ex23 Flashcards
Stem Cells
Cells with the ability to self-renew and differentiate into specialized cell types, playing a key role in development, tissue repair, and medical research.
Pluripotency
The ability of stem cells to differentiate into all three germ layers: endoderm, mesoderm, and ectoderm.
DNMT (DNA Methyltransferase)
Enzyme responsible for adding methyl groups to DNA, regulating gene expression by modifying chromatin structure.
De novo DNA Methylation
Establishes new methylation patterns on unmethylated CpG sites during development, mediated by DNMT3A/B.
Maintenance DNA Methylation
Preserves methylation patterns during DNA replication, mediated by DNMT1, ensuring epigenetic memory in somatic cells.
Active DNA Demethylation
TET enzymes oxidize 5-methylcytosine to intermediates like 5-hydroxymethylcytosine, followed by base excision repair (BER) to replace the modified base.
Passive DNA Demethylation
Occurs when DNMT1 fails to maintain methylation during replication, leading to progressive dilution of methylation over cell divisions.
Fragile X Syndrome
Caused by CGG expansion in the 5’ UTR of the FMR1 gene, leading to hypermethylation, chromatin condensation, and transcriptional silencing.
Endothelial Cells
Key cells in the vascular wall that regulate vascular tone, form a selective barrier, and mediate inflammation, playing roles in thrombosis and angiogenesis.
Atherosclerosis
A progressive disease involving lipid accumulation, inflammation, and plaque formation in arterial walls, leading to myocardial infarction or stroke.
Myeloid-Derived Suppressor Cells (MDSCs)
Cells that suppress T-cell activity, secrete immunosuppressive cytokines, and promote tumor growth in the tumor microenvironment.
Tumor-Associated Macrophages (TAMs)
Macrophages in the TME that exhibit M1 (anti-tumor) or M2 (pro-tumor) phenotypes, contributing to immune evasion and angiogenesis.
Immune Checkpoint Inhibitors
Drugs like anti-PD-1 or anti-CTLA-4 antibodies that block inhibitory signals, reactivating T cells to attack tumor cells.
Resistance to Immune Checkpoint Therapy
Mechanisms include low antigen expression, upregulation of alternative checkpoints, increased Tregs and MDSCs, and physical barriers like dense extracellular matrix.
Plasmid
Circular DNA molecule in bacteria that can carry multiple resistance genes and is transferred between cells via horizontal gene transfer.
Efflux Pump
A protein that actively exports antibiotics out of bacterial cells, reducing their intracellular concentration and conferring multi-drug resistance.
De novo Methylation
Establishes new DNA methylation patterns on CpG sites during development or differentiation, mediated by DNMT3A and DNMT3B.
Maintenance Methylation
Copies existing DNA methylation patterns onto the daughter strand during replication, mediated by DNMT1, preserving epigenetic memory.
Heteroplasmy
The presence of both normal and mutated mitochondrial DNA within a single cell, contributing to variable expression of mitochondrial diseases.
Neoantigens
Tumor-specific antigens arising from mutations, which are recognized by the immune system and are targets for T cell-mediated immunity.
PD-1
An immune checkpoint receptor on T cells that, when bound to PD-L1 on tumor cells, inhibits T cell activation and promotes immune evasion.
TET Enzymes
Involved in active DNA demethylation by oxidizing 5-methylcytosine to 5-hydroxymethylcytosine, enabling base excision repair.
Angiogenesis
The formation of new blood vessels, driven by VEGF and promoted by tumor-associated endothelial cells to supply nutrients and oxygen to tumors.
Tumor Microenvironment (TME)
A complex network of cancer cells, immune cells, stromal cells, and extracellular matrix, which shapes tumor progression and therapy responses.
Thrombosis
The formation of a blood clot in a vessel, which can result from plaque rupture in atherosclerosis, leading to myocardial infarction or stroke.
TAM (Tumor-Associated Macrophages)
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.
CAFs (Cancer-Associated Fibroblasts)
Stromal cells in the TME that produce extracellular matrix components and secrete growth factors, supporting tumor invasion and immune evasion.
MDSCs (Myeloid-Derived Suppressor Cells)
Immature myeloid cells in the TME that suppress T-cell and NK cell activity, promoting tumor growth and immune evasion.
Tregs (Regulatory T-cells)
Immunosuppressive T cells that inhibit anti-tumor immune responses, contributing to tumor immune evasion in the TME.
VEGF (Vascular Endothelial Growth Factor)
A protein secreted by tumor and stromal cells to promote angiogenesis and ensure a blood supply for tumor growth.
PD-L1
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.
Neoangiogenesis
The process of forming new blood vessels within the tumor, often driven by VEGF and critical for supplying nutrients and oxygen to growing tumors.
Checkpoints
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.
Checkpoint Inhibitors
Therapies targeting PD-1, PD-L1, or CTLA-4 to block immune suppression and restore T cell-mediated anti-tumor activity.
Heterochromatin
Tightly packed chromatin that is transcriptionally inactive, often associated with DNA methylation and histone modifications.
Fragile X Syndrome
Caused by CGG expansion in the FMR1 gene leading to CpG methylation, chromatin condensation, and loss of gene expression.
5-Methylcytosine
A DNA modification resulting from cytosine methylation, commonly found at CpG sites and associated with transcriptional repression.
Base Excision Repair (BER)
A DNA repair pathway involved in active DNA demethylation after TET-mediated oxidation of methylated cytosines.
Plaque Rupture
The breaking of a fibrous cap in atherosclerotic plaques, exposing thrombogenic material and triggering clot formation.
Neoantigen Escape
Tumor cells evade immune detection by downregulating neoantigen expression or altering MHC molecule presentation.
Th1 Cells
A subset of CD4+ T cells that produce IFN-γ, promoting cellular immunity against intracellular pathogens and tumors.
Th2 Cells
A subset of CD4+ T cells that produce IL-4, IL-5, and IL-13, promoting humoral immunity and responses against extracellular parasites.
IL-17
A cytokine produced by Th17 cells and ILC3s, crucial for defense against extracellular bacteria and fungi, especially at mucosal surfaces.
IL-10
An immunosuppressive cytokine produced by Tregs, MDSCs, and TAMs, dampening inflammation and anti-tumor immune responses.
TME Composition
Includes immune cells (Tregs, MDSCs), stromal cells (CAFs), tumor cells, and cytokines, all influencing cancer progression and therapy resistance.
Chromodomain Proteins
Proteins that recognize and bind methylated histones, such as H3K9me3, influencing chromatin structure and gene expression.
Bromodomain Proteins
Proteins that bind acetylated histones, promoting transcriptional activation by recruiting transcriptional machinery.
Histone Acetyltransferases (HATs)
Enzymes that add acetyl groups to histones, loosening chromatin structure and enhancing gene transcription.
Histone Deacetylases (HDACs)
Enzymes that remove acetyl groups from histones, tightening chromatin structure and repressing gene transcription.
Tumor Angiogenesis
The process by which tumors stimulate the growth of new blood vessels to ensure oxygen and nutrient delivery.
Neoantigen Presentation
The display of tumor-specific antigens on MHC molecules, critical for T cell recognition and anti-tumor immunity.
Efflux Pump Overexpression
A mechanism of drug resistance where bacterial or cancer cells actively pump out therapeutic agents, reducing efficacy.
PD-1/PD-L1 Axis
An immune checkpoint pathway where PD-L1 on tumor cells binds PD-1 on T cells, inhibiting T cell activation and promoting immune evasion.
Epigenetic Writers
Enzymes like DNMTs and HATs that add epigenetic marks (e.g., methylation, acetylation) to DNA or histones to regulate gene expression.
Epigenetic Readers
Proteins like bromodomain or chromodomain proteins that recognize and bind epigenetic marks to mediate downstream effects.
Epigenetic Erasers
Enzymes like TETs, HDACs, or demethylases that remove epigenetic modifications, resetting chromatin states.
CpG Island
A DNA region rich in CpG sites, often found in gene promoters, where methylation regulates gene expression.
Base Excision Repair (BER) in Demethylation
A DNA repair mechanism that removes oxidized bases during active DNA demethylation mediated by TET enzymes.
Tumor-Associated Dendritic Cells (DCs)
Immune cells in the TME that present antigens to T cells but may become dysfunctional, limiting anti-tumor responses.
Antigen Escape
A resistance mechanism where tumor cells downregulate MHC or mutate to reduce neoantigen presentation, avoiding immune detection.
Checkpoint Therapy Resistance
Mechanisms like TME remodeling, compensatory checkpoint activation, or antigen loss that reduce the effectiveness of immunotherapies.
Histone Modifications
Post-translational changes such as methylation, acetylation, or phosphorylation that regulate chromatin structure and gene activity.
IFN-γ
Produced by Th1 cells, CTLs, and ILC1s, critical for activating macrophages and promoting cellular immunity against intracellular pathogens.
TGF-β
An immunosuppressive cytokine produced by Tregs and TAMs, involved in tumor progression and immune evasion in the TME.
