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Question 1
What type of cell is a permanent cell?
Germ cell
Prokaryotic cell
Somatic cell
Eukaryotic cell
Question 2
Which category of cells includes stable cells?
Germ cell
Somatic cell
Prokaryotic cell
Eukaryotic cell
Question 3
Signaling molecules used for cell to proliferate/divide?
1. mitogens 2. growth factors 3. survival factors
Question 4
What type of cells are labile cells?
Eukaryotic cell
Germ cell
Somatic cell
Prokaryotic cell
Question 5
What is a mitogen?
Apoptosis
Necrosis
Cell regeneration
Autophagy
Question 6
Which signaling molecules stimulate protein synthesis and inhibit protein degradation?
growth factors
inhibitors
degraders
suppressors
Question 7
What type of factors suppress apoptosis?
cell elimination factors
death factors
destruction factors
survival factors
overexpression is associated with tumors
Question 8
How long does it take for liver cells to complete one cell cycle?
days
months
hours
Epidermal: complete cycle <1 day liver: years for one cell cycle
Question 9
Steps of interphase
G1 phase S phase G2 phase
Interphase
G1 phase
G0 phase
Question 10
What occurs during G1?
• longest phase • cell grows • organelles synthesize energy and proteins
Question 11
Purpose of G1 checkpoint?
M checkpoint
S checkpoint
checks for DNA damage and right proteins
G1 checkpoint
Question 12
What phase immediately follows the G1 phase in the cell cycle?
Mitosis
S phase
G2 phase
Interphase
Question 13
What happens if DNA damage is detected during the G1 checkpoint?
Apoptosis
Cell enters S phase
Cell undergoes mitosis
Cell produces energy
Question 14
What phase do cells enter after G1 if they become terminally differentiated?
G0
G2
Interphase
S phase
Question 15
Which of the following cell types typically become terminally differentiated in the G0 phase?
epidermal cells
red blood cells
neurons
white blood cells
Question 16
Which cell types commonly reenter the cell cycle in response to growth factors or after injury?
hepatocytes and fibroblasts
adipocytes
fibroblasts
sperm cells
Question 17
What happens during S phase?
Synthesis • DNA is replicated
Question 18
What is the primary function of telomeres during DNA replication?
Control cell division timing
Facilitate DNA repair
Maintain the stability of chromosomes
Maintain the stability of chromosomes • ensure proper replication of DNA ends • serve as a sign for chromosome health
Question 19
What happens to telomeres in each replication cycle?
Split into smaller pieces
Remain unchanged
Often shortened maintained in various tumors
Often shortened
Question 20
What enzyme is responsible for maintaining telomeres in various tumors?
RNA polymerase
Telomerase
Telomerase
DNA polymerase
Question 21
What is the phase immediately before mitosis?
Prophase
G2 phase
Anaphase
Interphase
Question 22
What must happen to organelles during the G2 phase?
Cell must synthesize proteins
Cell must duplicate organelles
Cell must replicate DNA
Cell must divide organelles
Question 23
What is the final checkpoint before entering mitosis?
Final G2 checkpoint • no DNA damage after replication
Final G1 checkpoint
Final S checkpoint
Final M checkpoint
Question 24
Phases of mitosis?
Cell Respiration
Glycolysis
Meiosis
Prophase Metaphase Anaphase Telophase
Question 25
What happens during the prophase of mitosis?
Microtubules form the mitotic spindles.
Chromosomes line up at the cell equator.
Chromatids are pulled apart by the spindle apparatus.
• nuclear membrane disintegrate • chromatin → chromosomes • two-centriole pairs migrate to opposite poles = centrosome • prepare for formation of mitotic spindle
Question 26
What role does the inhibitor of sister chromatid separation (ISS) protein play during metaphase?
• Chromosomes line up at the cell equator • mitotic spindles form • ISS protein holds the two sister chromatids together and degraded afterwards
Pulls chromatids apart.
Forms the mitotic spindles.
Holds the two centrioles together.
Question 27
What occurs during the anaphase of mitosis?
Nuclear membrane disintegrates.
Microtubules form the mitotic spindles.
• chromatids are pulled apart by the spindle apparatus • migrate to the opposite sides of the cell
Chromosomes line up at the cell equator.
Question 28
What happens during telophase?
• Final stage • Daughter chromosomes are at the spindle poles • nuclear membranes are formed
Question 29
What is cytokinesis?
• cytoplasm is divided by cleavage • starts in the late anaphase and continues through telophase
Question 30
What are the main families of regulatory molecules involved in cell cycle control?
GTPases
Histones
Transcription Factors
Calcium Channels
Question 31
What can cyclin-dependent kinase inhibitors (CKIs) do to the cell cycle?
stop or arrest the cell cycle at various phases
enhance DNA repair
promote cell division
increase cell size
Question 32
What is the programmed form of cell death?
Autophagy
Necrosis
Apoptosis
Mitosis
Question 33
Which type of cell death is associated with injury or disease?
Apoptosis
Autophagy
Mitosis
Necrosis
Question 34
What is apoptosis?
active process of cellular self-destruction
• occurs in normal and pathologic conditions
Cell repair
Cell migration
Cell division
Question 35
What does apoptosis require for energy?
Oxygen
Nitric oxide
Lactate
Glucose
Question 36
T/F: Apoptosis can be intrinsic or extrinsic
True
Nuclear fragmentation
Chromatin condensation
Cell shrinkage
Question 37
What is the intrinsic pathway also known as?
cytoplasmic pathway
mitochondrial pathway
nuclear pathway
receptor pathway
Question 38
What can trigger the intrinsic pathway?
anti-apoptotic signals
proliferative signals
Exposure to oxidative stress, hypoxia, protein misfolding
pro-inflammatory signals
Question 39
What does the intrinsic pathway activate?
• Activates
proapoptotic
signals • leading to activation of caspase signaling (procaspase to caspase)
Question 40
What triggers the Extrinsic pathway?
Exposure to death signals from outside cell (e.g: TNFα)
Question 41
What does the extrinsic pathway activate?
activate a sequence of molecular signaling events that activate caspase signaling.
Question 42
Untitled question
• cleavage of cellular proteins and the cytoskeleton • weakened cell membrane develop blebs → break off + phagocytosed by macrophages • Intactness of membrane in apoptosis reduces inflammation
Question 43
What is the primary characteristic of membranes during apoptosis?
Cell swells
Cell size increases
Membranes remain intact
Membrane ruptures
Question 44
What happens to the cell size during apoptosis?
Cell size increases
Cell size reduces
Cell remains unchanged
Cell divides
Question 45
What is a potential consequence of the failure of apoptosis?
Failure may lead to tumor development
Cell grows rapidly
Cell becomes immortal
Cell becomes sterile
Question 46
What is the regulated pathway of apoptosis?
overexpression of BCL-2 leads to acute myeloid leukemia
overexpression of BCL-2 leads to follicular lymphoma
underexpression of BCL-2 leads to chronic lymphocytic leukemia
underexpression of BCL-2 leads to follicular lymphoma
Question 47
What is the process where cells swell and burst, potentially leading to necrosis?
Osmosis
Mitosis
Cells swell + burst → inflammatory response → membrane damage Nucleus undergo pyknosis → karyolysis
Apoptosis
Question 48
What is pyknosis?
Autoimmune response
Allergic reaction
Hypersensitivity
shrinkage with dense genetic material)
Question 49
What is karyolysis?
nuclear dissolution and lysis of chromatin
Question 50
What process describes the fragmentation of the nucleus during apoptosis?
Karyolysis
Pyknosis
Fragmentation into nucleosome-size fragments
Karyorrhexis
Question 51
What is the typical state of the plasma membrane during necrosis?
Altered structure
Unchanged
Disrupted
Fragmented
Question 52
What is the usual outcome of cellular contents during necrosis?
Enzymatic digestion, may leak out of cell
Absorbed by adjacent cells
Fragmented
Intact
Question 53
Types of necrosis?
1. coagulative 2. liquefactive 3. gangrenous 4. caseous 5. fat 6. fibrinoid
Question 54
When and where is coagulative necrosis seen?
Secondary to ischemic injury multiple organs: spleen, kidney, heart and liver
Question 55
What type of necrosis is characterized by a coagulative, gelatinous, opaque-clear appearance with preserved tissue structure?
Coagulative necrosis
Necrobiosis
Fatty necrosis
Colliquative necrosis
Question 56
What causes coagulative necrosis?
electrolyte imbalance
protein denaturation
enzymatic digestion
viral infection
Question 57
When is liquefactive necrosis seen?
cases of ischemic injury to the brain, and bacterial abscess
Question 58
Cause of liquefactive necrosis?
release of hydrolytic enzymes → complete digestion of damaged area
Question 59
Appearance of liquefactive necrosis?
soft, liquefied tissue appearance
Question 60
Cause of gangrenous necrosis?
Secondary to ischemia
Question 61
What is the microscopic appearance of
dry
gangrene?
liquefactive necrosis
colliquative necrosis
fibrinoid necrosis
coagulative necrosis, tissue appear dried, no infection and has brownish black color.
Question 62
What is the appearance of
wet
gangrene?
liquefactive necrosis appearance due to bacterial and inflammatory leukocytes action
Question 63
Where can gangrenous necrosis commonly be observed?
lungs
brain
lower limbs or GI
heart
Question 64
What causes caseous necrosis?
• secondary to tuberculosis • Usually observed in lungs
Question 65
Caseous necrosis characteristics
affected area will have a soft, granular, yellowish “cheese-like” appearance
Question 66
What type of inflammation is seen around the necrotic focus in caseous necrosis?
chronic inflammation
acute inflammation
surrounded by macrophages and other inflammatory cells = granulomatous inflammation
abscess formation
Question 67
What triggers fat necrosis?
Minor bruises
Severe burns
Acute appendicitis
Chronic pancreatitis
Question 68
What is the cause of fat necrosis?
Viral infections
Exposure to extreme cold
Release of bile acids
leakage and digestive action of lipases on adipocytes
Question 69
Pathophysiology of fat necrosis?
Lipases break down triglycerides → free fatty acids → saponification (when combined w/ calcium)
Question 70
What is the morphological appearance of affected area in fat necrosis?
Yellowish tint
Brown patches
Purple spots
Greenish hue
Question 71
What is fibrineroid necrosis?
Necrotic nerve tissue
Necrotic muscle tissue
necrotic connective tissue that histologically resembles deposited fibrin fibers
Necrotic skin tissue
Question 72
What causes fibrineroid necrosis?
Allergic reactions
Infectious diseases
hypersensitivity reactions (II and III) and blood vessel damage in hypertensive crisis
Autoimmune disorders
Question 73
Cancer definition?
autoimmune disorders
“diseases in which abnormal cells divide without control and are able to invade other tissues.”
heart disease
diabetes
Question 74
What process can lead to cancer if it fails?
programmed cell death
cell growth
cell differentiation
cell division
Question 75
What does the term 'neoplasm' refer to?
Benign tumors only
new and abnormal tissue growth
Normal tissue growth
Inflammatory responses
Question 76
Which type of tumor remains localized and can undergo surgical removal?
Invasive tumors
Benign tumors
Malignant tumors
Neoplasms
Question 77
What are malignant tumors?
refers to lesions that can invade adjacent tissues and metastasize
Question 78
What are the two basic components of tumors?
Parenchyma and epithelium
Parenchyma and non-neoplastic stroma
Epithelium and mesenchyme
Neoplasia and stroma
Question 79
What does the term 'parenchyma' in tumors refer to?
Connective tissue
Inflammatory cells
Transformed or neoplastic cells
Necrotic tissue
Question 80
What constitutes the non-neoplastic stroma in tumors?
Supporting host-derived tissue
made up of: • connective tissue • blood vessels • host-derived inflammatory cells
Invasive cells
Tumor cells
Necrotic tissue
Question 81
Which cancer is the most frequently diagnosed among males according to the data?
Melanoma
1. prostate 2. lung 3. colorectal 4. bladder 5. melanoma
Bladder
Colorectum
Question 82
Top five most frequent cancers in females?
1. breast 2. lung 3. colorectal 4. corpus uteri 5. melanoma
Question 83
general causes of cancer
1. genetic factors 2. environmental factors 3. others
Question 84
What are genetic risk factors that can increase the risk of cancer?
Physical injuries
Numerous gene mutations (acquired and germline)
Dietary habits
Environmental toxins
Question 85
Which germline mutation increases the risk for breast cancer and ovarian cancer?
TP53 mutations
EGFR mutations
BRCA-1 and -2 mutations
APC mutations
Question 86
What condition is caused by APC mutations, increasing the risk for several cancers?
Leukemia
Familial Adenomatous Polyposis (FAP) including colon and rectal cancer
Sarcoma
Lymphoma
Question 87
Which virus is associated with an increased risk of cervical/oropharyngeal cancer?
Epstein-Barr virus
• HPV = risk of cervical/oropharyngeal cancer • Epstein-Barr virus, EBV = B-cell lymphoma • Hep. B/C infection = hepatocellular carcinoma
herpes simplex virus
hepatitis B virus
Question 88
What type of radiation can cause DNA damage and increase the risk of cancer?
gamma rays
infrared radiation
thermal radiation
sound waves
Question 89
Other causes of cancer?
cell cycle dysregulation and genome instability
Question 90
general differences between benign and malignant tumors?
Distant spread
• Degree of differentiation • Rate of growth • Local invasiveness • Distant spread
Degree of differentiation
Local invasiveness
Question 91
Nomenclature of benign tumors?
---OMA
Invasive
Malignant
Highly differentiated
Question 92
Nomenclature of malignant tumors?
Local invasiveness
epithelial: carcinoma mesenchymal: sarcoma
Cell size
Distant spread
Question 93
What is the benign tumor of the glandular epithelium?
Carcinoma
Adenoma
Sarcoma
Epithelioma
Question 94
What is the malignant tumor of the epithelium - glandular tissue?
Adenocarcinoma
Osteoma
Adenoma
Rhabdomyosarcoma
Question 95
Untitled question
untitled answer
Question 96
What is an oncogene?
A mutated form of proto-oncogenes that stimulates cell growth and division.
A gene that controls cell differentiation
A gene that regulates cell death
A gene that inhibits cell growth
Question 97
What do most oncogenes encode for?
Transcription or growth factors to enhance cell survival.
Hormones
Enzymes
Cell membrane receptors
Question 98
Which type of mutation can produce an oncogenic effect?
Both alleles mutation
No mutation
A single allele mutation.
Multiple allele mutations
Question 99
which oncogenes induce cell transformations?
EGFR
TP53
K-RAS = pancreatic, lung, colon, and endometrial tumors N-RAS = melanomas H-RAS = cancers of the adrenal gland and thymus
BRCA1
Question 100
What percentage of human tumors have different MYC mutations?
Around 45%
Around 35%
Around 15%
Around 28%
Question 101
What is the primary role of tumor suppressor genes?
Regulate cell differentiation
Inhibit apoptosis
Enhance cell proliferation
Promote cell division
Question 102
What happens when tumor suppressor genes lose their function?
The transformed cell phenotype can develop • protein products stops cell cycle progression and promotes apoptosis
Cell death
Cell fusion
Cell migration
Question 103
Which family of proteins help regulate apoptosis?
Gain of function mutation
Epigenetic modification
BCL-2 family of proteins
Transcriptional activation
Question 104
What is the role of BAX in apoptosis?
anti-apoptotic
cell proliferation
DNA repair
pro-apoptotic
• activated following cell damage or normal cell turnover mechanisms • genes are often down-regulated or functionally inactivated by mutations
Question 105
What effect does upregulated expression of BCL2 have on apoptosis?
activates cell division
induces cell senescence
promotes apoptosis
has no effect
Question 106
What is carcinogenesis?
Genetic expression
Molecular integration
Cell division
accumulation of driver and passenger mutations
Question 107
What are driver mutations also known as?
benign mutations
neutral mutations
oncogenic mutations
passenger mutations
Question 108
What are driver mutations?
neutral mutations
benign mutations
• directly contribute to the development or progression of cancer • mutations that alter gene function • give a growth advantage to the prospective tumor cell
passenger mutations
Question 109
What are passenger mutations?
benign mutations
pathogenic mutations
• 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
oncogenic mutations
Question 110
What comprise the mutated gene sets of a cancer tumor
mix of passenger and driver mutations together
Question 111
What process do tumors use to ensure adequate nutrient supply?
necrosis
mitosis
angiogenesis
apoptosis
Question 112
What factors control the development of new vessels?
angiogenic factors and angiogenic inhibitors
neural factors
hormonal factors
immune factors
Question 113
What mechanism do cancer cells use to promote angiogenesis?
increase cell differentiation
increase the secretion of angiogenic factors and decrease the release of angiogenic inhibitors
decrease cell death
increase cell division
Question 114
Which processes can lead to cancer metastasis?
Cell division
1. Loosening cell–cell contacts via inactivation of E-cadherin 2. Degradation of ECM 3. Migration and invasion
RNA transcription
DNA replication
Question 115
What do tumors express to potentially evade the immune system?
normal cell antigens
viral antigens
bacterial antigens
tumor associated antigens and tumor specific antigens
Question 116
What can lead to the spontaneous regression of some tumors?
Successful chemotherapy response
Successful radiation response
Successful surgery response
Successful immunosuppression response
Question 117
What is the characteristic form of cellular metabolism in cancer cells known as?
Glycolysis effect
Pasteur effect
Warburg effect
Krebs cycle effect
Question 118
What amino acid precursor is utilized by cancer cells from the lactate they generate?
nucleotide precursor
carbohydrate precursor
• consume glucose to generate energy quickly • use lactate as an amino acid precursor → support growth of daughter tumor cells
fatty acid precursor
Question 119
What process do normal cells use to maximize glucose use?
Krebs cycle
Glycolysis
Calvin cycle
Electron transport chain
Question 120
What are the systemic effects of the tumor mass?
Local effects only
Viral infections
Inflammatory responses
• depends on tumor size and location • physical pressure or loss of normal tissue function • bone marrow failure • ischemia
Question 121
What are Paraneoplastic Syndromes
Symptoms triggered by the tumor but not attributed to the direct effect of the tumor mass
Question 122
What causes paraneoplastic syndromes?
Genetic mutations
• substances released from the tumor • immune response targeting the tumor
Direct pressure from the tumor
Bacterial infections
Question 123
What is cachexia?
"Wasting away syndrome"
• excessive weight loss • marked weakness • taste alterations • muscle wasting • altered protein, lipid, and carbohydrate metabolism • decreased quality of life
Question 124
What is the primary cause of cachexia in cancer patients?
Viral infection
Chronic inflammation
Cancer cells activating inflammatory cytokines
Bacterial infection
Question 125
What is the role of Proteolysis-inducing factor (PIF) in cachexia?
causes calcium mobilization from bone
increases bone density
• induces protein degradation • apoptosis via activation of caspases • inhibits protein synthesis • increase proteolysis
promotes lipolysis of adipose tissue
Question 126
What is the role of Lipid-mobilizing factor (LMF) in cachexia?
Parathyroid hormone-related protein (PTHrP)
Interleukin-6 (IL-6)
Proteolysis-inducing factor (PIF)
promotes lipolysis of adipose tissue + increase fatty acid oxidation
Question 127
What does Parathyroid hormone-related protein (PTHrP) cause in cachexia?
causes calcium mobilization from bone and hypercalcemia
inhibits apoptosis
increases protein synthesis
promotes lipolysis of adipose tissue
Question 128
Role of Proinflammatory cytokines (TNF alpha, interferon gamma and IL-6) in cahexia?
LMF
PTHrP
Interferon gamma
contribute to inflammatory process and generalized weakness
Question 129
What is the primary method used for diagnosing and staging tumors?
A combination of clinical interviews and patient history
A combination of X-rays, CT scans, and MRI
A combination of clinical exam, imaging, tissue biopsies and histochemistry/immunohistochemistry, blood biochemistry and tumor markers, and genetics/immunophenotyping
A combination of blood tests and genetic screening
Question 130
What are tumor markers?
Types of cancer treatments
Non-cancerous growth indicators
Tumor markers include hormones, enzymes, genes, antigens, and antibodies.
Markers of normal cell function
Question 131
Which hormone is elevated in hepatocellular carcinoma?
Alpha fetoprotein
Beta globulin
Testosterone
Estrogen
Question 132
Which hormone is elevated in non-Hodgkin's lymphoma?
CD20 is elevated
Question 133
Which antigen is elevated in prostate cancers?
Lung cancer antigen
Prostate-specific antigen (PSA)
Breast cancer antigen
Colon cancer antigen
Question 134
What type of tumor can produce catecholamines?
Benign tumors of the adrenal medulla (pheochromocytoma)
Kidney tumors
Liver tumors
Pancreatic tumors
Question 135
What is one use of tumor markers?
1. identify individuals at high risk 2. diagnosis of a specific type of tumor 3. To follow the clinical course of treatment/monitor remission
To diagnose viral infections
To treat existing cancers
To monitor bone health
Question 136
Which marker can aid in the diagnosis of pituitary tumors?
CA 125
CEA
AFP
ACTH
Question 137
Management strategies of cancer?
Immunotherapy
Hormone therapy
Radiation therapy
Targeted therapy
Question 138
What is this?
Surgery
Targeted therapy
Radiation therapy
atrophy
Question 139
What is one of the key recommendations for cancer prevention according to the World Cancer Research Fund International?
Avoid all dairy products
hyperplasia
Eat only organic food
Consume at least 5 servings of red meat daily
Question 140
Which of the following is NOT a recommendation for cancer prevention?
Limit alcohol consumption
Limit consumption of fast foods and foods high in fat, starches, or sugars
dysplasia
Increase daily intake of fruits and vegetables
Question 141
What is this?
Avoid all physical exertion
metaplasia
Stay in bed all day
Sleep for 20 hours a day
Question 142
What is the term for the condition where cells become larger but remain normal in number?
Hypertrophy
Hyperplasia
Dysplasia
Atrophy
Question 143
Which cellular adaptation involves an increase in the number of cells?
Hypertrophy
Atrophy
Metaplasia
Hyperplasia
Question 144
What term describes the replacement of one mature cell type with another?
Atrophy
Dysplasia
Metaplasia
Neoplasia
Question 145
What does Atrophy refer to?
Complete congenital lack of a tissue
Development of immature cells
Reversible change in cell type
Increase in cell size
Question 146
What is Neoplasia?
new growth. Neoplasm refers to new and abnormal tissue growth.
Increase in cell number
Complete congenital lack of a tissue
Decrease in cell size
Question 147
What is Anaplasia?
Complete congenital lack of a tissue
Reversible change in cell type
lack of differentiation in neoplastic cells.
Increase in cell size
Question 148
What is Aplasia?
Decrease in cell size
Increase in cell number
complete congenital lack of a tissue.
Development of immature cells