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cancers
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cancers, in general
-Involves uncontrolled growth of cells
-Higher incidence in men over age 55 (mostly prostate / breast)
-Second-leading cause of death in the US
-Many people can survive cancer tho
-screening is ESSENTIAL
immune cells’ roles in fighting cancer
Cytotoxic T cells: Kill tumor cells & produce cytokines
Natural killer cells and activated macrophages lyse tumor cells
B cells produce antibodies that bind to tumor cells
roles of the immune system in fighting cancer
goal: to reject or destroy cancer cells
Some cancer cells have changes on their surface antigens called Tumor-Associated Antigens (TAAs) → the immune system recognizes these as cancerous thru Immunologic Surveillance
Thru Immunologic Escape, cancer cells evade our immune system (suppressor T cells, blocking antibodies bind TAAs, preventing recognition)
genetic link to cancers
2 types of normal genes that can be affected by mutations:
Protooncogene – Fxn: regulates normal cellular processes. Mutations can alter them to function as oncogenes (these can change a normal cell to a malignant one)
Tumor-suppression genes – Fxn: regulates cell growth & cell cycle. Mutations can make them inactive.
Ex- BRCA-1, BRCA-2, APC gene
classifications of tumors: benign vs malignant
-Benign – well-differentiated (early cancer, restricted to one area)
-Malignant – can invade and metastasize in other areas of the body (vascularized & grow quickly)
histologic classifications of cancer
Appearance of the cells and the degree of differentiation
Grade 1 – differs slightly from normal cells and are well differentiated
Grade 2 – more abnormal and moderately differentiated
Grade 3 – More abnormal and poorly differentiated
Grade 4 – Immature and primitive and undifferentiated; cell of origin is difficult to determine
Grade 5 – cannot be assessed
clinical staging of cancers
Determines the extent of the disease process of the cancer
Stage 0 – cancer in situ (localized and shows no tendency to invade or metastasize)
Stage I – tumor growth limited to the tissue of origin
Stage II – limited local spread
Stage III – extensive local and regional spread
Stage IV – metastasis (invasion of other tissues)
oncofetal antigens & tumor markers
Malignancy signs, found in both cancer cells & fetal cells. Occurs as a result of the cells un-differentiating into stem cells
Ex: CEA (colon cancer), AFP (liver cancer), CA-125 (ovarian cancer), CA19-9 (pancreatic and gallbladder cancer), PSA (prostate cancer), CA 15-3 & CA 27-29 (breast cancer)
Tumor markers: kRAS (colon), HER-2 (breast)
Early warning signs of Cancer (CAUTION)
C- change in bowel / bladder
A- a lesion that won’t heal
U- unusual bleeding / discharge
T- thickening or lump you can feel
I – indigestion or difficulty swallowing
O- obvious changes in a mole
N- nagging cough or persistent hoarseness
diagnoses of cancer
BIOPSY is key
Cytology studies, Chest x-ray, CBC, chemistry profile, Liver function studies, Endoscopic examinations, PET scan, Tumor / genetic markers, Molecular receptor status (ex- estrogen and progesterone), Bone Marrow examination
TNM classification system
determines the extent of the cancer disease process
T - Tumor size
T 0 – no evidence of primary tumor
Tis – Carcinoma in situ (all histologic features of cancer except invasion)
T 1-4 – Ascending degrees of increases in tumor size
N - Degree of regional spread to the lymph nodes
N 0 – No evidence of disease in lymph nodes
N 1-4 – Ascending degrees of nodal involvement
N x – Regional lymph nodes unable to be assessed clinically
M- Metastasis
M 0 – No evidence of distant metastases
M 1-4 – Ascending degrees of metastasis, including distant nodes
rTNM
Restaging done after extensive Tx
stages of cancer
Initiation (stage I) → mutations in cellular genes
Promotion (stage II) → reversible proliferation of the altered cells (lowering dietary fat, obesity, cigarette smoking, alcohol consumption, and stress)
A complete carcinogen –> initiator and promotor (smoking)
Latent period (1-40 yrs) comprises both the initiation and promotion stages (period where there are cancer cells present, but no mass). For the disease to become clinically evident, the cell must reach a palpable 1cm mass
Progression (Stage III) → Increased growth rate, invasiveness, & metastasis of the tumor
Metastasis is the spread of the cancer from the primary site to a distant site
chemical carcinogens
Certain chemicals over a period of time have a greater incidence of cancer
ex- benzene, arsenic, formaldehyde, and certain drugs
increase risk of leukemia
Tx for radiation exposure
Take potassium iodide to decrease risk of thyroid cancer
Don’t use any moisturizer -> it retains the radiation
The younger the person, the higher their risk of getting radiation cancer
Wash the body, Burn their clothes
After a radiation bomb, stay inside for 14 days (stock up on food & water)
viral carcinogens
Certain viruses, termed oncogenic, induce malignant transformation in the cells they infect.
Burkitt’s lymphoma – from EBV (mono can increase risk of this)
Kaposi’s sarcoma – from AIDS
Hepatocellular carcinoma – from hepatitis B virus
Cervical, anal, head/ neck cancer - from Human papillomavirus
radiation carcinogen
Exposure to radiation damages the cells
Higher incidence of cancer in occupations like radiologists, radiation chemists, aircrews, and uranium miners.
Leukemia & lymphoma -> After the Atomic Bomb in Hiroshima/Nagasaki
Thyroid cancer -> from receiving head and neck radiation
Skin cancer -> UV radiation from tanning beds
biology of cancer: proliferation & differentiation
proliferation: the body’s cells are programmed to divide every so many days, depending on if they are healthy. In cancer, the cell will divide regardless whether or not it’s healthy → so if it’s mutated, this mutation will carry on. Cells that multiply with these problems create a pyramid effect
healthy cells also have contact inhibition-bladder cells remain in the bladder, etc. This doesn’t happen with cancer cells
differentiation: in a biopsy of a healthy cell, it clearly looks like the type of cell that it is. But in cancer, it has mutated so much that its original type of cell is unrecognizable (it has un-differentiated, possibly into a stem cell)
well-differentiated cell = good sign
un-differentiated/ de-differentiated cell = a bad sign, the cancer has spread & they can’t tell the original site
cancer Tx in the cell cycle
chemo Txs target cells in a specific stage of their cell cycle. This is why chemo tx often includes multiple drugs, to target cancer cells in multiple stages