Cell Division and cell cycle control and cancer Quiz 3/Exam 3 – Flashcards

In eukaryotes, this process has two important aspects. The first is the division of the nucleus, called karyokinesis. The second is cytokinesis, the formation of the cell membrane between the two nuclei to split the newly forming "daughter" cells. The nucleus has the genetic material or chromosomes, structures made up of DNA strands and associated proteins that contain a cell's genetic information, which divide during karyokinesis. Prokaryotic cells (like bacteria) have one chromosome, whereas animals have multiple chromosomes with numbers that vary in different species. Prokaryotes typically reproduce through binary fission!!!: asexual reproduction marked by a cell dividing in half. have a simplistic genome. Eukaryotic cells divide through either mitosis or meiosis.

Mitosis is the process of producing exact copies of the "parent" cell's chromosomes and segregating them into separate nuclei. As in binary fission, the two cells created through this process contain all the same parts and typically identical genomes. In contrast, meiosis produces daughter cells that contain half the number of chromosomes of the parent cell and so are not exact copies. Meiosis occurs in sexual reproductive cells and is an essential process in the formation of haploid gametes.

Prokaryotes, the earliest cells to appear in evolutionary history, divide by binary fission. In binary fission, the prokaryotic cell copies its genome, doubles in size, and then splits into two identical cells. have a simplistic genome but have still lots of info to replicate. Most bacteria possess just one circular chromosome that floats freely in the cytoplasm and is not contained within a nuclear membrane

Like binary fission, eukaryotic cell division usually results in two identical daughter cells, each with the same number of chromosomes as the parent cell. Most eukaryotes have more chromosomes than prokaryotes. Humans have 23 pairs, or 46 chromosomes. n eukaryotes, this process has two important aspects. The first is the division of the nucleus, called karyokinesis. The second is cytokinesis, the formation of the cell membrane between the two nuclei to split the newly forming "daughter" cells. Unlike prokaryotes, eukaryotic cells also contain membrane-bound organelles and nuclei, and these organelles must be either divided equally among the daughter cells or reconstructed within the daughter cells. Prokaryotes typically reproduce through binary fission!!!: asexual reproduction marked by a cell dividing in half.

Now we know that mitosis is a small part of the cell's life cycle. Mitosis (M phase) alternates with interphase. In interphase — the phase in which the cell grows and the DNA replicates in preparation for mitosis Interphase occurs in three subphases: G1 phase (first gap, in which the cell grows, a cell's DNA is arranged into long, thin, chromatin fibers), S phase (synthesis, in which the chromosomes are duplicated), and G2 phase (second gap, in which the cell grows more and prepares to begin the process of mitosis. Centrioles, mitochandria and others replicate spindle formation begins). Proteins, organelles, and cytoplasm production occurs during the gap phases, but DNA is synthesized ONLY during the S phase!!! Not surprisingly, based on the eukaryotic genome's size, copying the genome is a major task of the cell cycle, the life cycle of a cell from the time it first forms until it divides S PHASE: Specialized proteins unwind the DNA double helix and hold it in place while enzymes work to copy the nucleotide sequence. Enzymes constantly proof read the copy and correct errors. Once the copies are complete, the chromatin fibers coil tightly and fold into thick chromosomes. Two copies of the same chromosome are paired into sister chromatids. Cells that divide infrequently spend most of their time either in the G1 phase or in an extended, nondividing phase called G0 phase. Cell centrosome duplicates during interphase in both plants and animal cells. However, plants do not have centrioles.

Before and during replication, a cell's DNA is arranged in long, thin chromatin fibers. Specialized proteins unwind the DNA double helix and hold it in place while enzymes work to copy the nucleotide sequence. Enzymes constantly proofread the copy and correct errors. Once the copies are complete, the chromatin fibers coil tightly and fold into thick chromosomes. Two copies of the same chromosome are paired into sister chromatids, which are attached along their length but most closely near the center. Under a light microscope, each pair of sister chromatids looks like a small X, because they are bound in the middle by a DNA-protein complex called the centromere. A nuclear envelope surrounds the duplicated chromosomes

DNA-protein complex which attaches the two sister chromatids.

DNA and proteins that make up the chromosomes

Main microubule organizing center (MTOC). Organizes the microtubules of the spindle during mitosis. The cell's centrosome, a structure that organizes microtubules during mitosis, duplicates during interphase in an animal cell. The two centrosomes stay together near the nucleus. The centrosomes of plant cells function much like animals cells, although they do not contain centrioles.

These five stages are called prophase, prometaphase, metaphase, anaphase, and telophase. All the phases Interphase Prophase Metaphase Anaphase Telophase Cytokinesis (I probably made ana that cold)

During prophase in organisms the chromatin condenses into chromosomes (they look like X) visible with a light microscope. each pair of sister chromatids looks like a small X, because they are bound in the middle by a DNA-protein complex called the centromere At this point, the nucleoli (structures in the nucleus where ribosomal RNA is produced) disappear, and the mitotic spindle begins to take shape. Asters, short microtubules, radiate around each centrosome. In prophase, tubulin protein subunits add on to the microtubules connected to the centrosomes, lengthening the microtubules and beginning to push the centrosomes apart

The mitotic spindle is a structure that consists of microtubules and associated proteins. The mitotic spindle is a crucial organizing force in cell division. It moves the daughter chromosomes to their appropriate places in prophase. During metaphase, motor proteins move the chromosomes along microtubules to line up neatly in the middle of the cell.

kinetochore is the protein structure on chromatids where the spindle fibers attach during cell division to pull sister chromatids apart

Asters are short microtubules. They radiate around each centrosome in prophase. (later in metaphase the asters meet the cell membrane.)

During prometaphase, the chromosomes condense further, and each chromatid develops a kinetochore, a protein structure associated with specific DNA sequences at the centromere. Microtubules attach to the kinetochores to move them around. The Nuclear Envelope usually breaks into pieces at this point, and the mitotic spindle extends across the cell and through the nuclear space.

During metaphase, motor proteins move the chromosomes along microtubules to line up neatly in the middle of the cell. Their centromeres lie on the imaginary plane of the "metaphase plate," stretching across the middle of the cell. The two kinetochores of each sister chromatid face in opposite directions and are joined by microtubules to different centrosomes. Nonkinetochore microtubules interact to push the two centrosomes to opposite poles of the cell. The asters meet the cell membrane, completing the mitotic spindle.

Anaphase is the shortest stage. It may last only a few minutes. Proteins attached to the chromatids are cut apart, and the sister chromatids rapidly separate. (X chromosomes seperate) The newly formed daughter chromosomes move toward opposite ends of the cell, pushed and pulled by motor proteins along the kinetochore microtubules. The nonkinetochore microtubules lengthen, and the cell expands.

During telophase, two nuclei form and recreate the nucleoli. Fragments of the parent nuclear membrane and other intracellular membranes join to form a new nuclear envelope around each collection of chromosomes. The chromosomes loosen and straighten out to some extent. The microtubules break apart and mitosis is complete .

Shortly after mitosis, the cytoplasm finishes dividing through the process of cytokinesis . In animal cells, cytokinesis begins with a cleavage furrow, a narrow groove in the middle of the dividing cell, at the location of the metaphase plate. Actin microfilaments associated with the protein myosin circle around the inside of the cell at the cleavage furrow, forming a ring. The actin and myosin draw together, contracting the ring and pinching the cell membrane together. This pinching action separates the cytoplasm into two identical daughter cells.

Mitosis phase of cell. Then the cell proceeds through mitosis, the M phase, in which the chromosomes segregate. The M phase includes several stages: prophase, prometaphase, metaphase, anaphase, and telophase. The cell ultimately divides during cytokinesis.

All the parts of the parent cell are transferred, reformed, or reorganized in the daughter cells: the nucleoli, ribosomes, mitochondria, Golgi apparatus, lysosomes, endoplasmic reticula, and the microtubules and microfilaments of the cytoskeleton.

Plant cells have cell walls. Instead of a cleavage furrow forming, the Golgi apparatus generates vesicles that move along microtubules to the middle of the cell and join to form a cell plate. Cell wall materials gather within the cell plate, and the plate enlarges until it joins up with the edges of the plasma membrane. The plate separates down the middle, producing a new membrane and cell wall for each daughter cell

Mistakes in cell division can lead to uncontrolled cellular growth and can result in cancer and certain other disorders

Interphase takes up the larger proportion of the cell's life cycle. Mitosis about one hours. For eukaryotes it around 24 hours to do the whole cell cycle.

Mitosis is divided into five stages: prophase, prometaphase, metaphase, anaphase, and telophase. During prophase, chromosomes condense and the mitotic spindle begins to take shape. During prometaphase, the nuclear envelope breaks down and the mitotic spindle expands. Chromosomes line up in the middle of the cell during metaphase with sister chromatids facing opposite ends of the cell. The chromatids separate during anaphase, and motor proteins move them along microtubules to opposite ends of the cell. During telophase, two new nuclei form, completing mitosis. Shortly after the end of mitosis, proteins form a ring around the middle of the cell and tighten into a noose, separating the cytoplasm and cell membranes into two cells. This process is called cytokinesis.

Cell division typically results in two daughter cells identical to the parent cell. Prokaryotic cell division commonly occurs by binary fission. This process results in replication of the single circular chromosome and cytoplasm expansion. The cell membrane pinches together to form two new cells, each with a complete genome. Prokaryotes may also reproduce under some conditions using endospores, budding, or multiple fission.

Division of the nucleus during cell division.

G1 Correct This answer is correct because if a cell is not to divide, it should not replicate its DNA by entering S phase; thus, G1 is the last phase before the cell commits to dividing itself. Once a cell enters S phase, it has already committed to duplicating itself along with its genetic material.

The nuclear membrane breaks apart. Correct This answer is correct because the nuclear membrane breaks apart in prometaphase, allowing the mitotic spindle to stretch through the nuclear space.

The system that controls which phase a cell is in is called the cell cycle control system. The times at which the cycle can be stopped or pushed forward are called checkpoints. In general, animal cells' default mode is to stop at the checkpoint, the way you would stop at a military checkpoint if guards asked you to

The times at which the cycle can be stopped or pushed forward are called checkpoints. In general, animal cells' default mode is to stop at the checkpoint.At these checkpoints in the cell cycle, existing conditions are considered and the cell decides whether it is safe to proceed or stop and not divide. Protein signaling pathways are the guards that interact with molecules involved in the cell cycle, such as components of the DNA replication machinery and microtubules, to decide whether or not a cell should continue. Checkpoints are at G1 (before the cell copies its DNA), G2 (before it enters mitosis), and M checkpoint (before the DNA separates), among other points.

The most important checkpoint in mammals seems to be the G1 checkpoint. If the cell is not given the go-ahead at this point, it goes into G0 phase and stops dividing. Most highly differentiated cells in the human body, including mature muscle cells and neurons, remain in G0. Some cells, like liver cells, can leave G0 and reenter the cycle to repair an injury.

The Big Checkpoints are at G1 (before the cell copies its DNA), G2 (before it enters mitosis), and M (before the DNA separates), among other points (there are other like in S phase and etc.).

As the early experiment in fusing cells indicated, the cell cycle is regulated substantially by proteins in the cell's cytoplasm!!!! Many proteins involved in cell cycle regulation are cyclin-dependent kinases (Cdks)

A kinase is an enzyme that catalyzes the addition of a phosphate group to a molecule. A cyclin is a protein whose concentration in the cell varies cyclically. Kinases whose activities are determined by cyclins are Cdks. Cyclin-Cdk complexes are formed from a protein kinase subunit and a cyclin subunit. When the two subunits associate, they form the holoenzyme. In most cases, the concentration of the kinase subunit is relatively constant, whereas the concentration of the cyclin subunit oscillates. The kinase is completely inactive without its cyclin partner, but in addition to the formation of the cyclin-Cdk complex, activation of the holoenzyme requires the phosphorylation of a key residue in the kinase subunit.

The holoenzyme is made of two subunits: the kinase subunit and the cyclin subunit. The holoenzyme is activated when the cyclin and kinase subunits form a complex and the kinase subunit is phosphorylated.

Cyclin is synthesized during the S and G2 phases. During G2, when cyclin has reached critical concentration, it forms a complex with Cdk, creating MPF. MPF is a holoenzyme that phosphorylates proteins needed for mitosis to proceed. MPF triggers mitosis by phosphorylating proteins, in some cases activating additional enzymes. If these proteins are not phosphorylated, the cell cycle halts at the M checkpoint. It phosphorylates proteins in the nuclear envelope, promoting the nuclear envelope's breakdown during prophase. MPF may also help chromosomes to condense and the mitotic spindle to form in prophase. In anaphase, MPF's actions cause its cyclin component to be broken down. The kinase remains in the cell in inactive form until new cyclin molecules are synthesized. The cyclin-Cdk complex then re-forms.

One mechanism that regulates the cell cycle is the concentration of cyclin. Cyclin increases in concentration throughout the G1, S, and G2 phases (synthesized during S and G2 phase). Near the end of the G2 phase, the cyclin molecules combine with a cyclin-dependent kinase (Cdk), forming maturation-promoting factor (MPF). MPF is a holoenzyme that phosphorylates proteins needed for mitosis to proceed. If these proteins are not phosphorylated, the cell cycle halts at the M checkpoint. After mitosis, cyclin is broken down and must build again for mitosis to repeat.

They peak at the same time because cyclin is part of MPF; it binds to Cdk to create MPF. They rise at different rates because cyclin is produced throughout S phase and G2 phase, but MPF is only created when cyclin binds to Cdk

Other than Cdks, two more types of kinases, Polo-like kinases (Plks) and Aurora kinases, act at the M checkpoint and during mitosis and cytokinesis to help regulate and prevent errors in centrosome duplication, assembly of the mitotic spindle, chromosome separation, and cytokinesis. These types of errors may lead to errors in cell division. Similar to the Cdks, Plks and Aurora kinases are also activated by phosphorylation.

Cdks, Plks and Aurora kinases are different kinase families that regulate the cell cycle. Different Cdks operate at different stages of the cell cycle. Plks and Aurora kinases control cell cycle events in different ways, ranging from centrosome function, spindle assembly, and chromosome segregation to cytokinesis (M phase) . Together these enzymes regulate the cell cycle and ensure that it happens correctly. (cyclin attaches to cdks to make MPF phosphorylates proteins which starts mitosis).

At the M checkpoint, a complex of different proteins activates the enzyme "separase," which catalyzes the separation of sister chromatids. At this point in the cell cycle, it is crucial that the chromosomes be lined up at the metaphase plate with the sister chromatids facing in different directions, so that when the chromatids separate exactly one from each pair will go to each daughter cell. At the checkpoint, the cell checks whether each chromatid is attached to the mitotic spindle at its kinetochore. If some of the kinetochores are not attached to the spindle, anaphase does not start. If they are all attached securely, separase is activated and anaphase proceeds

At the M check point, the cell checks whether each chromatid is attached to the mitotic spindle at its kinetochore. This ensures that the chromatid can be pulled to poles in anaphase, and that the resulting cells will have an equal number of chromosomes. If some of the kinetochores are not attached to the spindle, anaphase does not start.

many signals that the cell cycle responds to are internal. But the cell cycle also responds to external signals. Aspects of the environment that cells normally monitor include nutrients, growth factors, and space. Most types of mammalian cells also won't divide unless the environment contains specific growth factors, proteins that stimulate cell division

growth factors, proteins that stimulate cell division. Most types of mammalian cells also won't divide unless the environment contains specific growth factors. Different cells require different factors or combinations of factors

Many cells will stop dividing if they are too crowded. This phenomenon is called density-dependent inhibition

cells will stop dividing if they are too crowded. Cells in a Petri dish will keep dividing until a single layer of cells covers the surface of the dish, and then they will stop. If a scientist removes some cells, the cells will again start dividing until they fill in the gap. This inhibition occurs because proteins on the surfaces of neighboring cells bind to each other. Cell division keeps going while the surface proteins on some cells remain unbound but stops once all the cells have neighbors.

Cancer cells, in contrast, may not show density-dependent inhibition. They may keep dividing despite crowding, forming multiple layers. The reason for the loss of this density-dependent inhibition may be that the cells produce additional external growth factors or the cells may have abnormal signal transduction pathways that bypass normal growth checks.

anchorage dependence. (the second other kind is density dependent reaction). Most animal cells must be attached to a surface or tissue to divide. Most animal cells divide only if attached to a surface; in the body, they attach to tissues. In cancer cells, this check may not function, and cells that should show anchorage dependence may keep dividing without needing to be anchored or attached at all.

Cancer is the uncontrolled growth of abnormal cells in the body. How are cancer cells different from normal cells? They may not stop dividing when they are crowded or when they are free-floating. They may speed past the G1 checkpoint into S phase without confirming their readiness. If they stop dividing, they stop at random points in the cycle, not at the usual checkpoints. A cancer cell may divide indefinitely

Although failure of any of several cell cycle controls can lead to uncontrolled growth, a single cell that has undergone this type of transformation into a cancer cell is usually recognized and destroyed by the immune system. If the immune system fails to catch the cell in the place where it started. These cell masses form benign tumors, abnormal tissue growths that do not spread to other parts of the body. Benign tumors often do not cause serious health problems. If a benign tumor is causing problems by pressing against normal tissue — for example, pressing against the urethra and blocking urine flow — it can usually be surgically removed. People who have cancer have malignant tumors. Malignant tumors contain cells that can spread to new tissues and proliferate in different parts of the body. This process is called metastasis. Multiple mutations are required for a cell to display both uncontrolled growth and metastasis. Mutations often accumulate over time before cancer develops.

If the immune system fails to catch the cell in the place where it started. These cell masses form benign tumors, abnormal tissue growths that do not spread to other parts of the body. Benign tumors often do not cause serious health problems. If a benign tumor is causing problems by pressing against normal tissue — for example, pressing against the urethra and blocking urine flow — it can usually be surgically removed

People who have cancer have malignant tumors. Malignant tumors contain cells that can spread to new tissues and proliferate in different parts of the body. This process is called metastasis. Multiple mutations are required for a cell to display both uncontrolled growth and metastasis. Mutations often accumulate over time before cancer develops.

Process by which malignant tumors spread to other parts of the body

Compared with normal cells from the same tissues, cancer cells look physically different. They are often less well differentiated and less clearly organized than normal cells because they have many mutations and proceed through the cell cycle without pausing at the normal checkpoints. Cancer does not just occur in animals, plants can also have uncontrolled growth that results in cancerous tumors

Genes that cause cancer are called oncogenes. The normal forms of these genes are called proto-oncogenes. Researchers have identified a number of proto-oncogenes. Cyclin D1 is one; another is ras, short for "rat sarcoma," so named due to its initial discovery in rodents. The ras gene codes for a G protein that relays a signal from a growth factor outside the cell to begin a cascade that ends with the synthesis of a protein that stimulates the cell cycle. As in cyclin D1 protein, an abundance of ras protein pushes the cell towards proliferation. About 30% of human cancers display mutations in the ras gene. Oncogenes such as ras cause cells to proliferate because their protein products stimulate cell division

Other genes involved in cancer inhibit cell division. How is this possible? When genes that normally halt cell division or induce apoptosis (programmed cell death) do not do their jobs, cell division becomes uncontrolled. These genes are called tumor suppressor genes, not oncogenes. The gene most frequently altered in human cancers is a tumor suppressor gene called p53. p53 is mutated in more than half of human cancers. Normally, p53 acts to pause cell cycle progression while DNA is repaired or to induce apoptosis (cell death). When p53 does not work properly, cell cycle progression can proceed unchecked thus leading to mutated/damaged cell to go through cell cycle. p53 pauses the cell cycle while repairs are made or induces apoptosis of damaged cells. Loss of p53 could cause unregulated cell division even if DNA damage was sustained, which can result in cancer.

As well as reacting to internal cues, the cell cycle reacts to external cues. Cells will not divide if the environment lacks crucial nutrients, and most animal cells will not divide without specific growth factors being present in the environment. Extracellular signaling molecules can initiate a cascade reaction by binding to a transmembrane receptor. Receptor tyrosine kinases and G protein-coupled receptors are two receptor types important in cell signaling pathways. Normal animal cells usually exhibit density-dependent inhibition and anchorage dependence, meaning they will not proliferate if crowded or unattached to a surface.

A gene that normally halts cell division or induces apoptosis. (example p53) The genes that regulate these processes are called tumor suppressor genes, so named because they halt uncontrolled cell division and suppress tumor formation. Errors in tumor suppressor genes inhibit the cell from repairing damage and prevent the organism from disposing of damaged cells.

Cancer is caused by breakdowns in cell cycle control. Its relevance to cancer makes cell cycle control an active area of scientific research. Oncogenes such as ras stimulate uncontrolled proliferation, whereas tumor suppressor genes such as p53 inhibit cell cycle progression. In many cases, mutations accumulate over time before the cancer becomes malignant, or acquires the ability to spread to other tissues

the central role it plays in maintaining healthy cells. Normally, p53 pauses the cell cycle while repairs are made or induces apoptosis of damaged cells. (cell death). When p53 does not work properly, cell cycle progression can proceed unchecked thus leading to mutated/damaged cell to go through cell cycle. (its a tumor supressor gene) It is frequently inactivated in all types of cancer because of the central role it plays in maintaining healthy cells. Cellular stressors, such as metabolic stress, errors in mitosis, DNA damage, or oncogene activation, all trigger the p53 pathway. If the damage is not severe, p53 activates the transcription of DNA repair enzymes in an attempt to fix the damage; however, in the case of excessive damage or severe stress, p53 may initiate apoptosis, instead.

oncogenes and tumor suppressor genes altered? Three main events can change how genes are expressed: the number of copies of the gene in one cell changes, the gene's location changes, or a mutation develops within either the gene or its control element and is not corrected. an oncogene may be overexpressed if the cell has more copies of the gene, if either the gene or its control element mutate, or if the gene moves to a part of the genome where a control element enhances its transcription.

G0 Correct This answer is correct because most human cells are in G0, the phase in which they are neither dividing nor preparing to divide (Interphase?). Some cells divide frequently, but others divide rarely.

A cell that passes the G1 checkpoint usually begins the process of cell division. Correct This answer is correct because this is why the G1 checkpoint has particular importance in mammalian cells.

Proto-oncogenes encode proteins that promote cell division, regulate cell differentiation, and inhibit cell death. They are most active during embryonic development, during the time when an organism is rapidly increasing its cell numbers. As an organism develops into an adult, proto-oncogenes are turned off in many cell types. There are only a few cell types, such as skin cells and the cells that line the intestines, in which proto-oncogenes remain active throughout adulthood to enable the continuous replacement of damaged cells. A proto-oncogene becomes an oncogene when it acquires a mutation or is altered in a way that increases its activity and encourages cells to continue to divide, regardless of the presence of growth inhibitory signals

A proto-oncogene becomes an oncogene when it acquires a mutation or is altered in a way that increases its activity and encourages cells to continue to divide, regardless of the presence of growth inhibitory signals. In this way, oncogene mutations contribute to tumor formation and cancer progression. A mutation in a proto-oncogene that leads to uncontrolled cell division is classified as an oncogene mutation The root "onco" is Greek for tumor, and the prefix "proto-" means first.

Errors in both gene types may lead to cancer. Errors in proto-oncogenes result in oncogenes, which accelerate cell division. Errors in tumor suppressor genes inhibit the cell from repairing damage and prevent the organism from disposing of damaged cells.

Proto-oncogenes become oncogenes if (affectedby mutations/more than one): Transcription is up-regulated. This occurs if the promoter is mutated to become more active or if the gene is moved to a new area of the genome that is more actively transcribed. Gene amplification occurs. Extra copies of the gene may result in more protein synthesis, which may cause increased activity. The gene is mutated to produce a hyperactive protein.

Tumor suppressor genes may become harmful if they acquire loss-of-function mutations. These mutations may result in: The down-regulation of transcription. The loss of functional protein expression. The gene product not being sufficiently active.

Environmental factors, or mutagens, may also lead to mutations in the DNA. Some mutagens are chemicals, such as food preservatives, the reactive oxygen byproducts of aerobic respiration, or chemicals found in cigarette smoke. Mutagens may also be physical, such as X-rays and UV light. Mutagens that have been experimentally shown to cause cancer in animal studies are called carcinogens.

Cancer may also result from a viral infection. Viruses often increase or alter the expression of host genes. Virus-related genetic changes may trigger a proto-oncogene to become an oncogene or may inhibit a tumor suppressor gene. HPV (human papillomavirus), for example, is a virus that has been shown to inactivate p53 and is linked to the incidence of 99% of cervical cancers

One essential point to understand is that, in general, no single mutation will result in cancer. From what we can tell, most cancers contain more than 60 different mutations On its own, the conversion of a single proto-oncogene to an oncogene is not carcinogenic because of the intricate safety net of tumor suppressor genes. Similarly, the loss of a single tumor suppressor gene is not enough to cause cancer because transformed

A number of genetic changes are needed to convert a healthy cell to a cancerous cell. The common mutations needed for a cell to become cancerous are: 1) cell division despite a lack of growth factors, 2) cell division despite the presence of growth inhibition signals, 3) evasion of apoptosis, 4) indefinite cell division, 5) initiation of angiogenesis, 6) ability to metastasize, 7) activation of unusual metabolic pathways, 8) evasion from the immune system, 9) increased mutation rate , and 10) increased recruitment of local inflammatory molecules.