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Cancer Terminology

by: Rachael Couch

Cancer Terminology Biol 2311

Rachael Couch
GPA 3.9

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I am a TA for the course this year and got a 98 on exam 4 from studying these notes when I took the class. These are my notes- study them and you WILL do well!
Introduction to Biology
John Burr
Class Notes
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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


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