastic syndromes and cachexia.
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This document discusses chemical carcinogenesis and the initiation and promotion stages. Initiation results from exposure to a carcinogenic agent and causes permanent DNA damage (mutations). Promotion alone cannot cause tumors, but can induce tumors in initiated cells by causing proliferation and clonal expansion of initiated cells. The document also discusses various carcinogens like radiation, viruses, and bacteria that can cause cancer through direct DNA damage or indirect mechanisms like chronic inflammation. It also summarizes tumor immunity, how tumors evade the immune system, and some clinical aspects of cancer like paraneoplastic syndromes and cachexia.
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Cancer develops through a multistage process of genetic mutations that alter the normal control of cellular growth and proliferation. The initial step is initiation by carcinogens, which cause DNA damage and mutations in proto-oncogenes and tumor suppressor genes. This gives cells a selective growth advantage. Promotion makes the environment favor growth of these mutated cells. Finally, progression leads to increased proliferation and metastasis. Oncogenes stimulate growth while tumor suppressors inhibit it. Loss of control over these genes, through acquired or inherited mutations, drives carcinogenesis.
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Cancer arises from mutations in genes that control cell division, apoptosis, and DNA repair. There are three main classes of cancer genes: proto-oncogenes that become activated oncogenes, tumor suppressor genes that are inactivated, and mutator genes that increase mutation rates. The two-hit model explains that tumors often develop when both copies of a tumor suppressor gene acquire mutations. For example, the tumor suppressor gene RB is mutated in the inherited cancer retinoblastoma following the two-hit model. Cancer development can also be caused by viruses introducing oncogenes or through exposure to carcinogens and radiation inducing mutations.
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Cancer is characterized by uncontrolled cellular growth and proliferation that can spread to other parts of the body. It is caused by both external factors like chemicals, radiation, viruses and internal factors such as genetic mutations. Cancer development is driven by changes in oncogenes and tumor suppressor genes. Tumor markers are substances produced by cancer cells or the body in response to cancer that can be detected in bodily fluids or tissues and used to diagnose certain cancer types. Some common tumor markers are CEA for colon cancer, AFP for liver cancer, and PSA for prostate cancer.
Oncogenic virus-host cell interaction
Oncogenic viruses can interact with host cells in ways that promote oncogenesis through both direct and indirect mechanisms. Direct mechanisms include viruses introducing oncogenes that alter cellular signaling pathways and disrupt cell cycle control. Indirect mechanisms involve evading immune responses, establishing chronic infections, and inducing chronic inflammation. Specific oncogenic viruses discussed include EBV, HPV, HBV, HCV, HTLV-1, and KSHV. Each virus employs distinct strategies to activate cancer hallmarks in host cells, with EBV and HPV expressing oncoproteins that mimic cellular signaling and proliferation factors, while HBV/HCV cause liver damage and HBV/HTLV-1 inhibit apoptosis.
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This document discusses cancer and its genetic basis. It begins by introducing cancer and how it is caused by the accumulation of genetic damage over time through mutations in genes that control cell growth. Key points include: cancers originate from mutations in somatic cells, not germ cells; carcinomas make up over 90% of cancers and originate from endodermal or ectodermal tissues; the ability of cancer cells to invade and metastasize distinguishes malignant from benign tumors. The document then covers specific genetic mutations and cellular processes involved in cancer development.
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Lung cancer is a malignant tumor that can be categorized as small cell or non-small cell. Small cell lung cancer grows faster but is more responsive to chemotherapy. It can be limited, confined to the chest, or extensive, having spread outside the chest. Symptoms often appear after the cancer has invaded tissues or spread. Small cell lung cancer accounts for 20% of lung cancer cases and has a median survival of 16-24 months with treatment for limited stage disease. Risk factors include cigarette smoking and second-hand smoke exposure. Treatment depends on stage and typically involves chemotherapy and radiation.
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Cervical cancer develops in the cervix, the lower part of the uterus. It begins as pre-cancerous changes to cervical cells and can progress to cancer. About 10,520 new cases are diagnosed in the US each year, with risks highest for those who are sexually active at a young age or have HPV. Screening via Pap tests can detect cell abnormalities early when treatment is most effective. Treatment options depend on cancer stage and may include surgery, radiation, chemotherapy, or vaccines.
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Interceptive orthodontics refers to procedures that eliminate or reduce malocclusion in the developing dentition. Local factors that can cause malocclusion include delayed eruption, retained primary teeth, infraocclusion, ectopic eruption, hypodontia, diastema, crowding, and thumb sucking. Treatment for these local factors may include extractions, space maintenance, serial extraction, or appliances to redirect eruption. The timing of interceptive treatment is important to address developing issues before malocclusion worsens.
Interceptive orthodontics
Interceptive orthodontics refers to procedures that eliminate or reduce malocclusion in the developing dentition. Local factors that can cause malocclusion include delayed eruption, retained primary teeth, infraocclusion, ectopic eruption, hypodontia, diastema, crowding, and thumb sucking. Treatment for these local factors may include extractions, space maintenance, serial extraction, or appliances to redirect eruption. The timing of interceptive treatment is important to address developing issues before malocclusion worsens.
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The document discusses various types of maxillary and mandible fractures, including LeFort fractures and their associated signs and symptoms. It recommends treating open fractures within 48 hours to restore normal occlusion and refers various complex injuries, such as those involving the intracranial cavity, cervical spine, orbit, or facial nerves. The summary emphasizes stabilizing the patient, thoroughly examining for other injuries, managing soft tissues, and referring complex cases for appropriate treatment.
Spread of tumours
Tumors can spread through direct extension into surrounding tissues, through the lymphatic or vascular systems, or by transcoelomic spread through body cavities. Lymphatic spread is common for carcinomas and follows drainage routes to regional lymph nodes. Vascular spread occurs via blood vessels either as tumor emboli or growing along vessel walls. Certain primary tumors have tendencies to metastasize to specific organs, such as prostate cancer spreading to bone. Transcoelomic spread involves cavities such as the peritoneal, pleural, or pericardial spaces, potentially causing malignant ascites or pleural effusions. Perineural spread grows along nerve bundles.
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This document summarizes key aspects of deciduous and permanent dentition development from birth through the mixed dentition stage between ages 6-12 years. It describes the typical sequence of tooth eruption, features of primary teeth, development of spacing as permanent teeth emerge, and transient crowding that can occur during the mixed dentition phase. Normal occlusion is defined, including requirements that all teeth be present and make proper contact within and between arches.
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Cleft lip and palate is a congenital abnormality caused by failure of fusion of structures like the lip, alveolus, hard and soft palate during embryonic development. It has an incidence of 1 in 600 live births for cleft lip and palate, and 1 in 1000 for isolated cleft palate. Treatment involves surgical repair of clefts as well as management of associated issues like feeding problems, hearing loss, dental abnormalities, and speech and facial growth defects. Secondary surgery may be needed to improve cosmetic or functional outcomes.
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