Chapter 27. Amenorrhea Berek & Novak’s Gynecology 14 th edition (p 1035~1068) R3 Jung Mi Byun.
Novak’s gynecology 6 Molecular Biology and Genetics 부산백병원 산부인과 R3 박영미.
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Transcript of Novak’s gynecology 6 Molecular Biology and Genetics 부산백병원 산부인과 R3 박영미.
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Novak’s gynecology 6Novak’s gynecology 6
Molecular Biology and Molecular Biology and GeneticsGenetics
부산백병원 산부인과부산백병원 산부인과R3 R3 박영미박영미
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• Cell Cycle
• Modulation of Cell Growth and Function
• Immunology
• Factors that Trigger Neoplasia
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Cell CycleCell Cycle
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Normal cell cycleNormal cell cycle
• Phases of cell cycle : G1, S, G2, M
• Duration of cell cycle : about 24hrs. – Variations in cell cycle time : different durations of the G1
• Three subpopulations of cells– Terminally differentiated cells
• RBC, Striated muscle cells, uterine smooth muscle cells
– Quiescent cells (G0)• fibroblasts
– Dividing cells • GI tract, skin, cervix
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Normal cell cycleNormal cell cycle
• G1 Phase– Synthesis of enzymes & regulatory proteins
necessary for DNA synthesis– Duration (8 ~ 100 hrs)
• S Phase– Nuclear DNA content of the cell is copied.
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Normal cell cycleNormal cell cycle
• G2 Phase– RNA & Protein synthesis– Repair of errors of DNA replication
• M Phase– Nuclear division occurs
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Normal cell cycleNormal cell cycle
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Genetic Control of the Cell Genetic Control of the Cell Cycle Cycle
• To successfully complete the cell cycle, a number of cell-division-cycle(cdc) genes are activated
• Two checkpoints– G1/S boundary : cell commits to proliferation – G2/M boundary : repair of any DNA damage must be completed
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Genetic Control of the Cell Genetic Control of the Cell Cycle Cycle
• Cell Division Cycle Genes
– Factors that regulate the cell cycle checkpoints : • proteins encoded by the cdc2 family of genes• cyclin proteins
– Cyclins• Regulate the checkpoint at the G1/S boundary• Inhibit progression through the cell cycle in the presence of D
NA damage
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Genetic Control of the Cell Genetic Control of the Cell Cycle Cycle
• Cell Division Cycle Genes
– The p53 tumor suppressor gene : • participate in delay of the cell cycle in order for DNA repair to
be completed
– Mitosis is initiated by activation of the cdc2 gene at the G2/M checkpoint.
• MPF (mitosis promoting factor) : p34 cdc2 protein, specific cyclins : catalyzes protein phosphorylation & drives the cell into mitosis
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Genetic Control of the Cell Genetic Control of the Cell CycleCycle
• Apoptosis
– The regulation & maintenance of normal tissue mass requires a balance between cell proliferation & programmed cell death, or apoptosis
– Example• Deletion of the interdigital webs • Palatal fusion • Development of the intestinal mucosa • During the menstrual cycle : reduction in the number of endo
metrial cells. • Follicular atresia
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Genetic Control of the Cell Genetic Control of the Cell CycleCycle
• Apoptosis
– Characteristics • Histological : cellular condensation & fragmentation of the nucleus • Biochemical : increase in transglutaminase expression & fluxes in intracellular calcium concentration • Molecular : complex interactions between the bcl-2, c- myc, p53, ced-9
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Modulation of Cell Growth Modulation of Cell Growth and Function and Function
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Oncogenes & Tumor Suppressor GenesOncogenes & Tumor Suppressor Genes
• Among the genes that participate in cell growth and function, proto-oncogenes & tumor suppressor genes are particularly important
• Proto-oncogenes – Encode : growth factors, membrane & cytoplasmic receptors, proteins that play key roles in the intracellular signal transduction cascade, nuclear DNA binding proteins – Positive effects upon cellular proliferation
• Tumor suppressor genes : – inhibitory regulatory effects on cellular proliferation
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Oncogenes & Tumor Suppressor GenesOncogenes & Tumor Suppressor Genes
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Steroid Hormones Steroid Hormones
• Estrogen
– diffuses through the cell membrane– binds to estrogen receptors that are located in the nuc
leus – the receptor-steroid complex binds to the DNA at spec
ific sequences, estrogen response elements (EREs) – gene expression, protein synthesis
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Steroid HormonesSteroid Hormones
• Mutations of hormone receptors
– Absence of E2R-a in a male human• Incomplete epiphyseal closure• Increased bone turnover• Tall stature• Impaired glucose tolerance
– Mutations of the androgen receptor• Androgen insensitivity syndrome
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Growth Factors Growth Factors
• Growth factors exert positive or negative effects upon the cell cycle by influencing gene expression related to events that occur at the G1/S cell cycle boundary
• Because of their short half-life in the extracellular space, growth factors generally act over limited distances through autocrine or paracrine mechanisms.
• The regulation of ovarian function occurs through autocrine, paracrine, and endocrine mechanisms.
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Growth FactorsGrowth Factors
• The growth & differentiation of ovarian cells : influenced by the IGFs (insulin-like growth factors) * IGF-1 --> granulosa cell
: increase in cAMP, progesterone, oxytocin, proteoglycans,inhibin * IGF-1 --> theca cell
: increase in androgen production : theca cell --> TNF-a, EGF produce
* EGF : acts on granulosa cells to stimulate mitogenesis
• Disruption of these autocrine and paracrine intraovarian pathways
-> polycystic ovarian disease and disorders of ovulation
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Growth FactorsGrowth Factors
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Intracellular Signal Intracellular Signal TransductionTransduction
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Some Intracellular Signalling Proteins Act as MolecSome Intracellular Signalling Proteins Act as Molecular Switchular Switch
Ser/Thr kinaseSer/Thr kinase
Tyr kinaseTyr kinase
Large trimeric GTP binding protein (G protein)Large trimeric GTP binding protein (G protein)
Small monomeric GTPasesSmall monomeric GTPases
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Intracellular Signal Intracellular Signal TransductionTransduction
• Gene Expression-> transmission of external signals -> transcription and translation of specific genes -> the structure, function, proliferation of the cell
• Genetic errors -> result in abnormal structure and function-> premalignant, malignant, benign neoplasm of the female genital tract
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• Amplification
– An increase in the copy number of a gene
– Increasing the amount of template DNA
– common event in malignancies of the female genital tract
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• Point mutations
– The codon sequence alteration
– Qualitatively altering the gene product
– Point mutations of the p53 • The most common genetic
mutation in solid tumors• In approximately 50% of ov
arian cancers and 30-40% of endometrial cancers
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• Deletions and Rearrangements
– Gross changes in the DNA template
– Synthesis of a markedly altered protein product
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ImmunologyImmunology
- Immunologic - Immunologic Mechanisms - Mechanisms -
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Adaptive immune response Adaptive immune response
• Humoral immune responses : production of antibodies : specific antigen-binding sites that react with foreign an
tigens
• Cellular immune responses : antigen-specific immune responses : mediated directly by activated immune cells
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• 면역반응은 면역작용을 수행하는 기전이 세포에 의해서 나타나는지 단백질에 의해서 나타나는지에 따라 다시 세포매개성면역반응과 체액성면역반응으로 구분한다
• 세포매개성 면역반응
– cytotoxic T cell 이나 자연살해세포의 경우처럼 세포가 직접 항원을 제거하는 경우
– 문제가 있는 세포를 직접 파괴 함으로서 항원과 함께 문제가 된 세포를 죽이는 방법으로 , 주로 종양세포에 대한 면역반응이나 바이러스에 감염된 세포에 대한 면역반응에서 볼 수 있다
• 체액성 면역반응 – 항체나 보체처럼 체액이나 혈액에 녹아있는 물질 , 즉 세포와는
독립적으로 존재하는 단백질에 의하여 나타나는 면역반응 – 세포와는 독립적으로 항원과 반응하므로 , 세포와 연관되어 있지
않는 세균 등과 같은 항원에 대한 면역반응에서 볼 수 있다
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B Cells, Humoral Immunity, and Monoclonal B Cells, Humoral Immunity, and Monoclonal AntibodiesAntibodies
• B lymphocytes : the cells that synthesize and secrete antibodies
• Bone marrow stem cell -> Pre-B cell -> B cell -> plasma cell : produce antibodies
• Monoclonal antibodies – react with tumor-associated antigens – Immunotoxin-conjugated monoclonal antibodies
• directed to human ovarian adenocarcinoma antigens
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T Lymphocytes and Cellular T Lymphocytes and Cellular Immunity Immunity
• T lymphocytes : acting as helper cells in both humoral & cellular respo
nses : acting as effector cells in cellular responses
• T cells can respond to antigens -> when these antigens are presented in association with MHC molecules on antigen-presenting cells.
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T Lymphocytes and Cellular T Lymphocytes and Cellular ImmunityImmunity
• Two major subsets of mature T cells
– T helper/inducer cells : express the CD4 cell surface marker
– T suppressor/cytotoxic cells : express the CD8 cell surface marker
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Monocytes and Macrophages Monocytes and Macrophages
• Myeloid cell
• Important roles in both innate and adaptive immune responses
• Macrophages– express MHC class II molecules – effective antigen-presenting cells for CD4 T cells– ingesting and killing microorganisms– cytotoxic, antitumor killer cell
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Natural Killer cellsNatural Killer cells
• Nonspecific killing of tumor cells and virus-infected cells
• Innate form of immunity that does not require
an adaptive, memory response
• But the anti-tumor activity can be increased by exposure to several agents
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Cytokines, Lymphokines, and Immune MediaCytokines, Lymphokines, and Immune Mediatorstors
• Cytokines called
– Monokines if they are derived from monocytes
– Lymphokines if they are derived from lymphocytes
– Interleukins if they exert actions on leukocytes
– Interferons if they have antiviral effects
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- Interleukins - • IL-1
– Involved in fever & inflammatory responses
– Source : macrophages, phagocytic cells of the liver & spleen, s
ome B cells, epithelial cells, certain brain cells, the cells lining the synovial spaces
– Initiation of early events in immune responses
– Act as a B-cell activation-inducing factor
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• IL-2
– T-cell growth factor
– Proliferation-inducing effects
– Source : activated T cells
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• IL-3 – Increase the early differentiation of hematopoietic cell
s
• IL-4, IL-5, IL-6 – B-cell stimulating factor
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• IL-6– Induction of cytotoxic T-lymphocyte differentiation
– Induction of acute phase reactant production by hepatocytes
– Activity as a colony-stimulating factor for hematopoietic stem cell
• IL-8, IL-10 – cytokine synthesis inhibitory factor
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- Interferons -
• Three types : IFN-a, IFN-b, IFN-r --> interfere with viral production in infected cells --> direct antitumor effects
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Factors that Trigger Neoplasia Factors that Trigger Neoplasia
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Advanced Age Advanced Age
• Single most important risk factor
• Cancer Dx : 50 % of the population by 75 years of age
• Accumulation of critical genetic mutations over time
• Exposure to exogenous mutagens, altered host immune function
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Environmental Factors Environmental Factors
• Smoking
– The best known example of mutagen exposure that is associated with the development of lung cancer
– Cigarette smoking and cervical ca. is associated
– Exposure of the transformation zone to cigarette smoke mutagens increase the DNA damage and cellular transformation
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Environmental FactorsEnvironmental Factors
• Radiation
– Radiation induced cancer : the result of DNA damage that is not repaired
– Radiation induced cancer is approximately 10% greater in women than in men
: gender specific cancer, including breast cancer
– Radiation therapy for cervical cancer is associated with a small increase in the risk of colon cancer and thyroid cancer
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Immune Function Immune Function
• Immunosuppressed renal transplant patients -> 40-fold increased risk of cervical cancer
• HIV-infected patients with depressed CD4 cell count -> increased risk of cervical dysplasia, invasive disease
• High dose chemotherapy with stem cell support -> increased risk of developing a variety of solid neoplasms
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Diet Diet
• Dietary fat -> risk of colon & breast cancer
• Deficiency of folic acid & vitamin A & C -> cervical dysplasia & cervical cancer