Day 7, Lecture 3 (Aug 30): Cancer I: Introductory Nomenclature and Pathology

Question 1

Question 2

Most cancers of the colon are

Answer 2

adenocarcinomas

Question 3

Question 4

Question 5

Question 6

Question 7

Anatomic and Clinical Pathology

Answer 7

Question 8

Question 9

Characteristic microscopic morphology of Cancers

Answer 9

• Key microscopic features of malignancy
  
  • nuclear irregualrities (atypia)
    
    • irregular contours (jagged, notched, etc.)
    • Increased size (nucleus to cytoplasm ratio)
    • Large and/or multiple nucleoli
    • “open” chromatin or hyperchromasia (dark, from too much chromatin)
  • Overall pattern
    
    • invasion into surrounding tissues
    • irregular 3-D structures (jumbled 3D grouping; note

Question 10

List the distinguishing features of Benign and Malignant tumors

Answer 10

Question 11

• Cancers are graded and staged to guide managment
  
  • Define stage and grade

Answer 11

• Grade
  
  • degree of differentiation of the tumor
    
    • how?
      
      • microscopic examination
        
        • low-grade: well differentiated (looks like tissue of origin)
        • high-grade: poorly differentiated (does not look like tissue of origin (anaplastic)
• Stage
  
  • Anatomic extent of the tumor
    
    • how?
      
      • surgery
      • imaging
      • pathology
    • Designation:
      
      • “T_N_M_) where T= tumor size/extent, N=nodal status, and M=metastasis

Question 12

What should the cell to fat ratio of bone marrow be

Answer 12

• Cellularity: normally about 100-patient’s age

Question 13

Chronic Myelogenous Leukemia

Answer 13

• is characterized by BCR-ABL
• CML is chronic myeloproliferative disorder
• Spectrum of malignant granulocytic cells in the peripheral blood
• Presenation:
  
  • Discovered incidentally; anemia/fatigue; splenomegaly
• Can be mimicked by an increased in WBCs due to infection
• t(9;22) (balanced translocation between chromosomes 9 and 22) or BCR-ABL (the resultant fusion gene) required for diagnosis
• Targeted molecular therapy available (Gleevec, a.k.a. imatinib, a tyrosine kinase inhibitor) (note that TKIs end in “-nib”

Question 14

How do Tyrosine kinases inhibitors work on CML

Answer 14

Question 15

Question 16

A mutation in BCR-ABL can switch a threonine to Isoleucine and makes TKIs, like Gleevec not able to bind

Question 17

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Question 22

Question 23

can benign tumors kill

Answer 23

yes, if they are in critical location

Question 24