Intro To Oncology Flashcards
How does all cancer start?
Initiation: via exposure to carcinogens of some sort that causes genetic damage and mutations
Promotion: changes in environment of the body causes growth of mutated cells over normal cells usually caused by over expression of a mutated gene
General symptoms for cancer
Weakness, anorexia and fatigue
Extreme weight loss out of nowhere
Changes in bowel/bladder habits
Sores that don’t heal
Rectal bleeding
Changes in cough and voice (more hoarse)
Staging
Uses the “TNM” formula
T =. Size of the tumor (1-3)
N =. Nodal involvement (0-2)
- 1 = Tumor only in primary nodal chain
- 2 =. Tumor involves primary and secondary nodes
M =. Presence of absence of metastasis
- 0 = n/a
- 1 = met present
- general staging*
- 1 localized tumor
- 2-3 = local and regional
- 4 = metastatic
Types of treatment for cancers
Surgery
- excellent for early stage cancers
- implausible for metastatic
Radiation
- limited to localized tumors and good palliative treatments
- high dose = more damage
Chemotherapy
- given prior to surgery and also to metastatic cancers
- highest chance of causing death
Types of systemic chemotherapy
Neoadjuavant
- CMT given prior to surgery to increase efficacy to surgical resection
- not used for treatment of metastatic
Adjuvant
- CMT used to eradicate micrometastatic disease
- following up surgery and is used against treatment of metastatic disease
Palliative
- CMT given to decrease tumor size and prevent symptoms caused by presence of tumor
Significant clinical importance of the cell sizes of tumors
10^5 cells = angiogenic switch initiates (tumor gains its own blood supply)
10^9 (1g) cells = clinically can be detected before imaging
10^ 12 (1kg) cells = death of patient
Remission occurs between 10^1 - 10^9
- because it is difficult to detect before 10^ (1g), this is why cancer is difficult to cure and can come back*
Log cell kill model
A constant fraction of cells are killed by a dose of chemotherapy and not a constant number of cells.
* most common is 3-log kill drugs*
Alkylating agent MOAs
Interferes with DNA replication via attaching carbon chains to DNA strands and cells, preventing cell replication and marking cells for death.
Why are Nitrosoureas unique compared to other alkylation agents?
Only type of alkylation agent that can cross BBB, so used to treat brain tumors
Vinca alkaloids MOA
Bind to tubulin and prevents production of them. Cell cant complete mitosis and therefore the cell is marked for death
M-phase specific
Taxanes MOA
Exact opposite of Vinca alkaloids. Produces way to much tubulin in cells and causes cell arrest during mitosis, marking it for death
m-phase specific
Antimetabolities MOA
3 classes all of which function to inhibit various enzymes required for DNA synthesis
Antibiotics MOA
Bleomycin =. Binds to iron creating free radicals and causes DNA breakage
Dactinomycin = inhibits DNA polymerase indirectly by binding to DNA strands
Anthracyclines =. Binds to DNA and generates free radicals within it as well as inhibits topoisomerase 2
Mitomycin C = alkylation of DNA again
Chemoman
Diagram that helps show adverse side effects for specific chemos
Chemoprotective agents
Reduce side effects of specific chemotherapy agents
- 2% sodium thiosulfate solution = lowers nitrogen mustard damage
- hydration and Mensa = Neutralizes cyclophosphamide and ifosfamide metabolite “Acrolein” build up in the kidney
- leucovorin = antagonizes methotrexate and can be used to prevent toxicity
- Dexrazoxane = cheating agent that binds to free radicals caused by anthracyclines and limits bystander heart damage
