Stem midterm 2

  1. What are the most important CDK regulators of the cell cycle?
    CDK4 CDK6 for structure and CDK2
  2. Following mitogenic stimuli, quiescent cells enter the cells cycle and upregulate?
    D and then E_type Cyclins during G1
  3. Once cyclins D and E have been up regulated what happens?
    D associates with CDK4 and 6. E associates with CDK2
  4. One the cyclin-CDK complexes have been assembled, what happens?
    The complex enters the nucleus
  5. What is retinal blastoma?
    It is a regulator
  6. In G-2 phase CDK1 associates with cyclin B1 to form the CDK1/cyclin B complex. What happens?
    This brings the onset of mitosis and is tightly regulated.
  7. CDK1 The catalytic subunit and its positive regulator subunit cyclin B1 comprising aserine/threonine portion kinase, the CDK1/cyclinB1 complex is maintained by?
    P-Thr161 activates it and Kinase CAK mediates it
  8. During G2 phase the CDK1-cyclineB1 complex is inactive by?
    P-Thr14 and tyr15 by CDK1 inhibitory protein kinases.
  9. CDC25A mainly controls what?
    G1/s transition via de-p and activation of CDK2/cycline A and CDK2/cycline E
  10. CDC25B and C primarily required for?
    Entry into mitosis
  11. Dephosphorylation of THr14 and Tyr15 by CDC25B activates CDK1/B1 complex and triggers initiation of?
    Mitosis
  12. Later in prophase CDK1/cycli B is translocated in the nucleus where the complex is fully activated by CDC25C
  13. These can inhibit cyclin-CCDKs modulating the cell cycle by preventing or limiting cyclin-CDKs from phosphorylation get their normal substrates.
    CDK inhibitors
  14. What are the two classes of CDK inhibitors?
    Cip/Kip and INK4
  15. These inhibit CDK4, but eventually include inhibitors of CDK6 as well.
    INK4
  16. This inhibitor of cyclin-CDKs is a kinase inhibitor
    Cip/Kip
  17. The source of cancer depends on alterations of
    Regulatory control of the cell cycle, Cellular senscence, and apoptosis
  18. Alteration done to the cell can be done by
    Somatic mutations and genetic predisposition.
  19. Mutations tend to occur in
    Photo-oncogenes
  20. This theory is hat any. Cell type could become mutated and transformed into a cancer cell.
    Stochastic hypothesis.
  21. Accumulation. Of. Genetic and epigenetic alterations during tumors genesis can be caused by
    Loss of APC, DNA hypomethylation, activation of K-ras, loss of 18q TSG, and loss of p53
  22. For mutations of cells to cause cancer, 90% of these are from.
    The loss of APC
  23. What happens where there is no APC?
    Colon crypt cell migration will continue to have a flow, but instead it will continually proliferate without WNT signaling.
  24. Who was it that discovered that there was a similarity between cancer cells and cells encompassing an early-stage developing embryo?
    Virchow
  25. What are the 7 principals of stem cell theory?
    1: Cancer arises from tissue Stem cells. 2: the niche allows cancer stem cells to express the malignant phenotype. 3: cancers contain the same cell populations. As do normal tissue 4: cancers can be transplanted via cancer stem cells, but not via the transit-ampyfying cells of the cancer. %: products of the cancer cells that reflect stages in teal development can be used as markers of diagnosis, prognosis and treatment. 6: Maligant cells can become benign. 7:Differentiation. Therapy is targeted towards transit amplifying cells; when discontinued, cancer regrows from resistant cancer stem cells.
  26. This cancer theory believes that all tumor cells have tumorigenic potential. Cahemical carcinogenesis. Genetic mutations and epigenectic changes cause it.
    Stochastic model
  27. This. Cancer. Theory only the cancer stem cell has high tumorigenic potential. Not every cell within a tumor can for a new tumor. Undifferentiated cells within the tumor supported tumor growth.
    Hierarchy model
  28. These cells can self-renew and can give rise to cell types present witching that particular tumor or cancer.
    Tumor -initiating cells
  29. Tumor-initiating cells with malignant properties are referred t as
    cancer stem cells.
  30. Why are CSCs highly debated?
    Difficult to chararctize these cells as unique and hard to find origin
  31. What are the three pathways of CSCs?
    CSCs from mutations in stem or progenitor cell populations. Norm to mutationto cancercell to tumorigenisis to primary tumor. CSCs not eradicated by chemo drive tumor regrowth. Primary tumor to chemo to refractory CSC to relapse to relapsed tumor. CSCs escape a metastasizing tumor leading to new tumor growth. Primary tumor to tumor cell escape to metastatic CSC to metastasis to multiple tumors.
  32. What are the differences between ASC and CSCs?
    ASCs syetrical or asymmetrical division and. Differentiate into a variety of terminal lineages. CSCs symmetrical division. No stemness markers resembling ASCs. May or may not differenciatiate into terminal lineages. May have their own molecular and morphological properties. They do express pluripotent your factors: oct 4 annoy and Sox 2, but are not markers
  33. What. Are the. Properties of CSCs?
    Self-renewal, strong tumorigenic potential, and tumor heterogeneity
  34. For CSCs how is self renewal determined?
    Often determined by serial tumor transplantation in vivo or soft agar sphere formation in vitro.
  35. How is the strong tumorigenic potential determined in CSCs?
    Measured by the number of cells required for tumor induction. Varies from CSC to another.
  36. How is the tumor heterogeneity determined in CSCs?
    Ability to recapitulate the phenotype of the original tumor it was isolated from.
  37. Which of these signaling pathways in CSC transformation has been associated with stem cell self renewal?
    Bel-2 WNT Shh and Notch
  38. These CSCs are. Devastating. Form of cancer yet can be treated with high survival rate. Show CD44+ CD24-
    Breast
  39. These CSCs express CD133+ from human gliomas. Neurosphere assay of cells from glioblastoma and medulloblastoma.
    CNS
  40. These CSCs are typically due to non-genetic environmental influences. WNT signaling is involved in transformation and turmogenisis. Express CD133+
    Colon
  41. These CSCs are the most deadly malignacy. Originates in the ovarian epithelium. expresses CD44+
    Ovarian
  42. What have we found some succesful treatments for CDCs?
    Melanoma and Multiple Myeloma
  43. How do we treat melanoma?
    T-cells is chimeric antiugen receptors recoginze target antigens expressed by CDCs. CD20+
  44. this is the transformation of white blkood cells, plasma cell myeloma
    Multiple Myeloma
  45. what is the new treatment for multiple myeloma
    Rituximab, and anti CD20 antibody that decreases the clonogenic recovery of these cells
  46. These are the cells that give rise to gametes.
    Primordial germ cells PGCs
  47. PGCs are formed and migrate to?
    The gonadal ridge
  48. Once PGCs are at the gonadalk ridge what happens?
    one to two controled divisions happens: Meiosis and differentiation-oogenesis or spermatogenesis.
  49. One PGCs are in the male genital ridge what happens?
    proliferation ceases. PGCs transiently arrest in G0/G1
  50. Once PGCs are in the femail genital ridge what happens?
    proliferation ceases whne entering the first meiotic (phrophase) division as oocytes
  51. identification of Pimordial stem cell be done by
    TNAP, HoxB-, fragilis, and stella (Dppa3)
  52. PGCs in the epiblast will express Blimp1 and
    proliferation accelerates and under go specification.
  53. What initiates migration of primordial germ cells?
    E-cadherin and N-carderin
  54. What guides the primordial germ cells?
    stromal cell-derived factor 1 and g-protein coupled receptor CXCR4
  55. These are derived from Primordial germ cells. capable of indefinate proliferation. can go to germline. Express Stem cell factor + bFGF+LIF
    Embryonic germ cells
  56. Mouse and human EGCs express high amounts of TNAP and SSEA-1 how does this compare to hESCs?
    HESCs also express SEEA 3 and 4 they Embryonic Germ Cells also don't for teratomas
  57. These cells have the capacuty to give rise to gametes and also take on the properties similar to ESCs.
    Embryonic Germ Cells
  58. What is the first stem cell type expressed?
    Trophoblast stem cells
  59. Where are the trophoblast found?
    extraembryonic ectoderm and ectoplacental cone
  60. Trophoblast proliferation dependent on signals from ICM. Its sends out this. In its absence TB Giant cells differentiate.
    FGF signaling
  61. What are some unique things for trophoblast stem cells?
    heterogeneous even in stem cell conditions. committed population: can only become placenta and yolk sac. ESCs cannot do this. absense of FGF giant cell differnetiation. No Oct4 brachyury and HNF4
  62. this is the root cause in may placenta-based preganacy complications
    trophoblast differentiation.
  63. Amniotic FLUID stem cell facts
    round shape for 1 wk. plastic adherence. 80% confluency every 48hr to 72 hr. highly proliferative. have the same markers as other stemn cells. broadly multipotent
  64. What stem cells are rich in cord blood?
    Hematopoietic and mesenchymal stem cells.
  65. What is Graft-versus-host disease Gvd?
    A donors tissue is recongonized as forgein and is attacked by the recipients immune system.
  66. What is the negatives to Cord blood?
    if they have lukemia you cannot use the blood. Has to be a small person. only 1.9ml per 1lbs. Only 80-100ml. donate only once, cannot treat yourself, limiting # stem cells in collection. and may not completely incorporate
  67. What are some advantages of Cord blood stem cells?
    Readily available. Lower incidence of Graft-verus-host disease. can be frozen. Greater HLA disparity
  68. These form the blood and immune cells.
    Hematopoietic stem cells.
  69. how did till and McCulloch analyze bone marrow to fnd out which components were responcible for regenerating blood?
    Hematipoietic stem cells are injected into a mouse that has been irradated to kill its own blood producing cells. If the mouse recovers and all blood cells reappear, the transplanted cells are deemed to have included stem cells. These studies led to the discovery of two kinds of hemopoietic stem cells.
  70. What are the two differnt kinds of hemopoietic stem cells?
    Long-term and short-term.
  71. These hematopoietic stem cells can undergo two round of regneration and over months.
    Long-term cells (stem cells)
  72. These hematopoietic stem cells can immediately regenerate all the different types of blood cells but not long term.
    Short term stem cells (proginators)
  73. What are the markers for hematopoietic stem cells?
    CD 34 CD 59 cxcr4 cd133 no lin and no cd45
  74. what are the sources for hematopoietic stem cells?
    Bone Marrow, peripheral blood, fetal hematopoiesis.
  75. why is peripheral blood becomeing the choice source for hematopoietic stem cells?
    easier on donor, higher survival rates, contain twices as many hematopoetic stem cells than bone marrow, and engraft more quickly.
  76. Where are the primitive sources of hematopoietic stem cells?
    yolk sac, aorta-gonad mesonephros region, placenta, and fetal liver.
  77. Where are the definitives tissues that promote hematopoietics stem cells?
    bone marrow, spleen, thymus
  78. This primitive source of hematopoietic stem cells is the most studied, earliest hematiopoietic activity by day 7, appear as islands of blood, and are transient?
    Yolk sac
  79. In adults where can you find hematopoetic stem cells?
    in the bone withing complex microenvirmoents.
  80. Hematopoetic stem cells are anchored in the bone marrow through.
    cxcr4/sdf-1. if this is disrupted them it is motile
  81. These are also found in bone marrow/ express sca-1+ lin- cd45-. rare and very small. also express seea1 oct 4 nanog and rex 1. they have tri-lineage differntiation potential.
    Very small embryonic like stem sels. (VSELs)
  82. The heart is the first functional organ. it is developed during neurulation adn directionality provided by endoderm. The place it develops from is called?
    primitive streak
  83. whay are cardiac stem cells hard to find?
    heart tube is composed of cardiomyocytes lined by endocardiald. Those cardomyocytes continue to divide. the division ends after birth. Increase in size is due to hypertrophy. Heart does not have a reserve. repair rate is at 1% per year at 25 yrs. and as low as .45% in 75 year olds
  84. How can hematopoetic stem cells help the heart?
    improvement of global cardiac function and enhanced blood flow.
  85. these stem cells are cabable of multi-lineage or uni-lineage differntiation. more restricted potential. can give rise to osteoblasts, adiposecytes, chodrocytes, and myoblasts
    Mesenchymal stem cell
  86. Sources of the mesenchymal stem cell?
    Bone marrow, umbilical ciord, fat aspirants, connective tissue, skin, and placenta.
  87. Mesenchymal stem cells are positive and negative for what markers?
    + Cd105, cd73, cd90. - cd45, cd34, cd14 or cd11b cd19 or79 hla-dr
  88. what are some appealing characteristics to mesenchymal stem cells?
    can home to bone marrow, can be incorporated into other tissues, and low immunogenicity and suppress alloreqactive T cell response.
  89. Are mesenchymal stem cells pluripotent?
    no
  90. what is the benefit of Aging mesenchymal stem cells?
    they are larger, exhibit mor podia and spread further, conatin for actin fibers, and more senescence
  91. senescent afrter a few population doublings. Shortened telomeres are sensed as DNA damage. leads to activation of p53
    senescence
  92. what are the benefits of mesenchymal stem cells?
    free of ethical concerns and teratoma formation. Critical role in injury healing and treating immune and non-immune dieases.
  93. what are the three tissues in the skeleton?
    Cartlage, bone, and bone marrow
  94. what are the three important cell types in adult bone?
    Chondrocytes Osteoblasts and osteoclasts
  95. This is the cells of logitudinal bone growth, synthesize cartilageneous scaffolds for osteoblast attachment.
    Chondrocytes
  96. Thes bon cells produce collagen-rich matrix, cytokines, and activation factors for the osteoclasts.
    Osteoblasts
  97. The bone cells constantly reshape deposited matrix.
    osteoclasts bone marrow
  98. what are the three sources of bone tissue?
    neural crest cell ( skull) scleretome cells from somites ( chest) lateral plate mesoderm (arms and legs)
Author
MagusB
ID
345411
Card Set
Stem midterm 2
Description
midterm 2
Updated