Cancer is not a single disease; it is a myriad or collection of diseases with many different manifestations as there are many different types of tissues and cell types Cancer is a disease of abnormal gene expression. Cells are constantly evolving and have the natural selection pressures to change Common biological properties of tumor cells: 1) Deregulated clonal cell growth- all cells in a tumor originated from one single cell that acquired mutations that made it deregulated cancer cells are constantly testing different mutations so they are constantly changing.
2) Impaired cellular differentiation – cancer cells have lost the ability to differentiate. Cells stop growing once they differentiate so cancer cells can’t differentiate therefore they keep growing 3) Invasiveness -benign tumor are localized and encapsulated, malignant tumors invade surrounding areas 4) Metastatic potential- not only have they become invasive but they have spread to secondary or distal sites Cancer cells become deprogrammed.
Proto-oncogenes encode for positive mediators of cell proliferation and growth. They drive the proliferation of the cell ex: growth factor receptor Tumor suppressor gene encode negative growth regulatory factors. They counter the effects of protooncogenes.
In cancer cells they bypass the negative effects of these so they continue to grow Cancer epidemiology is the study of distribution of various cancer types among world populations with consideration of speci?c risk factors and etiologic agents involved in disease causation such as age, ethnicity or even exposure to carcinogens Cancer epidemiology is the study of cancer instance, mortality, risk factors, and attempting to relate and find causation A carcinogen does not necessarily cause cancer but it can cause a progression of the disease such as a benign tumor becoming malignant.
Any abnormal growth is cancer there is just a difference between malignant and benign. Neoplasticism disease is another name for cancer Cancer rates are closely tied with the rate of detection because a high incidence rate can lead to low mortality because if you ? nd it ? rst you can treat it easier We study cancer epidemiology in order to monitor long range trends in cancer incidence to investigate cancer etiology.
The average age at the time of cancer diagnosis for all tumor sites is 67 years old Cancer is associated with the aging process because DNA repair mechanisms break down leading to more mutations in DNA leading to possible degradation of cell regulation As a higher percentage of the population reaches 60, the incidence of cancer increases proportionally Additionally, as life expectancy of populations increase, due to a reduction in other causes of premature death, the average risk of cancer increases.
Cancer Statistics: The biggest cancers involves reproductive organs, digestive system, respiratory system and breast cancers. Reproductive has highest incidence Respiratory cancers are most deathly, then digestive then reproductive Respiratory cancer is most deathly in females There is an equal distribution of male and female cancers Skin cancers are the most common Basal and squamous cell carcinomas (SCCS) Types of Cancers: Reproductive cancers are prostate, cervical, ovary, uterine.
Digestive cancers are colon, rectum, pancreas, stomach, liver and esophagus Respiratory cancers include lung and bronchus Digestive and respiratory cancers are deep tissue cancers so hard to detect early Males are at the greatest risk of prostate then respiratory system then digestive system cancers. Prostate cancer has highest incidence rate with men The mortality rates for prostate and colorectal cancers have remained relatively unchanged. Women are at the greatest risk of breast then respiratory system then digestive system cancers.
Breast cancers have high rate of reoccurrence * Respiratory is the most deathly for both males and females. Early detection is critical in breast cancer, prostate and colorectal cancers * Leading sites for cancer incidence is lung, stomach, breast, colorectal and liver US incidence rate is very high but our mortality is not very high. Our incidence rate is number one but we are only eighth on mortality because we do so much early detection that our incidence rates are high but we can treat them so early then mortality levels are low Lung cancers have poor clinical result.
Various world regions have a lot of disparity between total numbers of cancer cases and the incidence/mortality rates due to differences in quality of healthcare and early screening and detection. Pediatric tumors Acute lymphocytic leukemia typically happens with children but can also rarely be seen later in life A lot of these cancers are stem cell related Pediatric cancers are clearly the exception to the rule of cancer incidence rate being related to advanced age Cancer incidence differs greatly with race and ethnicity.
African Americans tend to get the most cancers and also tend to have higher mortality rates Survival rate of a cancer is reported as ? ve year survival rate Pancreatic survival rate is only 4% Prostate cancer has 92% survival rate. One in three males will get prostate cancer so high incidence but if caught early it is so easy to treat Digestive and respiratory cancers have low 5-year survival rates because they are highly metastatic and once symptoms have developed they’ve usually already spread.
* It takes 10^9 cells to form a tumor that can be felt and 10^6 cells for a cancerous area to show up on an MRI or a CT scan * Chapter 1: Genetic Basis of Cancer Mendel establishes the basis of genetics: Your gene expressions determines your phenotype Genetic information is packaged into genes Alleles are different versions of a gene Dominant alleles are always expressed when present Recessive alleles are not expressed when a dominant allele is present Mendel created theory of inheritance.
The majority of observable traits results from a cooperative interaction between numerous genes instead of one gene one trait Two redundant copies of each gene therefore the genome is diploid Genotype drives phenotypes Incomplete dominance coexisting alleles that results in a hybrid phenotype Co-dominance two alleles are both expressed simultaneously Mendel genetics helps explain Darwinian evolution Darwin gives theory of evolution and the theory of natural selection and how that effects a cancer cell.
Mutations are responsible for changing the information content of a gene converting one allele into another or creating a new allele from a pre existing gene An allele that is present in the vast majority of healthy individuals in a population is referred to as wild type The collection of alleles present in the genome of all members of a population is the gene pool becomes progressively more heterogeneous as the species grow older Humans are a relatively young species and have one half as many alleles and genetic diversity as chimpanzees which are twice as old as a species.
Natural selection preferentially selects for mutations that confer an advantage to the population thus producing more descendants Non bene? cial random mutations are continually discarded and only the bene? cial ones are kept because they make the organism more ? t The majority of DNA in the human genome is non coding or junk DNA only about 1. 5% encodes protein structures and another 2% encodes gene regulatory information Therefore the majority of random mutations affect non essential DNA sequences are consider to be neutral mutations.
Genes retained for cellular viability are evolutionarily conserved. Mutations that target these sequences typically are lethal, and leave no descendants Many genes essential for embryogenesis physiology, and biochemistry for all mammals are conserved Ex: The genes involved in eye development are conserved between fruit ? ies and mice Each person has a unique genome with its own unique array of functionally silent genetic alterations.
Genetic polymorphisms- individual, functionally silent differences in DNA sequences that make each human genome unique that confers diversity to the gene pool. Mendelian genetics governs how both genes and chromosomes behave Identical set of chromosomes is present in almost all cells of an organism known as the karyotype This karyotype is duplicated each time a cell goes through a cycle of growth and division (cell cycle) Genes are carried on chromosomes and each chromosome may contain several thousand genes. The length of a chromosome is roughly proportional to the number of genes it carriers The speci?c location of a gene on an individual chromosome is a genetic locus.
The positions of many genes have been mapped Germ cells such as sperm and egg contain a haploid number of chromosomes (have a single copy of each chromosome and gene) The diploid number is regenerated after the sperm and egg combine during fertilization The rule of paired similar chromosomes is violated by sex chromosomes x and y Non sex chromosomes are known as autosomes The X chromosomes encodes approx.900 genes and the Y chromosomes encodes approx.
78 genes Females have XX Males have XY The number of genes on the x chromosomes provide functional redundancy also gives females an advantage if one gene on an X is defective, the second X can try to provide a fail safe. While females have two X’s they can only access information on a single X so get X-inactivation to silence almost all the genes on one of the chromosomes and this X then shrinks into a small particle called a Barr body.
Example of functional redundancy: colorblindness results from mutations of color sensing proteins of the Retina on the X chromosomes. Since females have two X’s get fail safe mechanism but males suffer from this more frequently. Chromosomes are altered in most types of cancer cells Normal chromosomal structure is euploid karyotype Aberrant chromosomal structure in cancerous cells is considered to be aneuploidy (simple deviation from the euploid karyotype).
Cancer cells possess genomic instability and chromosomal aberrations Can get chromosomes that are structurally normal that accumulate in multiple copies or chromosomes can undergo changes Translocation- segment broken off one chromosomal arm and fused to the arm of another chromosome Reciprocal translocations- chromosomal segments exchanged between chromosomes from different chromosome pairs Inversions- chromosomal segment becomes inverted Deletion- a segment of a chromosome is discarded and the flanking chromosomal regions are joined.
Gene Amplification- increases in the number of genes carried in a chromosomal segment HSR – Homogeneously staining region segment is copied many times and fused in a head to tail manner that creates DM’s Double minutes (DM) sub-chromosomal fragments which may be cleaved out of a chromosome and replicate in an autonomous manner. * Methods to detect subtle chromosomal alterations: Spectral karyotyping (SKY) chromosome painting and allows us to see ? ne genetic changes on each chromosome mFISH- m band Fluorescence In Situ Hybridization shows the position of the genes and chromosomal architecture.
Mutations causing cancer occur in both the germ line and the soma Mutations within the genomes of germ cells (sperm and egg) can be transmitted from parent to offspring and are the basis of hereditary cancer predisposition Somatic mutations affect the genome of non germ cells such as somatic cells and are non-transmissible to offspring through inheritance Most that we will study are somatic cancer, only ? ve to ten percent of cancers are hereditary Cancer is a clonal disease that originates from a single genetically altered cell that is cloned millions of times.
Genotype embodied in DNA sequences creates phenotype through proteins Molecular biology is the study of biological and genetic processes to determine their mechanisms is of function How gene mutations effect phenotype Central dogma: DNA RNA protein cell tissue organ organism Genotype drives the phenotype of the cell by controlling protein expression a cells phenotype can range from complex genetically templated behavioral traits to the morphology (shape and form) of cells and subcellular organelles to the biochemistry of cellular metabolism.
* * The unique structure and function of a protein is determined by its primary sequence of amino acids Cellular proteins form an elaborate intracellular framework or cytoskeleton- the connective framework secreted between cells is known as the extracellular matrix (ECM) * Interactions between a cell and the ECM provides communication with the microenvironment and surrounding cells. Malignant cancer cells can degrade the ECM to invade surrounding tissues Malignant cancers produce proteases in order to cut through these tissues.
Other cellular proteins function as enzymes for metabolic or biochemical processes or intermediary metabolism. Cellular motility (movement)is also important for normal cell processes and may allow cancer cells to become invasive or metastatic the reorganization of actin ? laments and cytoskeletal elements within leader cells contributes to tumor motility Protein networks within a cell that provide intracellular and intercellular communication are known as signal transducers Signal transduction molecules can be oncogenes and are frequently deregulated in cancerous cells.
DNA sequences are copied into RNA molecules through the process termed transcription Genes that are transcribed are actively expressed, while genes that are not transcribed are often considered to be repressed Pre-mRNA is then processed because it contains introns (have no info on them) and exons (have important sequences) Splicing cuts out the introns and are discarded and nearby exons are fused to give a full mRNA which is exported to cytoplasm Alternative splicing and exon shuffling increases the coding capacity of the human genome.
mRNA molecules are then translated by protein synthesizing factories into ribosomes (sequences of amino acids) This ribosome folds into a functional protein Post-translational modification occur where something can be added to the protein. polypeptides form higher order (tertiary or globular) structures are determined by their primary amino acid sequence and post translational modi? cations the addition of sugar (oligosaccharide) moieties to a protein is termed glycosylation.
Proteins involved in signal transduction may be reversibly phosphorylated other proteins may be acetylated and or methylated certain proteins are synthesized as a precursor and are processed by proteases that cut the protein into the mature form Gene expression patterns also control phenotype Gene expression patterns control phenotype with the estimated 34,000 genes within the genome These genes act combinatorially within individual cells to create the complex organismic phenotypes of the mammalian body.
The genome is selectively read by different cell types as a result of differentiation and development pluripotent stem cell goes to tissue speci? c stem cell to differentiated cell tissue organ organism Differentiation- process as cells in early embryo go through cycles of growth and division, the cells begin to assume distinct phenotypes. The majority of expressed genes are housekeeping genes essential to maintain cell viability and metabolic processes approximately 10000 to 15000 genes.
The minority of genes are tissue speci?c genes that encode proteins associated with a particular type of cell. Only about 1000 tissue-specific genes are responsible fro distinguishing, and differentiating the characteristics of the cell. Gene expression microarrays are important tools for studying comparative gene expression patterns in normal tissues and cancerous cells Since all cells have the same genetic templates, using this tool we are able to see what genes are expressed in different types of tissues. Transcription Factors control gene expression.
In order to get cell differentiation, clearly some genes need to be repressed and other expressed, and this must be coordinated by transcription factors. Gene expression is regulated by transcription Transcription factors (TFS) are proteins that bind to speci? c DNA sequences within the promoter regions of genes and determine if the gene will be transcribed or not. TFS’s bind to a sequence motif to make this decision. Transcription factors which functions as activators (positive regulators of transcription) bind to DNA sequences known as enhancers. Promoter region is where transcription will begin.
Other transcription factors function as repressors (negative regulators of transcription) * * Certain TFS’s can simultaneously affect the expression of a large cohort of responder genes to cause a phenotype this is known as pleiotropy In cancer cells, a malfunctioning, pleiotropicaly acting TF can orchestrate a large cohort of responder genes to create a cancer cell phenotype. A gene can be separated into the non transcribed control sequences and the transcribed sequences represented in the mRNA Metazoa are formed from components conserved over vast evolutionary time periods.
Gene Family- genes that are clearly related to one another in their information content and protein structures Ex: the globin gene super family evolved through repeated duplication of genes followed by the divergence of duplicated sequences Genes that are related to one another in the genomes of distinct species are said to be homologous to one another The counterpart of a closely related gene in another species is known as an ortholog (functionally replaceable) basically a functional homolog myc gene in chickens and myc gene in humans.
Gene cloning techniques revolutionized the study of normal and malignant cells Cellular genomes could be fragmented and used to create the DNA fragments known as genomic libraries Molecular biological DNA hybridization techniques are used to identify individual gene sequences the isolated DNA fragment is puri? ed and ampli? ed to yield a gene clone Complimentary DNA (cDNA) library corresponds to all mRNA sequences expressed within a particular cell type or tissue Complementary DNA copies of mRNA molecules were synthesized using reverse transcriptase.
Gene cloning using one of the two above methods facilitated the identi? cation of genes involved in oncogenesis and cancer development. Summary/Additional Information: Most of our current info on malignant cellular transformation and cancer has been derived from molecular studies using model organisms such as yeast fruit ? ies worms and mice because these have similar cellular functions, but they don’t live very long. Cancer is a disease of deregulated gene expression and somatic evolution Somatic evolution is pressure put on the cancer cell from surrounding environment.
Mutations that inactivate cellular DNA damage repair pathways make the cell prone to acquire additional mutations that support oncogenic transformation Mutation rate in any cell is 10^4 so every time a cell divides there is a chance of mutations. But we have many checkpoints that can prevent a cell from mutating Cancer cells are also known as a mutator cell All malignant cells aren’t metastatic but all metastatic are malignant Metastatic means it moves to a secondary organ. Chapter 2: The Nature of Cancer.
The retained ability for cells to proliferate and to participate in tissue morphogenesis (creation of shape) makes it possible for the maintenance of adult tissues throughout the life span of an organism. This process makes possible the maintenance of adult tissues including the repair of wounds and the replacement of dead or depleted cell populations (tissue speci? c stem cells ; egCD34+ lymphoblasts) All the cells in the body of complex organisms are members of cell lineages that can be traced back to the fertilized egg and the fertilized egg and spawn all the cells in the body through repeated cycles of growth and division.
Individual cells are endowed with great autonomy and versatility and carry a complete organismic genome Alterations in the genomic sequence of cells may allow them to gain access to information that is normally denied them in a differentiated state Mutations cause genes to acquire novel and or highly abnormal phenotypes in cancerous cells- these cells no longer contribute to normal morphogenesis. Tumors arise from normal tissues Tumors are derived from normal cells gone awry, resulting in masses of cells programmed only to grow and divide.
All tissues are composed of cells and cell products and cells arise through the divisions of pre existing cells. All the cells in the body of complex organisms are members of cell lineages that can be traced back to the fertilized egg. The fertilized egg can spawn all the cells in the body through repeated cycles of growth and division. The practice of histology or histopathology (microscopic analysis of normal and tumor derived tissue sections) led to the realization that tumors are derived from masses of cells Tumors are derived from the normal types of tissues in which they arise.
Many tumors move within the body and invade their surrounding tissues and organs. Certain cancers spread to distant sites or metastasize and found new colonies of tumor cells metastases Tumors are classified based upon their tissues of origin Cells within metastases can often be traced back to the primary tumor mass (where the disease of cancer had begun) Cells within tumor masses exhibit disorganized tissue architecture and structure compared to normal tissue.
Tumors are divided broadly into two categories depending on their aggressiveness: benign grow locally without invading adjacent tissues malignant invade nearby tissues and may spawn metastases Most tumors in humans are benign but in rare cases, may cause damage by expanding and pressing on vital organs or tissues Certain benign tumors may secrete dangerous levels of hormones that case physiological imbalances such as thyroid adenomas (premalignant epithelial growths) produce thyroid hormone and cause hyperthyroidism Pituitary adenomas produce growth hormone which can cause excessive growth of certain tissues- acromegaly.
The majority of cancer related deaths result from malignant tumors- metastasis results in approximately 90% of all cancer deaths Tumors arise from many specialized cell types throughout the body The majority of human tumors arise from epithelial tissues Epithelia are sheets of cells that line the walls of cavities and channels (skin covers the body) Beneath the epithelial cell layers is a basement membrane (basal lamina) separates the epithelial cells form the underlying laying of supporting connective tissue cells called the stroma. Endothelial cells form the inner linings of capillaries and larger vessels rest on a specialized basement membrane that separates them from an outer layer of specialized smooth muscle cells.
Epithelia spawn the most common cancers- Carcinomas These tumors are responsible for more than 80% of the cancer related deaths in the western world Types of carcinomas: mouth, esophagus, stomach, skin, liver, lung, etc. This group of tissues contains cell types that arise from all three of the primitive cell layers in the early vertebrate embryo. Epithelia of the lungs, liver, gallbladder, pancreas, stomach and intestines all derive from the inner cell layer the endoderm. Skin arises from the outer embryonic cell layer the ectoderm Ovaries derive from the middle cell layer the mesoderm.
Most carcinomas fall into two categories: 1) Squamous cell carcinomas- cancers of protective epithelia lining channels or cavities. Skin, nasal cavity, esophagus 2) Adenocarcinomas are cancers derived from specialized cells that secrete substances into the ducts or cavities that they line (have a lumen or mucous layer) Lung, colon, stomach Tumors can be found in organs where both types of carcinomas can coexists Non-epithelial malignant tumors First major class is derived from connective tissues that share a common origin in the mesoderm of the embryo.
These tumors, the sarcomas, are the soft tissue cancers. Sarcomas are derived from a variety of mesenchymal cell types such as: ? broblasts and related connective tissue, the major structural component of the extracellular matrix of tendons and skin osteoblasts assemble calcium phosphate crystals within matrices of collagen to form bone adipocyes store fat in their cytoplasm myocytes which assemble to form muscle An unusual tumor an angiosarcomaarises from precursors of the endothelial cells.
Second major class arise from the various cell types that constitute the blood-forming (hematopoietic) tissues [including cells of the immune system] Erythrocytes – red blood cells Plasma – antibody secreting cells T & B lymphocytes Leukemias are malignant derivaties of white blood hematopoietic cell lineages (T & B Lymphocytes) Lymphomas are tumors of the lympoid lineages B and T lymphocytes that aggregate to form solid masses in the lymph nodes Rather than the dispersed single-cell populations of tumor cells seen in leukemias Other types of hematopoietic malignancies:
Acute or Chronic Myelogenous leukemias are bone marrow cancers Chronic means cells are proliferating at a slow rate but are persistent Acute means cells are rapidly proliferating Hodgkin’s Disease that effects B lymphocytes Multiple myeloma Non-hodgkin’s lymphoma Third major class arises from cells that form various componnets of the central and peripheral nervous system Neuroectodermal tumors- orgins in the outer cell layer of the early embryo Glimos Glioblasttomas Neuroblastomas Schwannomas Medulloblastomas Anything with blast in the name involves stem cells.
Some types of tumors do not fit into the major classifications Melanomas derive from melanocytes, the pigmented cells of the skin and the retina These melanocytes arise from a primitive embryonic structure known as the neural crest Small Cell Lung Carcinomas (SCLCs) contain cells having many attributes of neurosecretory cells, such as those of neural crest origin in the adrenal glands that sit above the kidneys The switching of tissue lineage and resulting acquisition of an entirely new set of differentiated characteristics is termed transdifferentiation.
Cancer cells almost invariably, retain certain properties of their tissues of origin. Cancer cells which have lost all differentiation markers are said to have de-differentiated These tumors are anaplastic (undifferentiated) it is no longer possible to use histopathological criteria to identify the tissues from which they have arisen Cancers seem to Develop Progressively Tissue Architecture is a broad spectrum from normal to highly malignant.
The different gradations of abnormality may well re?ect cell populations that are evolving progressively away from normal and toward greater degrees of aggressive and invasive behavior. Hyperplastic- cells that deviate only minimally from those of normal tissues, but may nevertheless be abnormal in that they contain excessive numbers of cells. Appear reasonably normal and is not cancerous Metaplasia- a minimal deviation from normal where one type of normal cell layer is displaced by cells of another type that are not normally encountered in this site within a tissue. Even though the cells are in the wrong location they appear totally normal.
Dysplastic- cells within a tissue are abnormal cytologically (appearance is different) Variability in nuclear size and shape Increased nuclear to cytoplasmic ratio Increased mitotic activity Lack of cytoplasmic features typical of cellular differentiation. This is the transitional state between benign growths and those that are premalignant More abnormal growths in epithelial tissues are termed adenomas, polps, adenomatous polyps, papillomas and in skin called warts These growths form macroscopic masses with dysplastic cells that can be seen with the naked eye.
They are benign tumors that remain con? ned to a localized area contained by the basement membrane. Neoplasm- is the collection of growths both benign and malignant that just means new types of tissues Tumor progression- normal tissue evolves progressively into one that is highly malignant Normal Hyperplastic Dysplastic Neoplastic Metastatic Tumors are monoclonal growths Tumor cells originate from a single genetically altered cell that exhibits a progressively abnormal phenotype and growth characteristics.
Originally there were two theories: 1) Tumors were monoclonal 2) Tumors were polyclonal where a tumor was thought to be made up of many different types of cells To determine whether cancer cells originate from a single genetically altered cell, experiments were performed utilizing a natural nongenetic (epigenetic) marking event of one of female X chromosomes being silenced.
Characterized glucose 6 phosphate dehydrogenase in leiomyomas (benign tumors of the uterine wall).g6pd is an x linked gene that is heterozygous in 30% of African American woman therefore, tumor cells express only one form of g6pd as a result of x inactivation Each leiomyomas only had one form of G6PD so his meant the tumor descended from a single cell. Another experiment of this came from the observation of myelomas which derive from the B cell precursors of antibody producing plasma cells. Usually B-cell precursors have different subpopulations due to various immunoglobin (IgG) gene rearrangements.
However, in the patients all the myeloma cells produced the same antibody molecule. Clearly monoclonal origin. Clonal tumor cells may contain chromosomal aberrations that are present in the original abnormal cell that gave rise to the tumor mass. Cancer cells also continue to acquire genetic mutations and cells within distal metastases may be divergent compared to those within the primary tumor mass. Specific chemical agents can induce cancer Carcinogenics can either cause cancer or promote disease progression.
Benzo[a]pyrene is the major chemical carcinogen present in nicotine and cigarette smoke associated with development of small cell lung cancers. Many aromatic hydrocarbons are carcinogens. Both physical and chemical carcinogens act as mutagens Most chemicals are metabolized in the liver into a carcinogenic form and will get incorporated into a nucleotide, then screw up base pairing then cause cancer * The Ames test assesses the mutagenic potency of chemical compounds. Chemical carcinogens are metabolized by liver enzymes into their active xenobiotic forms.
The modi? ed chemicals are added to a histidine auxotrophic strain of salmonella bacteria which is unable to synthesize the amino acid histidine. Mutagenic chemicals induce genetic mutations in salmonella, causing the bacteria to revert back into the wild type form- which is able to produce histidine. The Ames test is currently used by the Food and Drug Administration as an initial screen for potential carcinogenic agents. Doesn’t tell us anything about tumorigenic potential, it just tells us if it is a mutagen.
To test tumorigenic potential, must put in animals to see Summary/Side Notes: Trying to ? nd biomarkers of disease progression to help in determining clinical outcomes in certain cancers found at different stages. Chapter 3: Viruses that Cause Cancer Oncogenic viruses are cancer causing viruses The study of these viruses led to the discovery of protoncogenes and oncogenes 15-20% of cancers are caused by viruses, most being related to the B-cell lymphomas The cytopathic (cell-killing) effects of viruses will cause the cell to die and release thousands of progeny viral particles to destroy the tissue.
However, certain tumor viruses instead of killing the host cell, force them to thrive and proliferate uncontrollably leading to cancer Most viruses have simple genomes, however, tumor viruses encode gene products that redirect cellular growth processes associated with cancerous cell proliferation Peyton Rous discovers a chicken sarcoma virus Originally, viruses were classified as infectious agents that were small enough to pass through filters Cancer was considered a candidate for an infectious disease Rous discovered that sarcomas in ch.