Exam 2 | Oncology + Glaucoma

Question 1

Oncogenes

Answer 1

• Mutated genes that tells cells to keep growing
• Not detected by body because it’s part of body systems and body actually activates them ⇒ B-cells and T-cells (adaptive immunity) doesn’t kill them → adapts to them instead

Question 2

Carcinoma in situ

Answer 2

• Encapsulated carcinoma
• Abnormal epithelial cell growth
• Localized/confined ⇒ hasn’t moved anywhere
• No invasion
• Variable progression ⇒ needs monitoring via ultrasounds

Question 3

Tumor-suppressor gene

Answer 3

• P53: tumor suppressor gene telling cell not to grow → tells cell to undergo apoptosis OR if cell is injured, tells it to repair and clean up itself
  
  • If turned off → cells keep growing bc nothing’s telling it to stop → bypasses apoptosis
  • About detection, damage control, and repair

Question 4

Caretaker genes

Answer 4

• In general:
  
  • Plays role in DNA damage
  • Involved in replication of DNA
  • Tells cell to encode specific DNA to repair normally bc cell was said to have been damaged
  • Malfunctions when there’s no P53 tumor suppressor gene in place (dependent) → tumor becomes aggressive and grows bc nothing’s telling it to stop
• P21: gene that helps w/ genomic stability by passing down DNA structures that have mature cell functions and mature structures so cell stays well differentiated and tries to set damaged cell to “right/good” path via encoding specific DNA to repair itself
  
  • Not seen in development of malignant cells
  • Tells cell it’s good to grow and pass on its good genes
• If tumor suppressor gene of P53 is off → it doesn’t stop cell from growing then caretaker genes can’t repair it bc P21 doesn’t know there’s an issue with the cell and general caretaker genes doesn’t tell cell to encode specific DNA to repair it normally → allows cell to proliferate w/ original mutated genes from parent → malignancy

Question 5

Process of abnormal cell growth that leads to anaplasia and tumor development | Biology of cancer cells

Answer 5

• Normal cell gets insults that damages DNA (ie. carcinogens, mutates, etc.)
• One of 3 things occur:
  
  • Cell successfully repairs itself and goes back to functioning normally
  • Cell is eaten by its own body
  • Cell repair doesn’t occur due to abnormal genetic mutation of a gene that suppresses cancer (P53) normally turned on is now turned off → caretaker genes fail to repair cell → cell divides with that genetic mutation → division of cell with mutated genes proliferates and spreads said genes to replicated cells and so on → irregular cell structures like anaplasia → tumor

Question 6

Anaplasia vs. Dysplasia

Answer 6

• Anaplasia: loss of cellular differentiation/specialization (therefore function) and normal cell structure (unorganized, irregular masses) ⇒ they’re rapidly dividing immature cells
  
  • Increased aggressiveness: more undifferentiated cells are = more likely to metastasize
  • Invades other tissues, irreversible, complete loss of cell differentiation, cells revert to undifferentiated state
• Dysplasia: reversible, appear immature or disorganized
• Dysplasia VS. Anaplasia: need biopsy to know which types

Question 7

Angiogenesis: vascular endothelial growth factor (VEGF) and basic fibroblast growth (bFG)

Answer 7

• Abnormal growth of resting endothelial cells (dormant tumor) secretes angiogenic cytokines (communicators), specifically…
  
  • Vascular endothelial growth factor (VEGF) → tells vasculature to grow by promoting new blood vessel formation
  • Basic fibroblast growth (bFG) → tells vasculature to grow by stimulating new blood vessel formation
• Endothelial cells of the preexisting blood vessels undergo sprouting where they extend towards dormant tumor with new blood vessels
• Dormant tumor and new blood vessels fuse
• Dormant tumor gets access to blood supply, nutrients, etc.
• Dormant tumor becomes aggressive
• Becomes malignant tumor, can invade nearby tissues, metastasize bc it now has access to bloodstream/lymphatic system and spread to other body parts

Question 8

Stages of Cancer 1-4

Answer 8

• Stage 1: small tumor confined to organ of origin/area/localized
• Stage 2: tumor grew and became locally invasive → going to nearby structures
  
  • Gotten bigger and a little bit beyond/encroaching on area where it was confined
• Stage 3: advanced to regional structures → moving towards lymph nodes nearby and deeper tissue
  
  • A little more advanced movements to nearby structures
• Stage 4: spread to distant sites and other tissues of body → full on metastasis
  
  • Aka “well advanced”

Question 9

Tumor Node Metastasis System (TNM)

Answer 9

• Tumor size: how big is it, has it broken skin or attached to cell membrane?
• Lymph node status: how many lymph nodes are involved/invaded?
• Metastasis: whether it’s metastasized or not/moved on to other parts of body or not?

Question 10

Endothelial Mesenchymal Transition (EMT)

Answer 10

• Endothelial mesenchymal transition: when tumor cells secrete protease to break down/degrade endothelial layer → creates space for tumor cells to move in and invade nearby endothelial tissues → tumor proliferates and invades bigger space of nearby tissue → tumor cells start to transition to mesenchymal cells that’s more mobile and allows for more metastasis in bloodstream/lymphatic
  
  • ↑ resistance to apoptosis
  • Doesn’t stay in basement membranes → they move → ↑ migratory capacity
• EMT is a state of the cell where once tumor cells are lodged in endothelial tissue due to protease degradation activity of the endothelial layer, it transitions to mesenchymal cell to better metastasize into the blood and lymph

Question 11

Open Glaucoma

Answer 11

• Gradual blockage of trabecular meshwork ⇒ pressure builds up because aqueous humor in anterior chamber builds up ⇒ builds up intraocular pressure ⇒ compresses optic nerve ⇒ vision loss
• Slow, gradual peripheral vision loss (tunnel vision)
• Hazy/cloudy vision
• Blurred vision

Question 12

Closed Glaucoma

Answer 12

• Occurs when iris displaced ⇒ weird angle between iris and cornea is blocked off ⇒ blocks outflow of aqueous humor ⇒ no drainage ⇒ trabecular meshwork prevents aqueous humor outflow ⇒ intraocular pressure builds up
• Physical blockage of drainage angle that happens quick
• Sudden, severe pain: stabbing, throbbing pain
• Can cause NV
• Blurred vision that can lead to tunnel or double vision
• Headaches from eye strain
• Halo around lights