Cell Kinetics

Question 1

Tissue and organ adaptation to injury

Answer 1

• Hyperplasia
• Metaplasia
• Dysplasia
• Desmoplasia

Question 2

Hyperplasia

Answer 2

• Tissue or organ adaptation to injury
• Increase in the number of cells due to activation of cell cycle kinetics; e.g. estrogen-induced endometrial hyperplasia; leukocyte response to cytokines released during infection

Question 3

Metaplasia

Answer 3

• Tissue and organ adaptation to injury
• substitution of epithelium type; eg. Barret’s esophagus- intestinal epithelium replaces squamous epithelium in GERD

Question 4

Dysplasia

Answer 4

• Tissue and organ adaptation to injury
• Potentially reversible mild to moderate upregulation and distortion of cell signaling w/ nuclear enlargement and cell proliferation
• Describes developmental defects: fibrous dysplasia of bone, renal dysplasia
• Also describes morphologic effects of abnormal cytogenetics w/ nuclear enlargement, increased nuclear/cytoplasmic ratio
• May serve as intraepithelial precursor lesion in the later development of malignant neoplasia

Question 5

Desmoplasia

Answer 5

• Tissue and organ adaptation to injury
• TGF activation adjacent to neoplasm w/ collagen formation (“hardness” of tumors)

Question 6

Benign Neoplasia

Answer 6

• New growth w/ focal and confined, slow, proliferation of uniform, mature cells, usually diploid w/ minimal threat to patient, who may be unaware of lesion

Question 7

Malignant Neoplasia

Answer 7

• New growth w/ rapid and disturbed proliferation of immature pleomorphic cells, usually aneuploid which invade across tissue boundaries, metastasize and usually cause morbidity (significant signs and symptoms of disease) and sometimes mortality

Question 8

Hamartoma

Answer 8

• Neoplasm-like process
• Developmental proliferation of cells native to organ e.g., hemangioma, anywhere; chondroma in lung, angiomyolipoma of kidney

Question 9

Choristoma

Answer 9

• Neoplasm-like process
• Developmental flaw; cell proliferation at ectopic sites e.g. pancreatic tissue in stomach

Question 10

Teratoma

Answer 10

• Neoplasm-like process
• Germ cell (ovary, testicle) aberration- parthenogenesis- with development of ectoderm, mesoderm, endoderm in varying stages of maturation

Question 11

Ploidy vs. Cancer cell doubling time

Answer 11

• The faster the doubling time the more aneuploid you’re going to find; meaning that if the cell is turning over rapidly theres going to be a lot of mistakes in the DNA; some of the chromosomes aren’t seperating

Question 12

Goals of Cancer Treatment

Answer 12

• Inhibit cell proliferation
• Induce apoptosis
• Promote terminal differentiation of cells

Question 13

Colchicine

Answer 13

• Delays development of HCC (hepatocellular carcinoma) in patients w/ hepatitis-related cirrhosis
• Anti-inflammatory (gout, psoriasis, scleroderma, etc.) agent interacts w/ inflammatory cell microtubules interfering w/ mitosis while inhibiting leukocyte adherence, motility and chemotaxis
• 9% of treated patients developed hepatocellular carcinoma vs 29% untreated group
• Time to HCC: 222 months tx group; 150 months untx group

Question 14

Taxol (Paclitaxel)

Answer 14

• Beneficial effect on ovarian, breast and lung carcinomas through inhibition of cell proliferation

Question 15

IL-15 treatment in cancer

Answer 15

• Effective for renal cell carcinoma; directs the epithelial differentiation of renal carcinoma stem cells

Question 16

Arsenic Trioxide Therapy

Answer 16

• For Acute Promyelocytic Leukemia
• Disrupt rusion protein RAR-a: PML causing cytodifferentiation
• Increased expression of caspases w/ induction of apoptosis