Cancer. Throughout the life of an individual, but particularly during development, every cell constantly faces decisions.

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1 Cancer Throughout the life of an individual, but particularly during development, every cell constantly faces decisions. Should it divide? Yes No--> Should it differentiate? Yes No-->Should it die? Yes-->Apoptosis No Proper development and tissue homeostasis rely on the correct balance between division and apoptosis. Too much apoptosis leads to tissue atrophy such as in Alzheimer s disease. Too much proliferation or too little apoptosis leads to cancer. cancer = unregulated cell proliferation apoptosis = programmed cell death necrosis = unprogrammed cell death Cell Cycle For recent reviews on this topic see: Johnson and Walker (1999) Cyclins and cell cycle checkpoints. Annu. Rev. Pharmacol. Toxicol. 39: See also Gilbert s website: The cell cycle is at the center of the decisions a cell makes. Dividing cells go through a cycle consisting of, G1 (growth or gap), S (DNA synthesis), G2 (growth) and M phase (mitosis). Specific events must happen in a particular sequence for the cell to replicate. During the G1 phase, the cell integrates mitogenic and growth inhibitory signals and makes the decision to proceed, pause, or exit the cell cycle. S phase is defined as the stage in which DNA synthesis occurs. G2 is the second gap phase during which the cell prepares for the process of division. M stands for mitosis, the phase in which the replicated chromosomes are segregated into separate nuclei and cytokinesis occurs to form two daughter cells. In addition, the term G0 is used to describe cells that have exited the cell cycle and become quiescent. When cells differentiate, they usually stop dividing and therefore exit the cell cycle. Most cells that stop dividing to differentiate do so in the G1 phase although some arrest in G2. An important checkpoint in G1 is referred to as start in yeast and the restriction point in mammalian cells. This is the point at which the cell becomes committed to DNA replication and usually to completing a cell cycle. Before beginning the cell cycle, the cell must assess whether sufficient growth has occurred (eg. are there enough ribosomes? Other cell constituents?), whether there is cellular damage and whether there is the proper complement of growth factor signaling. Another, checkpoint exists at

2 the G2 to M transition where cells become committed to divide. Again the cell must assess whether the chromosomes are completely replicated and whether there is cellular damage and proper growth factor signaling. The events of the cell cycle are regulated by a protein complex consisting of a cyclin dependent kinase (cdk) and a cyclin. Both the CDK and the cyclin are protein kinases. Different CDK/cyclin complexes regulate different phases of the cell cycle. In yeast, there is only one CDK that interacts with different phase-specific cyclins. In mammals, there are different CDKs and different cyclins for different phases of the cell cycle. Cyclins (and CDKs in mammals) are expressed cyclically; each cyclin is expressed only in the appropriate phase of the cell cycle and then is rapidly degraded. At each stage the CDK/cyclin complex performs 3 important functions: 1. They activate the cellular activities that are associated with that particular phase in the cell cycle. 2. They activate the CDK/cyclin complex that controls the next stage in the cell cycle. 3. They inactivate the CDK/cyclin complex from the previous stage in the cell cycle. Often they trigger their own inactivation or degredation. In this way, they control the forward progression of the cell cycle as well as the events of that particular phase. CDK/cyclin complexes are regulated in 4 major ways: 1. Association of the CDK and the cyclin (cyclin activates CDK) 2. Phosphorylation 3. Binding to cyclin dependent kinase inhibitors (CKIs) 4. Proteolytic degradation Phosphorylation Association of a CDK and cyclin is necessary but not sufficient for the formation of an active complex. The proper phosphorylation status is also required for activity. Phosphorylation of CDK/cyclin complexes can be either activating or inhibitory. As an example we will consider the regulation of MPF activity. (Remember from cleavage that MPF=maturation promoting factor, or mitosis promoting factor). MPF consists of a CDK (cdc2) and cyclinb. After association of these 2 proteins, the CDK is phosphorylated on a specific residue (tyrosine 15) by a kinase called wee1. This is an inhibitory phosphorylation therefore wee1 --- MPF. Then a second, activating phosphate is added to another residue (threonine 161) by a kinase called CAK (CDK activating kinase). However MPF is still not active because of the phosphorylated tyr15. MPF finally becomes activated when the inhibitory phosphate added by wee1 is removed by a phosphatase called cdc25 (or string). Then MPF is active and can trigger mitosis. Cyclins can also be regulated by phosphorylation.

3 CDK inhibitors (CKIs) There are 2 families of CKIs, the Cip/Kip family and the INK4 family. Members of the Cip/Kip family interact with all CDK/cyclin complexes. An example of this family, p21, will be discussed below in relation to checkpoint control. INK4 members interact with specific CDKs. For example, p16 interacts with the G1 CDKs (cdc4 and cdc6 in mammals) and either prevent their association with cyclind or inhibit the preassembled complex. p16 is also important in checkpoint control and will be further discussed below. Ubiquitin dependent proteolysis Ubiquitin dependent proteolysis is very important for rapidly degrading specific proteins. Ubiquitin is a 76 amino acid peptide that is ligated (attached) to proteins targeted for degradation. Additional ubiquitin peptides are sequentially added to the previous subunit in a process called polyubiquitination. This is catalyzed by a protein complex known as the ubiquitin ligase complex. Polyubiquitinated proteins are then recognized and degraded by a proteolytic complex known as the 26S proteosome. Ubiquitin dependent proteolysis is critical at 2 major steps in the cell cycle. Different ubiquitin ligase complexes act at each step and the mode of regulation is different. The progression from G1 to S-phase requires the action of a complex called SCF. SCF recognizes proteins that are phosphorylated on PEST sequences, sites that are common in proteins that are regulated by rapid turnover. Entry into S phase requires the proteolytic degradation of an S phase inhibitor called Sic. Sic is phosphorylated on it s PEST motif by the G1 cyclind. Thus Sic is targeted for polyubiquitination by SCF and subsequent degradation by the 26S proteosome, removing the inhibitor and allowing entry into S-phase. Ubiquitin dependent proteolysis is also important for maintaining the forward progression of the cell cycle. SCF ubiquitinates cyclind. CyclinD is phosphorylated by the same CDK that it activates and this phosphorylation targets it for ubiquitination by SCF and subsequent degredation. Another ubiquitin ligase complex, APC (Anaphase Promoting Complex) is important for the transition from metaphase to anaphase during mitosis. APC ubiquitinates M-phase cyclins. The regulation of APC is very complex but at it is partly regulated by phosphorylation of APC subunits. Phosphorylation of APC by the mitotic cyclin/cdk activates it to ubiquitinate mitotic cyclins. It s substrate specificity is controlled by different subunits becoming part of the complex. For example, degradation of mitotic cyclins is required for the onset of chromosome separation. Later, in telophase, APC begins degrading proteins involved in anaphase. One subunit that provided specificity for the mitotic cyclins is replaced by another subunit that confers substrate specificity for the anaphase proteins. Thus, SCF activity is regulated by modification of the substrates while APC activity is regulated by modification of the APC complex.

4 Checkpoint control The most important checkpoint is called start in yeast or the restriction point in mammalian cells. This is the point at which the cell commits to enter S phase. Since most cells exit the cell cycle in G1 to differentiate, passing start generally commits to undergoing an entire cell cycle. Cells assess whether adequate growth has occurred, whether proper growth factor signaling is present and whether any cellular damage is present before reaching the decision to pass start. Because defects in cell cycle checkpoint control can lead to unregulated cell division, many of the factors involved in checkpoint control were first identified as oncogenes. One central protein in regulating start is the retinoblastoma protein (Rb). Rb binds and inhibits a transcriptional activator called E2F. E2F activates the transcription of many cell cycle genes, including those involved in DNA synthesis as well as S phase cyclins. Rb dissociates from E2F when it is phosphorylated by cyclind, thereby allowing E2F to activate transcription and initiate S phase. Rb is also a negative transcriptional regulator of the CKI p16. In cells lacking Rb, p16 is overexpressed. The inactivation of Rb by cyclind allows expression of p16 which then inhibits the activity of the G1 CDK. Thus we see another example of how a cyclin promotes progression to the next phase while inhibiting the current or previous phase. CDK/cyclinD Rb E2F S phase Rb p16 G1 CDK CyclinD does not oscillate with the cell cycle. Growth factors regulate the expression of cyclind. This is one of the ways that growth factors feed information into the cell cycle. Thus cells cannot pass start without growth factor signals. Many growth factors signal to the cell cycle through ras and the MAP kinase pathway. When quiescent cells re-enter the cell cycle and divide (i.e. go from G0 to G1), cyclind is the first cyclin to be activated. The myc transcription factor is also required for the G1 to S transition. myc activates transcription of cdc25 which then activates the CDK complex, promoting cell cycle progression to S phase. Cells will not progress through the cell cycle if cellular damage is sensed. Cellular damage induces the expression of a transcription factor called p53. p53 inhibits both the G1 to S transition and the G2 to M transition. One of the genes whose transcription is activated by p53 is the CKI p21. Thus: Cellular damage p53 p21 CDK/cyclin Apoptosis For recent reviews on this subject see the following: King and Cidlowski (1998) Cell cycle regulation and apoptosis. Annu. Rev. Physiol. 60:

5 Norbury and Hickson (2001) Cellular responses to DNA damage. Annu. Rev. Pharmacol. Toxicol. 41: Also the Aug 28, 1998 issue of Science was a special issue on the topic of apoptosis and contains several informative reviews. Apoptosis is generally considered as programmed cell death whereas necrosis signifies unprogrammed cell death. The distinction between these was originally based on morphological criteria; apoptotic cells shrink while necrotic cells swell. It is not clear whether the distinction is quite so simple but there is a suite of morphological features that characterize apoptosis. Apoptotic cells lose substrate attachment and become rounded. Cells shrink, condense their chromatin, and display membrane blebbing. Apoptotic cells fragment their DNA into approximately 200 base-pair fragments. At the end of apoptosis, the cell is broken into multiple apoptotic bodies that are phagocytized by neighboring cells. Thus these morphological changes are the outward manifestations of the cell systematically dismantling itself and packaging itself up in membrane bound vesicles to be absorbed by neighboring cells. Because cellular contents are not released, this occurs with little inflammation. Apoptosis is an essential component of normal development and homeostasis as well as being critical for eliminating diseased or damaged cells. Approximately 50% of the neurons undergo apoptosis during mammalian embryogenesis. Severe mental retardation results if the extra neurons are not eliminated. In the immune system, autoreactive lymphocytes are eliminated by apoptosis and failure in this system results in autoimmune disease. Mutations in key components of apoptotic pathways are lethal. As a safeguard against disease, every cell in our bodies expresses the components of the apoptotic pathways and is ready for rapid self-destruction. In fact, it has recently become clear that cells must receive the proper set of signals to prevent apoptosis or they will self-destruct. Because of the importance of the correct balance between division and apoptosis for proper development and tissue homeostasis and the dire consequences of unregulated cell division, it is not surprising that the cell cycle and apoptotic response are closely connected. This is one of the safeguards we have against cancer (see below). There are 2 major pathways that control the apoptotic response: the mitochondrial pathway and the death receptor pathway. Both pathways utilize the same basic set of proteases, called caspases. Caspase Cascade The central machinery of apoptosis consists of a cascade of cysteine proteases called caspases. There are 2 major types of caspases, initiator caspases and effector caspases.

6 Initiator caspases activate effector caspases by proteolytic cleavave of an effector pro-caspase. The 2 most important initiator caspases are caspase-8 and caspase-9. These are associated with the 2 major pathways for initiating apoptosis. Caspase-8 is involved in receptor mediated apoptosis while caspase-9 is involved with the mitocondrial pathway. Mice deficient for either of these caspases usually die before birth and always within 3 days of birth. The mice show distinct defects for each caspase, some of which include brain deformities, heart malformations and blood overproduction. Initiator caspases are regulated by association with cofactors. Available evidence indicates that the cofactors facilitate caspase dimerization which leads to caspase activation. One model proposes that dimerization results in the proteolytic cleavage of each partner by the other, thereby activating the caspases. Effector caspases are the enzymes responsible for disassembling the cells. Substrates for effector caspases include: 1. apoptosis inhibitors (eg. Bcl2, Rb) 2. cell structures 3. other proteolytically activated enzymes gelsolin degrades cytoskeleton CAD caspase activated DNAse Caspases are ubiquitously expressed, therefore every cell is poised for rapid self destruction. Mitochondrial pathway The Bcl2 family of proteins are the central regulators of the mitochondrial pathway. Bcl2 is an inhibitor of apoptosis. Bcl2 binds and inhibits a protein called Apaf. Apaf is an activator of the initiator caspase-9. Therefore, Bcl2 -- Apaf! caspase-9! APOPTOSIS Bcl2 is located on the cytosolic face of several membranes including the outer mitochondrial membrane, the ER and the nuclear envelope. It is thought that Bcl2 may somehow monitor damage in these compartments. Bax is a protein,related to Bcl2, which inhibits Bcl2 thereby promoting apoptosis. It is thought that binding of Bax to Bcl2 releases Apaf to then activate caspase9. Thus, Bax -- Bcl2 -- APOPTOSIS, (net result, Bax! APOPTOSIS) CytochromeC is also an activator of Apaf and apoptosis. CytochromeC is released from damaged mitochondria. Death Receptor mediated pathways A number of cell surface receptors can induce apoptosis when activated by a signal ligand. One of the most well known of these is tumor necrosis factor (TNF) and the receptor TNFR. Another important one is Fas. Death receptors are plasma membrane

7 spanning proteins that have a conserved motif in their cytoplasmic domain called the Death Domain. The death domain mediates protein interactions with other death domain proteins. A protein called FADD (Fas-associated protein with death domain) associates with caspase-8 through the DED (death effector domain). This recruits caspase-8 to the receptor complex leading to its activation (possibly as a result of 2 caspase-8 molecules being brought into proximity so they can cleave and activate each other). Thus receptor mediated signaling can activate apoptosis independent of the mitochondrial pathway. TNF and other death signals can have very different effects on different cell types. TNF can signal division in some cells, differentiation in other cells, and apoptosis in yet other cell types. The response of a given cell depends on what other signals are being perceived and what proteins are expressed by that cell. In the case of TNF signaling, one protein of particular importance is a transcription factor called NF-ΚB. Cells that do not express NF-ΚB are induced to die by TNF while those that do express NF-ΚB are not. Sensitization of cells Inputs from different sources can act in combination to induce apoptosis. Cells that receive stimuli that are insufficient to induce apoptosis become more sensitive to induction by other stimuli. For example, mild DNA damage induces a low level of p53 expression. p53 inhibits the expression of Bcl2 and stimulates the expression of Fas. Therefore, both the mitochondrial and receptor mediated pathways become more sensitive to induction. Cancer Attributes of Cancerous Tumors " Cell migration (metastasis): alterations in Cell-to-Cell Interactions Are Associated with Malignancy. Metastatic cells break their contacts with other cells and the ECM in their tissue of origin, and as a result, metastatic cells can invade adjoining tissue or enter the circulation and establish themselves in a distant site. " Angiogenesis (formation of new blood vessels): tumor growth requires formation of new blood vessels to supply tumors with blood. Many tumors produce growth factors that stimulate angiogenesis " Unregulated cell division and growth (defects in cell cycle regulation). " Failure to undergo apoptosis in response to inappropriate division

8 Cancer is an extraordinarily rare event About 1 in 10 people will contract cancer at some point in their lives, and most of us have some sort of personal experience with someone we know having cancer. As such, we tend to think of cancer as common, and of course, it is a very serious disease. However, when one considers it in a developmental context, cancer is actually a very rare occurrence. First of all, cancer is rare before the age of forty. Then when one considers all the billions of cell divisions that occur under proper regulation, it is truly amazing how rarely a cell becomes malignant. The reason for the rarity of cancer is the elaborate safeguards cells have against inappropriate cell division. Normal cells require growth factor signals to instruct the cells to divide and not to undergo apoptosis. Links between the cell cycle and apoptotic machinery promote cell death for inappropriately dividing cells. For cancer to occur requires the failure of the apoptotic safeguard mechanisms as well as the deregulation of the cell cycle. Thus, most cancers require 2 or more mutations to deregulate the cell cycle and to overcome the apoptotic safeguards against inappropriate division. Links between Apoptosis and the Cell Cycle Because of the dire consequences of inappropriate cell proliferation, cells have evolved failsafe mechanisms to eliminate cells that divide when they are not supposed to. We tend to think of cancer as a common disease, but when one considers the millions of cells and cell divisions in every individual, and that only about 10% of people develop cancer (usually from a single defective cell and usually in older individuals), then it is evident that cancer is in fact an extraordinarily rare event. This is because of the failsafe mechanisms which allow cells to sense inappropriate proliferation and eliminate themselves. Several factors contribute to the rarity of cancers. One of these is the tight linkage between the cell cycle and apoptosis. Factors that promote cell division also promote apoptosis. Factors that inhibit apoptosis also inhibit cell division. There is a particularly tight relationship between the control of cell cycle checkpoints and apoptosis. p53 forms one of the key links between cell cycle regulation and apoptosis. Cell damage induces p53. p53 inhibits cell division by activating transcription of the CKI p21. p53 also induces apoptosis by inhibiting the expression of Bcl2 and activating the expression of Bax and Fas. P53! apoptosis P53-- cell cycle p53 knockout mice are viable and cells can be induced to undergo apoptosis by other means indicating that p53 does not have a direct role in apoptosis. However p53 mice nearly always die of cancer indicating that p53 is a tumor suppressor. Rb, the inhibitor of G1-S progression also inhibits apoptosis. Mice that are deficient in Rb die because of widespread apoptosis. Lack of p53 suppresses the apoptosis in Rb deficient cells indicating that Rb functions to suppress p53 dependent apoptosis. Rb is one of the targets of degradation by caspases during apoptosis.

9 Rb -- cell cycle Rb -- apoptosis Myc is a transcription factor and proto-oncogene. Myc is required at the G1-S transition and for quiescent cells to enter the cell cycle. Myc activates transcription of the cdc25 phosphatase which activates CDK. Thus Myc promotes cell division and in combination with the appropriate growth factors is an important component of normal cell proliferation. However, in the absence of growth factors, cells sense Myc induced cell division as inappropriate and undergo apoptosis. This is because Myc also induces p53. Myc! cell cycle Myc! apoptosis The apoptotic regulator Bcl2 also feeds back to inhibit the cell cycle by an unknown mechanism. Bcl2 -- apoptosis Bcl2! exit to quiescence Bcl2 -- re-entry to cell cycle Genetic Basis of Cancer There are 2 general classes of genes associated with cancers oncogenes and tumor suppressor genes. Gain-of-function mutations in proto-oncogenes convert them to oncogenes (cancer causing). Loss-of-function mutations in tumor suppressor genes can also cause cancer. Oncogenes Arise through gain-of-function mutations in Proto-oncogenes. Proto-oncogenes generally encode factors that function to promote cell division or inhibit apoptosis Examples of Proto-oncogenes " Growth factor signaling molecules (Growth factors, GF receptors, signal transduction molecules like ras, MAPK, etc.) " Transcription factors, such as myc " Apoptosis inhibitors such as Bcl2 At least three mechanisms can produce gain-of-function mutations to generate oncogenes from the corresponding proto-oncogenes. " Point mutations in a proto-oncogene that result in a constitutively acting protein product " Localized reduplication (gene amplification) of a DNA segment that includes a proto-oncogene, leading to overexpression of the encoded protein " Chromosomal translocation that brings a growth-regulatory gene under the control of a different promoter and that causes inappropriate expression of the gene In addition, oncogenes may be incorporated into viral genomes to generate tumor viruses.

10 Tumor Suppressor Genes Discovered because fusing cancer cells with some non-cancer cells inhibits tumor growth unless a particular chromosome is lost. In general, they inhibit cell cycle progression or promote apoptosis. Five broad classes of proteins are generally recognized as products of tumor-suppressor genes: Intracellular proteins that regulate or inhibit progression through a specific stage of the cell cycle. Examples include: o p16 cyclin-kinase inhibitor o Retinoblastoma (Rb) o p53 o p21 Receptors for paracrine factors (e.g. TGF-β) that function to inhibit cell proliferation Checkpoint-control proteins that arrest the cell cycle if DNA is damaged or chromosomes are abnormal Proteins that promote apoptosis o Death receptors o Bax Enzymes that participate in DNA repair Some Examples of Genetic Defects Common in Cancers Many cancers involve defects in the factors that regulate the cell cycle or induce apoptosis in response to inappropriate cell proliferation. Several examples follow: Deregulated Myc expression is associated with a number of cancers, but Myc alone is not sufficient to cause cancer. As mentioned, Myc alone induces apoptosis. However, if Ras is also deregulated then cancer can occur. Ras is a signal transduction molecule that acts downstream of growth factor receptors and deregulated Ras substitutes for the growth factor requirement. It is thought that deregulation of Rb is a ubiquitous feature of all cancers. This makes sense since Rb blocks the cell cycle at start. For cancer to occur, cells must get past this point somehow. Overexpression of Bcl2 causes increased tumorogenesis by oversuppressing apoptosis. Similarly, deficiencies in Bax are common in many types of cancer including colon cancer because these cells are defective in apoptosis initiation. Defects in death receptor signaling are associated with some cancers. For example, mutations in the FasR gene for the Fas receptor increase the frequency of Hodgkin s lymphoma. As mentioned, p53 is a tumor suppressor. Cells mutant for p53 no longer undergo apoptosis or cell cycle arrest in response to cellular damage. This makes these cells

11 susceptible to accumulating genetic defects that could result in cancerous proliferation. Mice lacking p53 are viable and healthy, except for a predisposition to develop multiple types of tumors. Oncogenic Viruses Retroviruses Contain an RNA genome Reverse transcription produces a DNA copy that integrates into the host genome Host genes occasionally get incorporated into the viral genome Infection by a retrovirus containing an incorporated oncogene can cause cancer. DNA viruses Do not integrate into the host genome Only a few examples of tumorogenic DNA viruses human papillomavirus (HPV) is tumorogenic encodes viral gene products that interfere with normal cellular regulation o One HPV protein, E7, binds to and inhibits Rb o another, E6, inhibits p53 o E5 protein causes sustained activation of the PDGF receptor o Together these proteins induce transformation and proliferation of the host cells transformation occurs in the absence of mutations to cell regulatory proteins Cancer Therapy There are 4 major types of cancer therapy. " Chemotherapy " Radiation Therapy " Angiogenesis suppression " Gene therapy: Many cancer therapies depend on induction of apoptosis by causing cellular damage. For example, radiation therapy causes damage to cells and dividing cells are the most sensitive. The idea is that actively dividing cancer cells will be induced to undergo apoptosis. Many other therapeutic agents work by similar means. However, some tumors become insensitive to therapy because of defects in the apoptotic machinery. One of the most common examples is defects in p53. Since p53 is the central regulator in damage induced apoptosis and cell cycle arrest, cells with defects in p53 no longer respond to agents such as radiation or certain drugs. Since tumors require angiogenesis for a blood supply to support tumor growth, some therapies target this process. The most common strategy is to develop and use inhibitors of growth factors that promote blood vessel development. The idea behind gene therapy is conceptually simple: replace a defective gene (such as P53) with a functional copy. Of course technically this is a huge challenge. How to get the functional gene into every cancer cell? Engineered viruses are the most promising vector right now. Yes, some of the same families of viruses that can cause cancer may be manipulated to deliver cancer suppressor genes to the defective cells.

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