Cancer Terminology Biol 2311
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This 5 page Class Notes was uploaded by Rachael Couch on Friday November 20, 2015. The Class Notes belongs to Biol 2311 at University of Texas at Dallas taught by John Burr in Fall 2014. Since its upload, it has received 61 views.
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Date Created: 11/20/15
Cancer Terminology 90% of cancers in humans are carcinomas; the remaining 10% are sarcomas and leukemias. Major types of cancers: Carcinomas derive from endo/ectoderm; cancers that originate in the skin, lungs, breasts, pancreas and other organs and glands Lymphomas cancers of lymphocytes Leukemia derive from bloodforming tissues; cancer of the blood Sarcoma derive from mesoderm; cancer of the bone, muscle, fat, or cartilages Melanomas cancers that arise in cells that make the pigment in the skin Properties of Benign versus Malignant Tumors Benign Malignant Encapsulated Nonencapsulated Noninvasive Invasive Highly differentiated Poorly differentiated Slow growth Rapid growth Little or no anaplasia Usually anaplastic No metastasis Metastasis How Cancer Arises The 30 trillion cells of the normal body are interdependent and regulate one another’s proliferation (growth/reproduction). Cancer cells become deaf to controls on proliferation and reproduce on their own accord Also, unlike normal cells, they migrate and invade nearby tissues or distant sites of the body. Tumors composed of these malignant cells become more aggressive over time and become lethal when they disrupt the tissues and organs needed for the survival of the organism. o The cells in a tumor descend from a common ancestral cell that at one point long ago initiated a program of inappropriate reproduction o The malignant transformation of a cell comes about through the accumulation of mutations in specific classes of the genes within it Two gene classes, which together constitute only a small proportion of the full genetic set, play major roles in triggering cancer o Protooncogenes encourage normal growth When mutated, can become carcinogenic oncogenes that promote excessive proliferation o Tumor suppressor genes inhibit abnormal growth When mutated, contribute to cancer o For a cancerous tumor to develop, mutations must occur in half a dozen or more of the founding cell’s growthcontrolling genes. o Altered forms of another class of genes may also participate in the creation of a malignancy by specifically enabling a proliferating cell to become invasive or capable of spreading (metastasizing) throughout the body Many protooncogenes code for proteins involved in growthsignaling o These pathways within a cell receive and process growthstimulatory signals transmitted by other cells in a tissue o Celltocell signaling usually begins when one cell secretes growth factors o Growth factors (proteins) move between cells and bind to receptors on the surface of other cells nearby Receptors span the outer membrane of the target cells o When a growthstimulatory factor attaches to a receptor, the receptor creates a proliferative signal to proteins in the cytoplasm o These downstream proteins then emit stimulatory signals to other proteins, in a chain that ends in the cell’s nucleus. o Within the nucleus, transcription factors respond by activating genes that help to push the cell through its growth cycle Cell growth becomes deregulated when a mutation in one of its protooncogenes causes excessive signaling in a critical growth stimulatory pathway, keeping it continuously active when it should be silent Some oncogenes force cells to overproduce growth factors o Sarcomas (cancer of connective tissue) and gliomas (cancer of nonneuronal brain cells) release excessive amounts of plateletderived growth factor o A number of other cancer types secrete too much transforming growth factor alpha o These factors act on nearby cells but may also turn back and drive proliferation of the same cells that just produced them Researchers have also identified oncogenic versions of receptor genes o These versions of receptor genes release a flood of proliferative signals into the cell cytoplasm even when no growth factors are present Other oncogenes in human tumors perturb parts of the signal cascade found in the cytoplasm o Ex: Proteins encoded by normal ras oncogenes transmit stimulatory signals from growth factor receptor to other proteins far down the line. The proteins encoded by mutant ras genes, however, fire continuously, even when growth factor receptors are not prompting them. Hyperactive Ras proteins are found in about a quarter of all human tumors. Summary of tumor development 1) Tumor development begins when a cell within a normal population sustains a genetic mutation that promotes proliferation when it would normally rest 2) The altered cell and its descendants continue to look normal but they reproduce too much (hyperplasia). After years, one in a million of these cells has another mutation that further loosens controls on cell growth. 3) In addition to proliferating excessively, the offspring of this cell appear abnormal in shape and orientation. This tissue is now said to exhibit dysplasia. Once again, after a time, a rare mutation that alters cell behavior occurs. 4) The affected cells become more abnormal in growth and appearance. If the tumor has not yet broken through any boundaries between tissues, it is called in situ cancer. This tumor may remain contained indefinitely. However, some cells eventually acquire additional mutations. 5) If the genetic changes allow the tumor to begin invading underlying tissue and to shed cells into the blood or lymph, the mass is considered to have become malignant. The renegade cells are likely to establish new tumors (metastases) throughout the body. These may become lethal by disrupting a vital organ. Fighting Cancer by Attacking Its Blood Supply Capillaries (tiny blood vessels) extend into almost every tissue in the body, replenishing nutrients and carrying off waste products Usually capillaries do not increase in size or number because they are lined with endothelial cells that do not divide. However, for example, during menstruation or when tissue is damaged, the vessels begin to grow rapidly. This proliferation of new capillaries is called angiogenesis (or neovascularization) and is typically shortlived and “turned off” after one or two weeks Tumor cells can “turn on” angiogenesis by releasing angiogenic proteins and suppressing angiogenesis inhibitors. As new blood vessels bring in fresh nutrients and proteins known as growth factors (angiogenic growth factors = vascular endothelial growth factors VEGF), the tumor mass can expand. Neovascularization appears to be one of the crucial steps in a tumor’s transition from a small, harmless cluster of mutated cells to a large, malignant growth capable of spreading to other organs throughout the body. Tumor cells usually can’t trigger angiogenesis when they first arise in healthy tissue. Unless the deranged cells become vascularized, the mass will not become larger than the size of a pea. If researchers can determine how mutated cells trigger angiogenesis and thus how to interrupt the process, they could have a new anticancer therapy. 1989 First clinical trial of an antiangiogenic agentinterferon alpha 1992 First antiangiogenic drug for cancer patients, TNP470 entered clinical trials. Endothelial cells (that make up the walls of a capillary) have receptors for vascular endothelial growth factor (VEGF). Binding of VEGF to these receptors causes the endothelial to proliferate and form new capillaries growing towards the source of VEGF (the cancer cells) Metastasis Metastasis is the process whereby cancer cells detach from the parent tumor and, by entering the vascular or lymphatic system, spread throughout the body and initiate new tumors at distant sites. The new tumors are called metastatic tumors or metastases. Tumor cells may enter the bloodstream directly by crossing the wall of a blood vessel or by crossing the wall of a lymphatic vessel that ultimately discharges its contents into the bloodstream. Tumor cells that have entered a lymphatic vessel often become trapped in lymph nodes along the way, giving rise to lymphnode metastases. Less than one in every thousand malignant tumor cell that enters the bloodstream will survive to produce a tumor at a new site Metastatic cancer cells usually enter capillaries near or in the primary tumor, and end up in the venous circulation. They pass through the heart. The first capillary bed they encounter after escaping the primary tumor is usually the lung. Slower flow rates of blood in a capillary bed facilitates the exit of metastatic cells through the thin walls of these blood vessels and into the neighboring tissues, where an escaped metastatic cell can proliferate to form a new tumor. So the lung is a common site for metastatic tumor growth for many types of cancer (melanoma, breast cancer, etc.) Exceptions: o In the case of colorectal cancers, the first capillary bed the metastatic cells encounter is the liver, so colorectal cancer often spreads first to the liver. o Sometimes cancer cells carry receptor molecules that are specific for some other cell type. Prostatic cancer cells, for example, often express receptors for adhesion molecules on bone cells and therefore often metastasize to bone. Summary of the process of metastasis: 1) Cells grow as benign tumors 2) Break through basal lamina 3) Invade capillary and travel through bloodstream 4) Adhere to blood vessel wall in liver 5) Escape from blood vessel 6) Proliferate in different area