17th lecture
* لتحميل المحاضرة ادخل الرابط التالي https://app.box.com/folder/19854514021Cancer: (Latin word crab) is defined as the new growth of abnormal cells. Oncology: the field of medicine that specializes in cancer, including the basic characteristics, classification, and origins of cancer.
* 17th lecture
An abnormal growth or tumor is generally characterized as benign or malignant. A benign tumor: is a self-contained mass within an organ that does not spread into adjacent tissues, do not ordinarily cause death unless they grow into a critical space such as the heart valves or brain ventricles. Malignant tumor (cancer): is uncontrolled growth of abnormal cells within normal tissue cells such as skin and bone marrow that have retained the capacity to divide, while mature cells that have lost this power (neurons, for instance) do not commonly become cancerous.
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Most cancerous growths show other characteristics, including: (1) Disorganized behavior and independence from surrounding normal tissues. (2) Permanent loss of cell differentiation. (3) Expression of special markers on their surface. As the initial (primary) tumor grows, it invades nearby tissues, enters lymphatic and blood vessels, and establishes secondary tumors in remote sites. This property of spreading is called metastasis, and the cancer is said to metastasize. Malignant tumors range in effects from those seen in pancreatic cancer) spread rapidly, almost always fatal, to as basal cell carcinoma of the skin, )much less aggressive, more treatable, and seldom fatal(.
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Although cancers are commonly referred to simply as bladder cancer, breast cancer, or liver cancer Carcinomas: cancers are originating from epithelial tissues Sarcomas: cancers are originating from mesenchyme (embryonic connective tissue) Descriptive name: such as Adenocarcinoma develops in glandular tissue such as the pancreas; Squamous cell carcinoma arises in the skin epidermis; Retinoblastoma occurs in the retina; Lymphosarcoma in the lymph nodes; Hepatoma(hepatic sarcoma) in the liver; Melanoma in the skin melanocytes. Leukemia, denotes cancer of the blood-forming tissues.
* 17th lecture
One-third of all U.S. citizens will develop cancer some time during their lifetime. Cancer is the second leading cause of death in humans (following heart and circulatory disease). Cancers currently on the increase melanoma (presumably due to increased levels of UV radiation entering the atmosphere), Kaposi’s sarcoma (in AIDS patients), thyroid cancer, esophageal cancer, and prostate cancer (because of an improved method of detection). Lung cancer accounts for the largest number of deaths in both sexes, followed by prostate cancer in men and breast cancer in women.Certain cancers are inherited or due to endogenous viral genomes, while many cancers reflect both hereditary and environmental factors (lung cancer). * 17th lecture
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*Cancer is clearly a complex disease associated with numerous physical, chemical, and biological agents . The evidence for the interrelationship between genes and cancer is derived from the following observations: (1) Cancer cells often have damaged chromosomes. (2) A specific alteration in a gene can lead to cancer. (3) The predisposition for some cancers is inherited. (4) Rates of cancer are highest in Immunodeficiency diseases (5) Mutagenic agents cause cancer. (6) Cells contain genes that can be transformed to cancer-causing oncogenes. (7) Tumor-suppressor genes (antioncogenes) exist in the normal genome.
* 17th lecture
There is a state of balance ensures that cells divide at a rate compatible with normal development and function. Cancer results when the system that organizes cell division is failure. Proto-oncogene: the gene complex controlling cell division by regulating the onset of mitosis. It is regulated by another gene called Tumor-suppressor gene (antioncogene): Gene that prevents the proto-oncogene from acting continuously and keeps the cell division cycle operating normally. If a genetic error (mutations) keeps the proto-oncogene switched on, it converts to an oncogene, causing the cell to divide continuously.
* 17th lecture
Common pathway for neoplasias. (a) Normal cell cycle and genetic controls. (b) Event that stimulates transformation into a cancer cell. Any agent that can alter the genetic control mechanisms can cause a cell to divide at incorrect times and in incorrect places.
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Oncogenic change occurs when a cell is infected by some viruses :RNA viruses Retrovirus utilizes an enzyme (reverse transcriptase) to synthesize viral DNA, which is subsequently inserted at a particular site on a host chromosome.Rous sarcoma virus, carry viral oncogenes whose products cause transformation of host cells into cancer cells. In T-cell leukemia retroviral genomes insert on host chromosomes sites can lead to activation of the cell’s own proto-oncogenes * 17th lecture
DNA viruses Human papillomavirus (HPV), causes (cervical carcinoma), inserts its genome directly into a chromosome in a way that overrides the usual cellular growth controls. Epstein-Barr virus (EBV) causes (Burkitt lymphoma), induces a chromosomal alteration that can interfere with cell death.
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Outcomes of viral infection. (a) A virus cango through the normal lytic cycle and destroy its host cell. (b) A possible mechanism for viral induction of cancer. DNA viruses and retroviruses can insert DNA into the host’s genome. If it inserts into a sensitive site (near a proto-oncogene), the cell can be converted into a tumor cell. *
Several cancers are associated with gross chromosomal changes or other aberrations that occur during mitotic divisions. translocation :a segment of one chromosome is transferred to another chromosome that is not its homologue. -Burkitt lymphoma ( the translocation chromosome 8 to chromosome 14). -Myelogenous leukemia almost are due to the translocation of a proto-oncogene on chromosome 9 to a different site on chromosome 22.
* 17th lecture
trisomies is a mistake in mitosis that produces cells bearing three rather than the usual pair of a particular chromosome. Such leukemia (occurring with chromosome 8 and 12) A second master regulator gene, P-TEN, codes for a protein to slow cell division. Disruption of this gene through mutation creates an aggressive cancer cell that is responsible for several rapidly growing tumors.
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Apoptosis: undergoing of abnormal, diseased, or old cells, the natural programmed death by Suicide genes . cancer cell have genetic defects that keep the suicide gene from being switched on, the cells never receive a death signal and thus become immortalized. Some viruses, such as the Epstein-Barr virus (Burkitt lymphoma), and papilloma viruses (warts), contain a gene called C-MYC that interferes with the onset of apoptosis and thereby allows infected cells to survive.
* 17th lecture
With the time, the genes that ordinarily regulate the repair of mismatched nucleotides are defective and can no longer detect and repair mutations, lead to accumulated mutations and increase the likelihood of cancer. Using monoclonal antibodies as immunotherapy that inactivate receptors on cancer cells, has been used successfully on breast cancer. Cancer development involves many complex interactions between genes, their products, and external signals received by the cell. The one unifying pathway for all of these cancers, is a genetic alteration that disrupts the normal cell division cycle and transforms a normal cell into a cancer cell.
* 17th lecture
Cell chemicals called cyclins act as chemical signals to promote cell division. cyclin D1, is important for the early growth phase of cells by turns on a set of enzymes called kinases that stimulate the replication of DNA. It turns out that the gene that codes for cyclin D1 (also called bcl1) is a type of oncogene. When a defect in the gene causes the cyclin to be overproduced or produced at the wrong time, the cell goes into a nonstop division mode.
* 17th lecture
The human retinoblastoma (Rb) gene on chromosome 13, which prevents retinal cancer and other cancers. Individuals who have inherited defective or mutated Rb genes, can develop retinal tumors, osteosarcoma (a form of bone cancer), breast cancer, and a form of lung cancer. p53 gene, becomes altered by simple missense mutations and has been implicated in 51 different tumors. p53 is a master regulator switch for the cell cycle that blocks the expression of the cyclin genes.
* 17th lecture
Several types of leukemia can be traced to the loss of a whole chromosome. The loss of part of a chromosome during cell division (chromosomal deletion) is also an important factor in some cancers. Many of colorectal carcinomas manifest a deletion of a small part of chromosome 17 Retinoblastoma occurs through deletions on chromosome 13 Gene amplification a process whereby numerous extra copies of a gene (proto-oncogene) are produced during DNA replication. Certain tumors arising in squamous cell tissue or tissue of the lung, brain, and breast are linked to gene amplification.
It appears that carcinogens are genetically alter or damage DNA in a way that activates or deregulates a proto-oncogene and transforms it into an oncogene. Although physical agents such as X rays and UV radiation have well-developed powers to mutate or damage DNA, most chemical carcinogens require at least two different stimuli. The initiating stimulus, is metabolized by the liver into a more reactive chemical that permanently alters the DNA of a particular target cell. Second chemical stimulus, called a promoter or co-carcinogen,that completes the transformation to cancer.
* 17th lecture
Transformation of malignant cell is appear as giant cells with bizarre shapes; show an abnormal, vacuolated cytoplasm; or possess enlarged, multiple nuclei. Some markers of cancer cells are surface receptors for receiving stimuli from growth factors (small polypeptides involved in cellular development that can favor cancerous growth). Some tumors secrete chemical factors that stimulate growth of additional circulatory vessels. Tumor cell become dislodged from a tumor, metastasize into the circulation, and are carried to distant sites. Such invasive tumor cells have the property of binding to and disrupting connective tissue barriers surrounding tissues and organs
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Many experts postulate that cells with cancer-causing potential arise constantly in the body but that the immune system ordinarily discovers and destroys these cells, thus keeping cancer in check. The primary types of cells that operate in surveillance and destruction of tumor cells are: Cytotoxic T cells. Natural killer (NK) cells. Macrophages. It appears that these cells recognize abnormal or foreign surface markers on the tumor cells and destroy them. Antibodies help destroy tumors by interacting with macrophages and natural killer cells In some cases, the cancer may not be immunogenic enough; it may retain self markers and not be targeted by the surveillance system. In other cases, the tumor antigens may have mutated to escape detection.
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Why patients with immunodeficiencies such as AIDS and SCID are more susceptible to various cancers ? because they lack essential T-cell or cytotoxic functions. Possible causes of cancerous transformation include: Irregularities in mitosis. Genetic damage. Activation of oncogenes. Infection by retroviruses. Immunotherapy offers the most promise in treating cancers, compared with surgery, radiation, or conventional chemotherapy.
* 17th lecture
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