1 / 214

Slackers Guide to Hematologic Cancers

Slackers Guide to Hematologic Cancers. Mike Ori. Disclaimer. These represent my understanding of the subject and have not been vetted or reviewed by faculty. Use at your own peril. I can’t type so below are common missing letters you may need to supply e r l

colum
Télécharger la présentation

Slackers Guide to Hematologic Cancers

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Slackers Guide to Hematologic Cancers Mike Ori

  2. Disclaimer • These represent my understanding of the subject and have not been vetted or reviewed by faculty. Use at your own peril. • I can’t type so below are common missing letters you may need to supply • e r l • I didn’t use greek letters because they are a pain to cut and paste in.

  3. What are the six hallmarks of cancer

  4. Evasion of apoptosis • Insensitivity to anti-growth signals • Self sufficiency of growth signals • Limitless replication potential • Sustained Angiogenesis • Tissue invasion and metastasis

  5. What is the Warburg effect

  6. It is the observation that cancer cells rely more heavily on glycolysis than on oxidative phosphorylation even in the presence of adequate oxygen supplies. Thus it is believed that the glycolysis is better suited to meet the metabolic demands of cancer cells.

  7. What is epigenetics • List a few epigenetic mechanisms in the cell

  8. Epigenetics refers to reversible but inheritable changes in gene expression that occur without mutations. Examples include • Methylation • Histone acetylation • Both examples limit the access of promoter regions to their respective promoters.

  9. What is the function of micro RNA

  10. miRNA are small (~22bp) RNA strands that function at the post transcriptional level to silence specific genes. Each miRNA may interact with multiple genes and thus can serve as an off switch post transcriptionally. • Some oncogenes control the expression of miRNA.

  11. What is mismatch repair?

  12. DNA replications “spell checker”. It makes sure A-T and G-C go together.

  13. What is Nucleotide excision repair

  14. Removal of pyrimidine dimers caused by UV radiation

  15. What is the function of p53

  16. P53 is a tumor suppressor gene. • It activates DNA repair genes • It can arrest the cell cycle at G1/S checkpoint • It can initiate apoptosis

  17. What is the function of ATM

  18. ATM is a tumor suppressor protein

  19. What is the function of Her2/neu/erb-b2

  20. An epithelial growth factor receptor whose gene is amplified in 25% of breast cancers. • Self-sufficiency in growth signals

  21. What drug targets her2 and what is its mechanism

  22. Trastuzumab is a monoclonal antibody directed against her2/neu/Erb b2. • It functions by binding to and disrupting erb b2

  23. What is BCR-ABL and how does it result in cancer

  24. BCR-ABL is a unique protein that from t(9:22) translocation that results in the fusion of the BCR promoter to the ABL tyrosine kinase in such a way that the kinase no longer requires a ligand for activation. • ABL is a proliferative kinase that is active in hematopoietic cells

  25. Describe the role of B-catenin and APC in cancer

  26. B-catenin is a cell proliferation enzyme that is sequestered by APC. • The deletion of one APC allele causes familial adenomatouspolyposis, an autosomal dominant condition that predisposes to colon cancer in early adulthood • Mutations in APC can lead to attenuated colon cancer forms

  27. What are the three benign types of lymphadenopathy

  28. Follicular • Expansion of B cells • Paracortical • Expansion of T cells • Sinus histiocytes • Surgical drainage

  29. What is the common gene involved with lymphoma translocation

  30. The heavy chain gene on CR14

  31. Why are immune cells susceptible to translocations?

  32. DNA cleavage is an important part of maturation of immune cells. This presents opportunity for abnormal joining.

  33. What is the etiologic classifications of lymphoma

  34. Translocations • Inherited • Downs, neurofibromatosis • Viruses • HTLV, EBV, HHV-8 • Environmental agents • Iatrogenic • Radiation

  35. Describe the relationship of lymphoma and leukemia

  36. Lymphocytic leukemias evolve to lymphomas late. Similarly, lymphomas may transform into lymphocytic leukemias.

  37. Describe follicular lymphoma

  38. Common indolent lyphoma • Back to back follicles • T(14:18) BCL-2 • Anti-apoptotic • May transform into diffuse large cell lymphoma

  39. Describe diffuse large cell lymphoma

  40. Large round lymphocytes • Alterations in BCL-6 • Germinal center formation disrupted

  41. Describe Burkitts Lymphoma

  42. Rapidly aggressive lymphoma • T(8:14) c-myc oncogene • Association with EBV • Starry sky pattern due to histiocytes

  43. Describe marginal zone lymphomas

  44. Associated with MALT in gut • Chronically inflamed tissue • H. pylori • Indolent but may transform to diffuse B-cell

  45. Describe hodgkins lymphoma

  46. Common cancer of young adults • Orderly progression from local nodes to spleen to liver to bone marrow • Reed-sternberg cells

  47. Describe Mycosis Fungoides

  48. T cell lymphoma • CD4+ • Band like infiltrates in dermis • Flat erythematous rash -> plaques -> tumor nodules • TX with local control early • Sezary syndrome • Widespread rash • Blood and lymph node involvement • Poor prognosis

  49. List the myeloid cells

  50. Granulocytes • Neutrophils • Eosinophils • Basophils • Monocytes • Erythrocytes • Megakaryocytes

More Related