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Question Bank
- 1What type of cell is a permanent cell?
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Somatic cell - 2Which category of cells includes stable cells?
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Somatic cell - 3Signaling molecules used for cell to proliferate/divide?
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1. mitogens 2. growth factors 3. survival factors - 4What type of cells are labile cells?
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Somatic cell - 5What is a mitogen?
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• activates cell proliferation/division via stimulating DNA synthesis • no mitogen signal = non-proliferating state - 6Which signaling molecules stimulate protein synthesis and inhibit protein degradation?
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growth factors - 7What type of factors suppress apoptosis?
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survival factors overexpression is associated with tumors - 8How long does it take for liver cells to complete one cell cycle?
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Epidermal: complete cycle <1 day liver: years for one cell cycle - 9Steps of interphase
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G1 phase S phase G2 phase - 10What occurs during G1?
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• longest phase • cell grows • organelles synthesize energy and proteins - 11Purpose of G1 checkpoint?
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checks for DNA damage and right proteins - 12What phase immediately follows the G1 phase in the cell cycle?
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S phase - 13What happens if DNA damage is detected during the G1 checkpoint?
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Apoptosis - 14What phase do cells enter after G1 if they become terminally differentiated?
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G0 - 15Which of the following cell types typically become terminally differentiated in the G0 phase?
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muscle, nerve cells - 16Which cell types commonly reenter the cell cycle in response to growth factors or after injury?
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hepatocytes and fibroblasts - 17What happens during S phase?
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Synthesis • DNA is replicated - 18What is the primary function of telomeres during DNA replication?
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Maintain the stability of chromosomes • ensure proper replication of DNA ends • serve as a sign for chromosome health - 19What happens to telomeres in each replication cycle?
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Often shortened maintained in various tumors - 20What enzyme is responsible for maintaining telomeres in various tumors?
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Telomerase - 21What is the phase immediately before mitosis?
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G2 phase - 22What must happen to organelles during the G2 phase?
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Cell must duplicate organelles - 23What is the final checkpoint before entering mitosis?
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Final G2 checkpoint • no DNA damage after replication - 24Phases of mitosis?
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Prophase Metaphase Anaphase Telophase - 25What happens during the prophase of mitosis?
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• nuclear membrane disintegrate • chromatin → chromosomes • two-centriole pairs migrate to opposite poles = centrosome • prepare for formation of mitotic spindle - 26What role does the inhibitor of sister chromatid separation (ISS) protein play during metaphase?
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• Chromosomes line up at the cell equator • mitotic spindles form • ISS protein holds the two sister chromatids together and degraded afterwards - 27What occurs during the anaphase of mitosis?
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• chromatids are pulled apart by the spindle apparatus • migrate to the opposite sides of the cell - 28What happens during telophase?
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• Final stage • Daughter chromosomes are at the spindle poles • nuclear membranes are formed - 29What is cytokinesis?
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• cytoplasm is divided by cleavage • starts in the late anaphase and continues through telophase - 30What are the main families of regulatory molecules involved in cell cycle control?
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Cyclins & CDKs - 31What can cyclin-dependent kinase inhibitors (CKIs) do to the cell cycle?
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stop or arrest the cell cycle at various phases - 32What is the programmed form of cell death?
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Apoptosis - 33Which type of cell death is associated with injury or disease?
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Necrosis - 34What is apoptosis?
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active process of cellular self-destruction • occurs in normal and pathologic conditions - 35What does apoptosis require for energy?
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ATP - 36T/F: Apoptosis can be intrinsic or extrinsic
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True - 37What is the intrinsic pathway also known as?
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mitochondrial pathway - 38What can trigger the intrinsic pathway?
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Exposure to oxidative stress, hypoxia, protein misfolding - 39What does the intrinsic pathway activate?
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• Activates proapoptotic signals • leading to activation of caspase signaling (procaspase to caspase) - 40What triggers the Extrinsic pathway?
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Exposure to death signals from outside cell (e.g: TNFα) - 41What does the extrinsic pathway activate?
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activate a sequence of molecular signaling events that activate caspase signaling. - 42Untitled question
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• cleavage of cellular proteins and the cytoskeleton • weakened cell membrane develop blebs → break off + phagocytosed by macrophages • Intactness of membrane in apoptosis reduces inflammation - 43What is the primary characteristic of membranes during apoptosis?
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Membranes remain intact - 44What happens to the cell size during apoptosis?
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Cell size reduces - 45What is a potential consequence of the failure of apoptosis?
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Failure may lead to tumor development - 46What is the regulated pathway of apoptosis?
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overexpression of BCL-2 leads to follicular lymphoma - 47What is the process where cells swell and burst, potentially leading to necrosis?
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Cells swell + burst → inflammatory response → membrane damage Nucleus undergo pyknosis → karyolysis - 48What is pyknosis?
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shrinkage with dense genetic material) - 49What is karyolysis?
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nuclear dissolution and lysis of chromatin - 50What process describes the fragmentation of the nucleus during apoptosis?
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Fragmentation into nucleosome-size fragments - 51What is the typical state of the plasma membrane during necrosis?
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Disrupted - 52What is the usual outcome of cellular contents during necrosis?
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Enzymatic digestion, may leak out of cell - 53Types of necrosis?
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1. coagulative 2. liquefactive 3. gangrenous 4. caseous 5. fat 6. fibrinoid - 54When and where is coagulative necrosis seen?
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Secondary to ischemic injury multiple organs: spleen, kidney, heart and liver - 55What type of necrosis is characterized by a coagulative, gelatinous, opaque-clear appearance with preserved tissue structure?
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Coagulative necrosis - 56What causes coagulative necrosis?
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protein denaturation - 57When is liquefactive necrosis seen?
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cases of ischemic injury to the brain, and bacterial abscess - 58Cause of liquefactive necrosis?
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release of hydrolytic enzymes → complete digestion of damaged area - 59Appearance of liquefactive necrosis?
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soft, liquefied tissue appearance - 60Cause of gangrenous necrosis?
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Secondary to ischemia - 61What is the microscopic appearance of dry gangrene?
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coagulative necrosis, tissue appear dried, no infection and has brownish black color. - 62What is the appearance of wet gangrene?
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liquefactive necrosis appearance due to bacterial and inflammatory leukocytes action - 63Where can gangrenous necrosis commonly be observed?
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lower limbs or GI - 64What causes caseous necrosis?
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• secondary to tuberculosis • Usually observed in lungs - 65Caseous necrosis characteristics
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affected area will have a soft, granular, yellowish “cheese-like” appearance - 66What type of inflammation is seen around the necrotic focus in caseous necrosis?
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surrounded by macrophages and other inflammatory cells = granulomatous inflammation - 67What triggers fat necrosis?
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trauma to the breast, acute pancreatitis - 68What is the cause of fat necrosis?
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leakage and digestive action of lipases on adipocytes - 69Pathophysiology of fat necrosis?
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Lipases break down triglycerides → free fatty acids → saponification (when combined w/ calcium) - 70What is the morphological appearance of affected area in fat necrosis?
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chalky white-like appearance - 71What is fibrineroid necrosis?
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necrotic connective tissue that histologically resembles deposited fibrin fibers - 72What causes fibrineroid necrosis?
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hypersensitivity reactions (II and III) and blood vessel damage in hypertensive crisis - 73Cancer definition?
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“diseases in which abnormal cells divide without control and are able to invade other tissues.” - 74What process can lead to cancer if it fails?
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programmed cell death - 75What does the term 'neoplasm' refer to?
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new and abnormal tissue growth - 76Which type of tumor remains localized and can undergo surgical removal?
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Benign tumors - 77What are malignant tumors?
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refers to lesions that can invade adjacent tissues and metastasize - 78What are the two basic components of tumors?
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Parenchyma and non-neoplastic stroma - 79What does the term 'parenchyma' in tumors refer to?
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Transformed or neoplastic cells - 80What constitutes the non-neoplastic stroma in tumors?
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Supporting host-derived tissue made up of: • connective tissue • blood vessels • host-derived inflammatory cells - 81Which cancer is the most frequently diagnosed among males according to the data?
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1. prostate 2. lung 3. colorectal 4. bladder 5. melanoma - 82Top five most frequent cancers in females?
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1. breast 2. lung 3. colorectal 4. corpus uteri 5. melanoma - 83general causes of cancer
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1. genetic factors 2. environmental factors 3. others - 84What are genetic risk factors that can increase the risk of cancer?
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Numerous gene mutations (acquired and germline) - 85Which germline mutation increases the risk for breast cancer and ovarian cancer?
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BRCA-1 and -2 mutations - 86What condition is caused by APC mutations, increasing the risk for several cancers?
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Familial Adenomatous Polyposis (FAP) including colon and rectal cancer - 87Which virus is associated with an increased risk of cervical/oropharyngeal cancer?
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• HPV = risk of cervical/oropharyngeal cancer • Epstein-Barr virus, EBV = B-cell lymphoma • Hep. B/C infection = hepatocellular carcinoma - 88What type of radiation can cause DNA damage and increase the risk of cancer?
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ionizing and ultraviolet radiation - 89Other causes of cancer?
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cell cycle dysregulation and genome instability - 90general differences between benign and malignant tumors?
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• Degree of differentiation • Rate of growth • Local invasiveness • Distant spread - 91Nomenclature of benign tumors?
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---OMA - 92Nomenclature of malignant tumors?
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epithelial: carcinoma mesenchymal: sarcoma - 93What is the benign tumor of the glandular epithelium?
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Adenoma - 94What is the malignant tumor of the epithelium - glandular tissue?
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Adenocarcinoma - 95Untitled question
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untitled answer - 96What is an oncogene?
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A mutated form of proto-oncogenes that stimulates cell growth and division. - 97What do most oncogenes encode for?
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Transcription or growth factors to enhance cell survival. - 98Which type of mutation can produce an oncogenic effect?
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A single allele mutation. - 99which oncogenes induce cell transformations?
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K-RAS = pancreatic, lung, colon, and endometrial tumors N-RAS = melanomas H-RAS = cancers of the adrenal gland and thymus - 100What percentage of human tumors have different MYC mutations?
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Around 28% - 101What is the primary role of tumor suppressor genes?
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Normally prevent uncontrolled cell growth. - 102What happens when tumor suppressor genes lose their function?
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The transformed cell phenotype can develop • protein products stops cell cycle progression and promotes apoptosis - 103Which family of proteins help regulate apoptosis?
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BCL-2 family of proteins - 104What is the role of BAX in apoptosis?
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pro-apoptotic • activated following cell damage or normal cell turnover mechanisms • genes are often down-regulated or functionally inactivated by mutations - 105What effect does upregulated expression of BCL2 have on apoptosis?
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inhibits apoptosis • Upregulated expression = inhibits apoptosis • seen in certain tumors like multiple myeloma - 106What is carcinogenesis?
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accumulation of driver and passenger mutations - 107What are driver mutations also known as?
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pathogenic mutations - 108What are driver mutations?
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• directly contribute to the development or progression of cancer • mutations that alter gene function • give a growth advantage to the prospective tumor cell - 109What are passenger mutations?
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• acquired mutations that don't normally affect cellular growth behavior • do not initiate carcinogenesis • aid the cancer formation process • increase the risk of drug resistance - 110What comprise the mutated gene sets of a cancer tumor
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mix of passenger and driver mutations together - 111What process do tumors use to ensure adequate nutrient supply?
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angiogenesis - 112What factors control the development of new vessels?
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angiogenic factors and angiogenic inhibitors - 113What mechanism do cancer cells use to promote angiogenesis?
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increase the secretion of angiogenic factors and decrease the release of angiogenic inhibitors - 114Which processes can lead to cancer metastasis?
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1. Loosening cell–cell contacts via inactivation of E-cadherin 2. Degradation of ECM 3. Migration and invasion - 115What do tumors express to potentially evade the immune system?
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tumor associated antigens and tumor specific antigens - 116What can lead to the spontaneous regression of some tumors?
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Successful immunosuppression response - 117What is the characteristic form of cellular metabolism in cancer cells known as?
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Warburg effect - 118What amino acid precursor is utilized by cancer cells from the lactate they generate?
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• consume glucose to generate energy quickly • use lactate as an amino acid precursor → support growth of daughter tumor cells - 119What process do normal cells use to maximize glucose use?
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Krebs cycle - 120What are the systemic effects of the tumor mass?
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• depends on tumor size and location • physical pressure or loss of normal tissue function • bone marrow failure • ischemia - 121What are Paraneoplastic Syndromes
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Symptoms triggered by the tumor but not attributed to the direct effect of the tumor mass - 122What causes paraneoplastic syndromes?
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• substances released from the tumor • immune response targeting the tumor - 123What is cachexia?
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"Wasting away syndrome" • excessive weight loss • marked weakness • taste alterations • muscle wasting • altered protein, lipid, and carbohydrate metabolism • decreased quality of life - 124What is the primary cause of cachexia in cancer patients?
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Cancer cells activating inflammatory cytokines - 125What is the role of Proteolysis-inducing factor (PIF) in cachexia?
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• induces protein degradation • apoptosis via activation of caspases • inhibits protein synthesis • increase proteolysis - 126What is the role of Lipid-mobilizing factor (LMF) in cachexia?
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promotes lipolysis of adipose tissue + increase fatty acid oxidation - 127What does Parathyroid hormone-related protein (PTHrP) cause in cachexia?
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causes calcium mobilization from bone and hypercalcemia - 128Role of Proinflammatory cytokines (TNF alpha, interferon gamma and IL-6) in cahexia?
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contribute to inflammatory process and generalized weakness - 129What is the primary method used for diagnosing and staging tumors?
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Combo of: • Clinical exam • Imaging • Tissue biopsies and histochemistry/immunohistochemistry • Blood biochemistry and tumor markers • Genetics / immunophenotyping - 130What are tumor markers?
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Tumor markers include hormones, enzymes, genes, antigens, and antibodies. - 131Which hormone is elevated in hepatocellular carcinoma?
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Alpha fetoprotein - 132Which hormone is elevated in non-Hodgkin's lymphoma?
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CD20 is elevated - 133Which antigen is elevated in prostate cancers?
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Prostate-specific antigen (PSA) - 134What type of tumor can produce catecholamines?
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Benign tumors of the adrenal medulla (pheochromocytoma) - 135What is one use of tumor markers?
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1. identify individuals at high risk 2. diagnosis of a specific type of tumor 3. To follow the clinical course of treatment/monitor remission - 136Which marker can aid in the diagnosis of pituitary tumors?
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ACTH - 137Management strategies of cancer?
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• Surgery • Radiation therapy • Chemotherapy • Immunotherapy • Targeted therapy - 138What is this?
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atrophy - 139What is one of the key recommendations for cancer prevention according to the World Cancer Research Fund International?
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hyperplasia - 140Which of the following is NOT a recommendation for cancer prevention?
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dysplasia - 141What is this?
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metaplasia - 142What is the term for the condition where cells become larger but remain normal in number?
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Hypertrophy - 143Which cellular adaptation involves an increase in the number of cells?
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Hyperplasia - 144What term describes the replacement of one mature cell type with another?
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Metaplasia - 145What does Atrophy refer to?
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Decrease in cell size (yielding reduced tissue mass) - 146What is Neoplasia?
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new growth. Neoplasm refers to new and abnormal tissue growth. - 147What is Anaplasia?
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lack of differentiation in neoplastic cells. - 148What is Aplasia?
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complete congenital lack of a tissue.