STUDY OF CANCER & Immune System LS601 Overview of cancer in addition to carcinogenesis Microevolutionary processes leading to cancer 1. Natural Selection in cells may disturb collaboration & predispose to cancer 2. Mutation, Competition in addition to natural selection among somatic cells create a microevolutionary environment promoting growth of selfish aberrant cells or cancer

STUDY OF CANCER & Immune System LS601 Overview of cancer in addition to carcinogenesis Microevolutionary processes leading to cancer 1. Natural Selection in cells may disturb collaboration & predispose to cancer 	2. Mutation, Competition in addition to natural selection among somatic cells create a microevolutionary environment promoting growth of selfish aberrant cells or cancer www.phwiki.com

STUDY OF CANCER & Immune System LS601 Overview of cancer in addition to carcinogenesis Microevolutionary processes leading to cancer 1. Natural Selection in cells may disturb collaboration & predispose to cancer 2. Mutation, Competition in addition to natural selection among somatic cells create a microevolutionary environment promoting growth of selfish aberrant cells or cancer

Lynn, Marlene, Host has reference to this Academic Journal, PHwiki organized this Journal STUDY OF CANCER & Immune System LS601 Professor Swapan K. Ghosh Lsghosh@scifac.indstate.edu 237-2416 Lectures From April 4-15,2003 Fact Sheet: · In 1996 554,740 deaths due to cancer in US alone. · Over 8 million cancer patient in US are alive · 5 million of those were diagnosed 5 years ago. · One of approx. 3 will experience cancer “CANCER IS A CRIMINAL-IT DOES NOT FOLLOW RULES” Dr. S. Otani CANCER: The term refers to 100 as long as ms of the disease. Almost every tissue can get trans as long as med into malignancy. Caused by : Uncontrolled growth by a cell that constitutes the tissue; The resulting impact on normal functioning of body organs in addition to disruption. The ability of the aberrant cell to migrate to a distant site in addition to invade neighboring tissues, a phenomenon called METASTASIS .

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Overview of cancer in addition to carcinogenesis Biology of cancer: Microevolutionary process Different stages of cellular trans as long as mation Basic properties in cancer cells Etiology: aberrant natural selection Molecular genetics of cancer: Oncogenes, Tumor suppressor genes Microevolutionary processes leading to cancer Animal bodies represent a society or ecosystem Individual members are cells that reproduce in addition to organize into assemblies or tissues Involves cell births, deaths, territorial boundary, population sizes, species propagation BUT virtually no competition as long as survival in addition to all cells collaborate in addition to sacrifice to produce germ cells ensuring propagation (All somatic cells die leaving no progeny) 1. Natural Selection in cells may disturb collaboration & predispose to cancer 2. Mutation, Competition in addition to natural selection among somatic cells create a microevolutionary environment promoting growth of selfish aberrant cells or cancer

SPECIFIC TOPICS General characteristics, classification, in addition to nomenclature of tumors Properties: How cancer arises, How cancer spread Grading in addition to staging Immunity in addition to cancer Therapy: surgery, radiation, chemotherapy in addition to biotherapy (immunotherapy) Classification: Carcinoma: cancer of epithelial tissues Adenocarcinoma: cancer of gl in addition to ular tissue; spread through lymphatics Sarcoma: cancer of stromal or mesenchymal layers of organs; spread via blood. Carcinosarcoma: mixtures of cancer cells from both epithelia in addition to mesenchma. Teratoma: cancer of stem cells. Undifferentiated neoplasms: poorly undifferentiated.

Terms in addition to Definitions Neoplasia : New aggressive growth of cells in addition to tissues putting pressure on neighboring tissues (Causing abnormal swelling or tumor) or invading neighboring tissues (cancer) Hyperplasia: Means too much cell proliferation or mitosis. This is abnormal but not cancer Dysplasia: A cell is not only proliferating excessively, but attains abnormal in addition to orientation; Pre-cancerous More TERMS: Metaplasia: conversion of one cell type into another, such as, stratified oesophagus or lung tissues (due to acidity or cigarette).The process is reversible in addition to is not cancer, but may lead to cancer. Metastasis: Spreading to distant sites. – First site where cancer is detected is called primary site in addition to the second site, secondary site. -Small clumps of cancer cells (emboli) Spread by migration through blood (called blood-borne or hematogenous) or through lymphatics (lymphogenous). -Cancer cells spread because they lose their molecular address where to go

More Jargons! Anaplasia: Primitive undifferentiated state of cell growth. Aplasia: A loss of normal appearance in addition to disorganizations of tissues. In situ cancer: abnormal growth at a particular site but no invasion of neighboring tissues. Benign in addition to fibrous. Invasive cancer: Lethal in addition to malignant as neighboring tissues are invaded. Characteristics of cancer cells Infiltration in addition to destruction of surrounding tissues. Loss of contact inhibition of growth. Anchorage independent in addition to aberrant chromosome numbers or aneuplody Variation in shapes in addition to sizes based on degree of differentiation. Uncontrolled mitosis or cell proliferation or growth rate. Less dependent on growth factors Often migration to distant sites in addition to loss of similarity with parent tissues.

Cancer classification Sporadic cancer: cancer without a family history; non-hereditary in addition to not affecting off-springs Mutations not present in the germline cells. Colon cancer mostly sporadic Hereditary cancer: Mutations are present in the germline cells in addition to predispose to inheritance towards developing cancer (familial). Breast cancer is an example Most Cancers originate from a single abnormal cell (Clonal origin) Cancer is essentially a genetic disease but not, in most cases, an inherited disease Cancer is nearly always of clonal origin Multiple mutations (at least TWO-HIT theory as proposed by Knudson) in cancer cells Same genes are often altered by carcinogens, radiation, viruses undergo translocation, amplification or deletion Cancer cells differently from normal cells

Experimental evidence of cancer clonality If cancer originates from one mutated cell, it could be traced by looking at fingerprints of genes in addition to /orproducts Tracking the identity of a marker X-chromosome that is inactivated in cancer cells in females Studying chronic myelogeneous lymphomas (CML) in addition to tracking Ph chromosome as markers Studying Myelomas in which Myc oncogene has translocated only to a specific Ig gene X-Chromosome inactivation in Females Only one of the two X chromosomes inherited are inactivated in a cell. If cancer is monoclonal origin, it would clearly have only one X-chromosome inactivated. No mixed inactivation be seen in any given tumor

How To Demonstrate Clonal Origin of Cancer Cells MYC GENE TANSLOCATION IN MYELOMAS Karyotype of a breast cancer cell depicting translocations (DIFFERENT COLORS)

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Abnormal cells in Pap smear What causes cancer Various factors Contribute to the cause of cancer. Carcinogens, that is, cancer producing agents can be of physical, chemical, or of biological nature. Physical: Radioactivity, UV radiation, X-rays. Chemicals: from cigarette smokes, in addition to shoots of chimney or coal: hydrocarbon (benzpyrene), DMBA, aromatic amine (in many synthetic dyes). Dietary factors: such as saturated fats, food additives, lack of fruits in addition to vegetables (anti-oxidants), alcohol, excess meat products Mutations by carcinogens

Biological factors: hormones in addition to viruses: estrogen in addition to pituitary hormones promotes breast tumor. Oncogenic viruses: leukemia viruses (Rous sarcoma virus) , Epstein-Barr virus (Burkitt’s lymphoma), Papilloma virus, Mammary tumor virus, Simian virus What causes cancer How Cancer Arises Cancer cells violate the civic rules that govern normal cells by not responding to go-signals as long as proliferation in addition to stop-signals as long as reproduction. Cancer cells descend from a common ancestral cell: clonal origin. But at some point one of the off-springs mutate that becomes worse with more mutation, in addition to finally the accumulated mutated cells disobey all civic controls of normal cells in a tissue, becoming invasive in addition to malignant. 3. Since mutations occur at the gene level, that is, DNA molecules that reside in the nuclei of the cells, most human cancer can be traced there. Proto-oncogenes from neighboring cells produce growth factors that encourage cell growth during cell cycle by producing growth-stimulatory signals. Mutation in these genes may cause cells divide without any signal from outside. One example is mutated ras gene. A quarter of all human tumors have mutated ras gene. Similarly myc gene family if abnormal causes leukemia, lymphomas. Receptors on the recipient cells that bind proto-oncogene growth factors may also mutate in addition to stimulate cell growth.Thus, in breast cancer, Erb-B2 receptors behave abnormally. Tumor suppressor genes that control unrestricted growth of cells in addition to inhibit cell growth. If they stop working, cancer cells grow wild in addition to uninterrupted. Example, pRB, P53 (tumor-suppressor gene protein), TGF-beta (inhibits cell growth)

In c, the switch is placed in the larger context of the many molecular interactions that regulate the cell cycle. Flipping the switch to “on” can be seen above the R point. Over-activity of the stimulatory proteins cyclin D, cyclin E in addition to CDK4 have been implicated in certain human cancers. Inactivation of various inhibitory proteins has also been documented. The affected proteins include p53, pRB, p16 in addition to p15. Mitochondria in apoptotic signaling Clinical Applications 1. Diagnosis – oncogenes c-myc in Burkitts Bcr/Abl CML 2. Detection of MRD Bcr/Abl CML 3. Prognosis n-myc neuroblastoma Her 2 breast cancer 4. Predictive oncology MEN Type II, Li-Fraumeni syndrome Retinoblastoma, Wilms tr, Breast ca.

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Lynn, Marlene is from United States and they belong to WDXX-FM and they are from  Selma, United States got related to this Particular Journal. and Lynn, Marlene deal with the subjects like International News; Local News; National News; Regional News

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