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Oncology Exam 1
Smith Biology and Pathophysiology of Cancer
| Term | Definition |
|---|---|
| Tumors that arise in different organs might have differnt pathologies but you could see underlying pathology in the breast that may be the same as in the colon meaning that you may choose? | the same drug agent if they both share the same pathology so there is no one drug for one type of cancer |
| What are the top 3 causes of human cancer? | Diet; Tobacco; Infection |
| What is the G1 stage of the cell cycle? | cells are sitting and they're trying to make some of the machinery that they need to actually do the DNA synthesis/replication |
| What is the S phase? | this is where DNA is synthesized |
| What is the G2 phase? | where the cells are stopping and tryig to make more machinery that they need to do division/mitosis |
| What is the M phase? | Mitosis where the daughter cells split apart *the the cells can go into G0 pahse where theyr waiting to do their thing or go to further differentiation/specialize or launch into G1 |
| cells spend _____% of the time in G1 where as its ____% in the S phase and _____% in the G2 phase. 2% of the time is spent in mitosis | 40; 39; 19 |
| Between the S phase and the G2 phase, cells will pause, why? | will take a little time to check that the DNA they replicated during the S phase was replicated accurately; purpose is to make new cells and prevent mutation (any errors are caught) but sometimes errors cna occur and mutation can cause a problem for the daughter cell and become cancerous |
| What are the ways ERRORS in DNA replication can be made? | 1. error of replication (S phase) 2. When a cell is in any of the phases and exposed to carcinogens, causing mutations --> cells start to divide out of control |
| What are Cdks and cyclins? | Cyclins and Cyclin-dependent kinase (CDKs) are key regulators of the cell cycle, with cyclins being proetins that bind to and activate CDKs, whcih are enzymes that phosphorylate other proteins, ultimately driving the cell cycle forward. These help push our cells getting to replicate when the SHOULD |
| Cyclin D is a proten that the cells produce. Cells produce cyclin which will then activate _____ ______ ______6 and cyclin D activates both ____ and ______ | cyclin dependent kinase 6; CDK6 and CDK4 |
| CDK4 and CDK6 get activated in the ____ phase and the presence of CDK 4 and 6 being activated pushes the cell into the ___ phase | G1; S |
| Cyclin E activates ______ and this pair will also push the cell through the cell cycle a little later in the G1 phase and pushing it a little futehr into the S phase | CDK2 |
| Cyclin A activates ______ moving the cell through the S phase | CDK2 |
| Cyclin A and B will activate _____ pushing the cells from the end of S phase into mitosis | CDK1 |
| Other things besides cyclines and CDKs that keep our DNA cell cyle normal also are? | DNA damage repair; Telomeres; Protein degradation (break down things that are no longer needed) |
| Besides certain parts of the cell cycle, what other times can cellular DNA be damaged by various factors including: | exposure to environmental agents like UV radiation, ionizing radiation, and certain chemicals, as well as by normal cellular processes like reactive oxygen species generation |
| What is the result of DNA damage? | unrepaired or improperly repaired DNA damage can lead to mutations, genetic disorders, cancer, and even cell death |
| how does DNA damage repair keep the cell cycle normal? Detection and repair: | Cells possess sophisticated mechanisms to detect and repair DNA damage, including single- and double-strand breaks, base modifications, and mismatches. |
| how does DNA damage repair keep the cell cycle normal? Cell cycle checkpoints: | Upon detecting DNA damage, cells activate cell cycle checkpoints, temporarily halting the cell cycle to allow time for repair. |
| how does DNA damage repair keep the cell cycle normal? Repair pathways | Several DNA repair pathways, such as base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), and homologous recombination (HR), are involved in repairing different types of DNA damage. |
| how does DNA damage repair keep the cell cycle normal? Apoptosis or Senescence: | If the damage is irreparable, cells may undergo programmed cell death (apoptosis) or enter a state of senescence to prevent the propagation of damaged cells and genomic instability. |
| How does Telomeres keep the cell cycle normal? Telomere function: | Telomeres are protective caps at the ends of chromosomes that prevent DNA degradation and chromosome fusions. -maintain chromosomal stability and prevent chromosomal degradation |
| How does Telomeres keep the cell cycle normal? Telomere Shortening: | Telomeres shorten with each cell division, and critically short telomeres can trigger a DNA damage response. |
| How does Telomeres keep the cell cycle normal? DNA damage response Activation: | Dysfunctional telomeres activate a DNA damage response, leading to cell cycle arrest and potentially senescence or apoptosis. |
| How does Telomeres keep the cell cycle normal? Telomerase: | In some cells, telomerase, an enzyme that elongates telomeres, can counteract telomere shortening and maintain telomere length. |
| how does protein degradation keep the cell cycle normal? Ubiquitination and Proteasome: | Proteins that are damaged, misfolded, or no longer needed are tagged for degradation via ubiquitination, a process where ubiquitin molecules are attached to the protein. |
| how does protein degradation keep the cell cycle normal? Cell cycle Regulation: | Protein degradation plays a crucial role in cell cycle regulation, ensuring the timely degradation of proteins that are no longer needed or are detrimental to cell cycle progression. |
| how does protein degradation keep the cell cycle normal? DNA damage response: | Protein degradation is also involved in the DNA damage response, removing damaged proteins and facilitating the repair process. |
| how does protein degradation keep the cell cycle normal? Proteasome: | The proteasome is a cellular complex responsible for degrading ubiquitinated proteins. |
| ________ provide a count down of how many times the cell is supposed to divide | Telomeres *cells can only replicate so many times (the count down is how many times left the cell has to replicate b/c the telomere will be too short and the cell will die |
| What is the protein degradation by ubiquitination? | is a cellular mechanism where proteins are tagged with ubiquitin molecules, marking them for degradation by the proteasome, a cellular machine that breaks down proteins. B/c the cell no longer needs cyclin or CDK4 after it has done its job so it doesn't confuse the cell; 26S proteasome degrades |
| what causes the cell cycle to go out of control? | damage to the DNA; -not getting replicated properly; -hyperactive proteins (ex: cyclins - activated due to damage); -exposed to something (ex: carcinogen); -hyperactive growth hormone |
| what is the multi-stage model of carcinogenesis | proposes that cancer development is a sequential process involving multiple genetic changes and stages, rather than a single event, and that these changes accumulate in a cell over time, leading to malignant transformation; *says that it takes more than 1 step or more than 1 stage for a cancerous tumor to develop; cancerous tumor is geneticially heterogenous (genetically different from each other) |
| Cancerous tumor ---> cells are geneteically _______ (different) | heterogenous |
| what are the names of the different stages of the multi-stage model of carcinogenesis | 1. initiation 2. promotion 3. progression |
| what is the initiation step of the multi-stage model of carcinogenesis | This is the initial, irreversible stage where DNA mutations occur in a cell, often due to exposure to carcinogens. These mutations can alter genes that regulate cell growth, differentiation, and DNA repair, potentially leading to dysregulated cellular processes. |
| what is the promotion step of the multi-stage model of carcinogenesis | In this stage, the mutated cells, now "initiated," proliferate and expand, forming pre-cancerous lesions. This stage is characterized by increased cell division and can be influenced by various factors, including hormones, growth factors, and inflammation. |
| what is the progression step of the multi-stage model of carcinogenesis | This stage involves further genetic and phenotypic changes in the pre-cancerous cells, leading to the development of a malignant tumor. This can include increased cell growth, invasion of surrounding tissues, and the ability to metastasize (spread to other parts of the body). |
| (T/F) need more than one kind of DNA damage to get a cancerous tumor | True |
| Explain how tumors can be genetically heterogenous | Tumor genetic heterogeneity arises from the accumulation of diverse genetic mutations and epigenetic changes during tumor cell division and expansion, resulting in a population of cells within a tumor with varying genetic profiles. |
| Why are genetically heterogenous cells in a malignant tumor a problem? | because they can lead to drug resistance, reduced effectiveness of targeted therapies, and potentially faster tumor growth and recurrence. |
| what are oncogenes | genes that, when mutated or over-expressed, can contribute to the development of cancer |
| what is the name of normal oncogenes | proto-oncogenes -oncogenes play essential roles in regulating cell growth, division, and differentiation |
| When proto-oncogenes become mutated or overexpressed, they turn into ____________________. | oncogenes -Oncogenes can disrupt normal cell control mechanisms, leading to uncontrolled cell proliferation and tumor formation. |
| Define oncogenes and their role in causing cancer | Oncogenes are mutated genes that, when activated, can cause uncontrolled cell growth and division, leading to cancer. They are derived from normal genes called proto-oncogenes that regulate cell growth and division |
| oncogenes de-reguate the normal cell cycle and cause out of control ____________________ | Proliferation; i.e. example of an oncogene: HER-2 |
| are oncogenes activated or deactivated in cancer | activated; When an oncogene is "activated," it means a proto-oncogene (a normal gene involved in cell growth) has undergone a change (mutation, amplification, or rearrangement) that causes it to function abnormally, driving uncontrolled cell growth and potentially leading to cancer. |
| (T/F) only one oncogene needs to be activated for the cell to go bad | True; same as for: "Both copies of the tumor suppressor gene need to be inactaviated for the cell to go bad" |
| describe tumor suppressor genes and their role in causing cancer. | Tumor suppressor genes (TSGs) normally act as "brakes" to control cell growth and prevent uncontrolled cell division, but when they are mutated or inactivated, cells can grow out of control, potentially leading to cancer |
| what is the normal function of tumor suppressing genes | is to inhibit inappropriate cell growth and proliferation by controlling the cell cycle |
| what can mutations to tumor suppressing genes cause | mutations may inactivate tumor suppressor genes, resulting in loss of control of cell cycle; ex: p53 |
| DNA repair genes are considered what? | Tumor suppressor genes: i.e. BRCA genes |
| Are tumor suppressor genes activated or inactivated in cancer? | inactivated; when tumor suppressor genes are inactivated--> it means the cells lose their ability to regulate cell growth and division, which can lead to uncontrolled proliferation and potentially cancer development |
| List some of the characteristics that cancer cells can acquire | Cancer cells acquire characteristics like uncontrolled growth, resistance to programmed cell death, and the ability to invade and spread, which are hallmarks of cancer. Cancer cells acquire characteristics like uncontrolled growth, immortality, and the ability to spread, due to genetic mutations and epigenetic alterations that disrupt normal cell processes |
| (T/F) acquired capabilities of cancer cells make cancer really hard to treat | True; contributes to the dangerous nature of a cancerous tumor |
| what functions do cancer cells acquire | 1. sustaining proliferative signaling (can keep sending out signals to itself to keep proliferating); 2. evading growth suppressors; 3. activating invasion and metastasis; 4. enabling replicative immorality (ie, never stops replicating) 5. inducing angiogenesisie, (i.e can grow blood vessels to bring more fluid and oxygen into the tumor that's growing); 6. resisting cell death (apoptosis) *these are all due to mutations that tend to occur as cells continue to replicate |
| is this benign or malignant: -often encapsulated, localized; -resembles cells in the organ from which they developed; -not cancerous due to (encapsulated or localized) and dont metastasize or spread | benign |
| is this benign or malignant: -invades and destroys surrounding tissue; -genetically unstable, abnormal architecture results in cells that are atypical of tissue or cell of origin; -cancerous | malignant *replicate too quickly, unstable, weird architecture and don't look like the cel from the organ in which they originated from |
| what is this: the spread of neoplastic cells from the primary tumor site to distant sites | metastasis |
| What differentiates benign from malignant tumors? | The key difference between benign and malignant tumors lies in their ability to spread and invade surrounding tissues; benign tumors are non-cancerous and don't spread, while malignant tumors are cancerous and can invade and spread to other parts of the body |
| Explain how our immune system helps us fight cancer? | The immune system plays a crucial role in fighting cancer by recognizing and destroying abnormal cells, potentially preventing or slowing down cancer growth, and some immune cells can even directly target and destroy cancerous cells. |
| Explain how our immune system helps us fight cancer? | Different cells fight different types of cancer. For example, one way the immune system fights cancer is by sending out a special form of white blood cells called T cells: The T cells see cancer as “foreign” cells that don't belong in the body. The T cells attack and try to destroy the cancerous cells. |
| steps of invasion and metastasis includes? | -angiogenesis or neovascularization (develops blood vessels into the tumor to bring in oxygen and nutrients into the growing tumor); -cells of the tumor detach from tumor and move into blood and lymph vessels; -attachment to inner vessels; -extravasation (meaning they go through the vessel into another kind of tissue --> ie they have spread to a new part of the body); -fight off host immune system; -angiogenesis again (grow blood vessels into themselves again) |
| Epigenetic changes in cancer--> we are realizing that its not just DNA damage that might be resulting in activation of oncogenes or the breakdown of tumor supressor genes; things that affect the structure of DNA--> the 2 epigenetic changes that we see that might be contributing to the pathology of cancer | 1. Methylation of DNA (genes are getting expressed more)--> could cause an oncogene to get expressed more than normally would or tumor suppressor gene not to be expressed. 2. Exposure to compounds that affect the histones from coiling of our DNA |
| What are examples of acquired capabilities of cancer cells? | Sustaining proliferative signaling; Evading growth suppressors; Activating invasion and metastasis; enabling replicative immortality; inducing angiogenesis; resisting cell death |
| Other topics in the development of carcinogenesis includes? | Mutator phenotype; Genetic hot spots; Multiplicity of mutations |
| What is the mutator phenotype? | As DNA damage occurs and doesnt get repaired, likely that the DNA damage that is int eh cell creates a cell that is more liekly to have more mutations to occur (i.e damage to a DNA repair enzyme and it can't work, then as the cell continues to divide, it cant fix any erros in DNA replication,and therefore it set with a phenotype making it more likely to mutate |
| Genetic hot spots are? | concept that the gene that get mutated in cancerous cells, they get mutated due to a structure in chemistry such that the structure that is easily mutated. see genes that drive cancer pathology and see the same mutation form pt to pt. b.c the gene has a chemical structure susceptible to damage to occur to it. |
| What is Multiplicity of mutations? | idea that the genes seen mutated over again from pt to pt. they have more than 1 place in the gene that can be mutated, so not only is each place that gets mutated a hot spot, but you end up seeing genes with many mutations in that one gene. classic example is tumor suppressor gene p53 (we depend on it being able to get the cells to perfrom apoptosis or to pause during the S phase and G2 phase but is often mutated in more than 1 spot in more than 50% of cases |
| What are the Treatment options for cancer? | Surgery; Irradiation; Chemotherapy; targeted therapies; Biologicals; Combinations |
| What is the Gompertzian Tumor Growth curve? shows over time the # of cells that could be in a tumor and Smith wanted to point out 2 things? | 1. cannot detect tumor until a size of 10^9 cells (fairly large and been a round fo awhile); 2. immune system can kick in but we think that immune system is able to identify and fight off up to 10^5 cells. |
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