ex23

Question 1

Stem Cells

Answer 1

Cells with the ability to self-renew and differentiate into specialized cell types, playing a key role in development, tissue repair, and medical research.

Question 2

Pluripotency

Answer 2

The ability of stem cells to differentiate into all three germ layers: endoderm, mesoderm, and ectoderm.

Question 3

DNMT (DNA Methyltransferase)

Answer 3

Enzyme responsible for adding methyl groups to DNA, regulating gene expression by modifying chromatin structure.

Question 4

De novo DNA Methylation

Answer 4

Establishes new methylation patterns on unmethylated CpG sites during development, mediated by DNMT3A/B.

Question 5

Maintenance DNA Methylation

Answer 5

Preserves methylation patterns during DNA replication, mediated by DNMT1, ensuring epigenetic memory in somatic cells.

Question 6

Active DNA Demethylation

Answer 6

TET enzymes oxidize 5-methylcytosine to intermediates like 5-hydroxymethylcytosine, followed by base excision repair (BER) to replace the modified base.

Question 7

Passive DNA Demethylation

Answer 7

Occurs when DNMT1 fails to maintain methylation during replication, leading to progressive dilution of methylation over cell divisions.

Question 8

Fragile X Syndrome

Answer 8

Caused by CGG expansion in the 5’ UTR of the FMR1 gene, leading to hypermethylation, chromatin condensation, and transcriptional silencing.

Question 9

Endothelial Cells

Answer 9

Key cells in the vascular wall that regulate vascular tone, form a selective barrier, and mediate inflammation, playing roles in thrombosis and angiogenesis.

Question 10

Atherosclerosis

Answer 10

A progressive disease involving lipid accumulation, inflammation, and plaque formation in arterial walls, leading to myocardial infarction or stroke.

Question 11

Myeloid-Derived Suppressor Cells (MDSCs)

Answer 11

Cells that suppress T-cell activity, secrete immunosuppressive cytokines, and promote tumor growth in the tumor microenvironment.

Question 12

Tumor-Associated Macrophages (TAMs)

Answer 12

Macrophages in the TME that exhibit M1 (anti-tumor) or M2 (pro-tumor) phenotypes, contributing to immune evasion and angiogenesis.

Question 13

Immune Checkpoint Inhibitors

Answer 13

Drugs like anti-PD-1 or anti-CTLA-4 antibodies that block inhibitory signals, reactivating T cells to attack tumor cells.

Question 14

Resistance to Immune Checkpoint Therapy

Answer 14

Mechanisms include low antigen expression, upregulation of alternative checkpoints, increased Tregs and MDSCs, and physical barriers like dense extracellular matrix.

Question 15

Plasmid

Answer 15

Circular DNA molecule in bacteria that can carry multiple resistance genes and is transferred between cells via horizontal gene transfer.

Question 16

Efflux Pump

Answer 16

A protein that actively exports antibiotics out of bacterial cells, reducing their intracellular concentration and conferring multi-drug resistance.

Question 17

De novo Methylation

Answer 17

Establishes new DNA methylation patterns on CpG sites during development or differentiation, mediated by DNMT3A and DNMT3B.

Question 18

Maintenance Methylation

Answer 18

Copies existing DNA methylation patterns onto the daughter strand during replication, mediated by DNMT1, preserving epigenetic memory.

Question 19

Heteroplasmy

Answer 19

The presence of both normal and mutated mitochondrial DNA within a single cell, contributing to variable expression of mitochondrial diseases.

Question 20

Neoantigens

Answer 20

Tumor-specific antigens arising from mutations, which are recognized by the immune system and are targets for T cell-mediated immunity.

Question 21

PD-1

Answer 21

An immune checkpoint receptor on T cells that, when bound to PD-L1 on tumor cells, inhibits T cell activation and promotes immune evasion.

Question 22

TET Enzymes

Answer 22

Involved in active DNA demethylation by oxidizing 5-methylcytosine to 5-hydroxymethylcytosine, enabling base excision repair.

Question 23

Angiogenesis

Answer 23

The formation of new blood vessels, driven by VEGF and promoted by tumor-associated endothelial cells to supply nutrients and oxygen to tumors.

Question 24

Tumor Microenvironment (TME)

Answer 24

A complex network of cancer cells, immune cells, stromal cells, and extracellular matrix, which shapes tumor progression and therapy responses.

Question 25

Thrombosis

Answer 25

The formation of a blood clot in a vessel, which can result from plaque rupture in atherosclerosis, leading to myocardial infarction or stroke.

Question 26

TAM (Tumor-Associated Macrophages)

Answer 26

Macrophages in the TME that can promote tumor growth (M2 phenotype) or initiate anti-tumor responses (M1 phenotype) depending on the signals in the microenvironment.

Question 27

CAFs (Cancer-Associated Fibroblasts)

Answer 27

Stromal cells in the TME that produce extracellular matrix components and secrete growth factors, supporting tumor invasion and immune evasion.

Question 28

MDSCs (Myeloid-Derived Suppressor Cells)

Answer 28

Immature myeloid cells in the TME that suppress T-cell and NK cell activity, promoting tumor growth and immune evasion.

Question 29

Tregs (Regulatory T-cells)

Answer 29

Immunosuppressive T cells that inhibit anti-tumor immune responses, contributing to tumor immune evasion in the TME.

Question 30

VEGF (Vascular Endothelial Growth Factor)

Answer 30

A protein secreted by tumor and stromal cells to promote angiogenesis and ensure a blood supply for tumor growth.

Question 31

PD-L1

Answer 31

A ligand expressed by tumor and immune cells that binds PD-1 on T cells, leading to suppression of T cell activation and immune evasion.

Question 32

Neoangiogenesis

Answer 32

The process of forming new blood vessels within the tumor, often driven by VEGF and critical for supplying nutrients and oxygen to growing tumors.

Question 33

Checkpoints

Answer 33

Molecular pathways like PD-1/PD-L1 and CTLA-4 that inhibit T cell activation, preventing autoimmunity but also exploited by tumors for immune evasion.

Question 34

Checkpoint Inhibitors

Answer 34

Therapies targeting PD-1, PD-L1, or CTLA-4 to block immune suppression and restore T cell-mediated anti-tumor activity.

Question 35

Heterochromatin

Answer 35

Tightly packed chromatin that is transcriptionally inactive, often associated with DNA methylation and histone modifications.

Question 36

Fragile X Syndrome

Answer 36

Caused by CGG expansion in the FMR1 gene leading to CpG methylation, chromatin condensation, and loss of gene expression.

Question 37

5-Methylcytosine

Answer 37

A DNA modification resulting from cytosine methylation, commonly found at CpG sites and associated with transcriptional repression.

Question 38

Base Excision Repair (BER)

Answer 38

A DNA repair pathway involved in active DNA demethylation after TET-mediated oxidation of methylated cytosines.

Question 39

Plaque Rupture

Answer 39

The breaking of a fibrous cap in atherosclerotic plaques, exposing thrombogenic material and triggering clot formation.

Question 40

Neoantigen Escape

Answer 40

Tumor cells evade immune detection by downregulating neoantigen expression or altering MHC molecule presentation.

Question 41

Th1 Cells

Answer 41

A subset of CD4+ T cells that produce IFN-γ, promoting cellular immunity against intracellular pathogens and tumors.

Question 42

Th2 Cells

Answer 42

A subset of CD4+ T cells that produce IL-4, IL-5, and IL-13, promoting humoral immunity and responses against extracellular parasites.

Question 43

IL-17

Answer 43

A cytokine produced by Th17 cells and ILC3s, crucial for defense against extracellular bacteria and fungi, especially at mucosal surfaces.

Question 44

IL-10

Answer 44

An immunosuppressive cytokine produced by Tregs, MDSCs, and TAMs, dampening inflammation and anti-tumor immune responses.

Question 45

TME Composition

Answer 45

Includes immune cells (Tregs, MDSCs), stromal cells (CAFs), tumor cells, and cytokines, all influencing cancer progression and therapy resistance.

Question 46

Chromodomain Proteins

Answer 46

Proteins that recognize and bind methylated histones, such as H3K9me3, influencing chromatin structure and gene expression.

Question 47

Bromodomain Proteins

Answer 47

Proteins that bind acetylated histones, promoting transcriptional activation by recruiting transcriptional machinery.

Question 48

Histone Acetyltransferases (HATs)

Answer 48

Enzymes that add acetyl groups to histones, loosening chromatin structure and enhancing gene transcription.

Question 49

Histone Deacetylases (HDACs)

Answer 49

Enzymes that remove acetyl groups from histones, tightening chromatin structure and repressing gene transcription.

Question 50

Tumor Angiogenesis

Answer 50

The process by which tumors stimulate the growth of new blood vessels to ensure oxygen and nutrient delivery.

Question 51

Neoantigen Presentation

Answer 51

The display of tumor-specific antigens on MHC molecules, critical for T cell recognition and anti-tumor immunity.

Question 52

Efflux Pump Overexpression

Answer 52

A mechanism of drug resistance where bacterial or cancer cells actively pump out therapeutic agents, reducing efficacy.

Question 53

PD-1/PD-L1 Axis

Answer 53

An immune checkpoint pathway where PD-L1 on tumor cells binds PD-1 on T cells, inhibiting T cell activation and promoting immune evasion.

Question 54

Epigenetic Writers

Answer 54

Enzymes like DNMTs and HATs that add epigenetic marks (e.g., methylation, acetylation) to DNA or histones to regulate gene expression.

Question 55

Epigenetic Readers

Answer 55

Proteins like bromodomain or chromodomain proteins that recognize and bind epigenetic marks to mediate downstream effects.

Question 56

Epigenetic Erasers

Answer 56

Enzymes like TETs, HDACs, or demethylases that remove epigenetic modifications, resetting chromatin states.

Question 57

CpG Island

Answer 57

A DNA region rich in CpG sites, often found in gene promoters, where methylation regulates gene expression.

Question 58

Base Excision Repair (BER) in Demethylation

Answer 58

A DNA repair mechanism that removes oxidized bases during active DNA demethylation mediated by TET enzymes.

Question 59

Tumor-Associated Dendritic Cells (DCs)

Answer 59

Immune cells in the TME that present antigens to T cells but may become dysfunctional, limiting anti-tumor responses.

Question 60

Antigen Escape

Answer 60

A resistance mechanism where tumor cells downregulate MHC or mutate to reduce neoantigen presentation, avoiding immune detection.

Question 61

Checkpoint Therapy Resistance

Answer 61

Mechanisms like TME remodeling, compensatory checkpoint activation, or antigen loss that reduce the effectiveness of immunotherapies.

Question 62

Histone Modifications

Answer 62

Post-translational changes such as methylation, acetylation, or phosphorylation that regulate chromatin structure and gene activity.

Question 63

IFN-γ

Answer 63

Produced by Th1 cells, CTLs, and ILC1s, critical for activating macrophages and promoting cellular immunity against intracellular pathogens.

Question 64

TGF-β

Answer 64

An immunosuppressive cytokine produced by Tregs and TAMs, involved in tumor progression and immune evasion in the TME.