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pathophysiology > lecture 10 cancer > Flashcards

lecture 10 cancer Flashcards

1
Q

all cells have…

A

several mechanisms/ genes to control (promote/ inhibit) growth
- constant renewal (hair follicles, gut lining)
- stable, but can renew/multiple rapidly when stimulated (hepatocytes, T cells)
- permanent, no renewal/ regenerative capacity (cardiac muscle, neurons)

tight regulation of cell cycle (so cells stay in their lane)

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2
Q

loss of control of cell cycle:

A

development of cancer - development from a single clone that escapes cell cycle regulatory control

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3
Q

cancerous tumors are characterized as: (3 ways)

A

benign vs malignant

solid (embedded but distinct from tissue) vs. invasive (mixed within host tissue)

in situ (one location where first formed) vs infiltrating (growth spread into surrounding tissue)

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4
Q

carcinogens

A
  • create mutations in DNA that disrupt a cell’s normal processes for regulating growth, leading to uncontrolled cellular proliferation
  • for most solid tumors in humans, latency period is between 10 and 40 years
  • degree of carcinogenicity can be route dependent (absorption, ingestion, inhalation, injection)
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5
Q

types of carcinogens and exposure types

A

-synthetic chemicals (asbestos, smoking, pollutants)
- naturally occurring substances (plant/ fungal toxins, Radon)
- radiation (X rays, UV)
- biologic agents: viruses and bacteria (direct/ indirect)
- aging

exposure types:
- lifestyle (obesity/ inflammation/food) - 97%
- occupation (wood dust, asbestos, radiation)
(environmental ones are most of our exposure)

group 1(carcinogenic to humans) –> group 2a (probably) –> group 2b (possibly) –> group 3 (not classifiable)

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6
Q

benign

A

slow, expansion, localized, well-differentiated, consider damage

SLOW GROWTH
growth character: expansion
remains LOCALIZED (can still do damage through growth - brain tumor) pushes - not infiltration
WELL-DIFFERENTIATED cells (closely resemble cells of origin) - primary factor to classify benign vs metastatic
- must consider damage to tissue replaced and damage from tumor volume/ position (remember that this is replacing healthy tissue and damage can create issues based on how much space it has)
- easily resectable by surgery

*sharp demarcation between the tumor and surrounding breast tissue

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7
Q

malignant

A

rapid, infiltrating, metastasis by bloodstream and lymphatics, poorly-differentiated

  • RAPID GROWTH
  • growth character: infiltrating
  • tumor spread: METASTASIS by BLOODSTREAM or LYMPHATIC channels to establish secondary sites that can also grow and spread (colon spread to liver, breast/ lung to brain)
  • degree of metastasis often defines cancer STAGING
  • cell differentiation: POORLY-DIFFERENTIATED cells (meaning you can’t tell what they are anymore, they don’t look like normal cells)
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8
Q

tumor classification - BENIGN

A

PREFIX-(cell of origin) and SUFFIX (oma)

prefixes and their meanings:
adeno = gland
angio = vessels
chondro = cartilage
fibro = fibrous tissue
hemangio = blood vessels
lymphangio = lymph vessels
lipo = fat
myo = muscle
neuro = nerve
osteo = bone

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9
Q

tumor classification - MALIGNANT

A

most fall into 3 groups:
- carcinoma
- sarcoma
- leukemia/ lymphoma

*have longer names than benign!!

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10
Q

carcinoma

A

EPITHELIAL TISSUE
- arise from surface, glandular or parenchymal epithelium
- most common: 85% of all tumours found in skin, large intestine, glands, stomach, lungs, prostate
- metastasis: LYMPH VESSELS
- subtypes: further classified by cell type or origin and organ
-adenoCARINOMA (ie. of pancreas - glandular/ secretory cells)
- squamous cell carcinoma (skin)

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11
Q

sarcoma

A

CONNECTIVE TISSUES (fat, bone, cartilage, muscle)
- arise from endothelium, mesothelium
- less common but SPREADS more quickly
- LITTLE DIFFERENTIATION; anaplasia (lack of form)
- metastasis: BLOODSTREAM
- fibroSARCOMA (fibroblasts) myoSARCOMA (muscle)
*muscle heart cells and brain cells don’t have a high risk of cancer because they don’t divide much)

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12
Q

leukemia

A

neoplasm (cancer) of blood cells
- usually not solid tumors
- instead, proliferates diffusely within BONE MARROW, overgrows and CROWDS out normal blood-forming cells
- neoplastic cells spill over into bloodstream and large number of abnormal cells circulate in the peripheral blood
- if they populate LN and spleen: LYMPHOMA (T/B cell)

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13
Q

neoplasm development

A
  • stepwise process, ongoing series of GENETIC CHANGES over time (NOT JUST ONE EVENT)
  • earlier stages have chance of resolution, control by immune surveillance/ destruction

cervical cancer ex.
- commonly begins in cervical cells in transformation zone (two types of cells meet/border)
- columnar epithelium (cervical canal leading to uterus) and squamous cells of cervix exposed in vaginal canal - particularly during sexual maturation
- columnar cells exposed to acidic environment of vagina are prone to metaplasia (conversion to different cell type) and become squamous cells (dysplasia)
- this process is susceptible to neoplasia and develop cervical intraepithelial neoplasia (CIN) - risk increased in HPV infection

*most cancers aren’t just from one mutation, often 3-4 until you get to carcinoma stage!!

*normal –>. mild dysplasia (CIN: abnormal growth starts)–> moderate dysplasia –> severe dysplasia –> carcinoma in situ

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14
Q

growth of neoplasms

A

cancers do not usually result from mutation of a single gene!

cancers occur as the result of MULTIPLE GENETIC INSULTS TO THE GENOME
- activation of oncogenes
- loss of function of one or more tumor suppressor genes
- additional random genetic changes (cell cycle/ growth/ death) - promotes growth or inhibits death

most cancers are MONOCLONAL - derive from a single cell, some cancers can have HETEROGENEITY if they derive from a stem cell

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15
Q

stem cell in cancer:

A

early in development, has the potential to become many different types of cell
- results in tumor with HIGH DEGREE OF HETEROGENEITY

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16
Q

tumour blood supply and necrosis

A

fast growing neoplasms may outgrow blood supply (can be used as a therapeutic target)
- tumors get blood from tissues they INVADE
-malignant tumors frequently induce NEW blood vessels to proliferate in other normal tissues to supply the demands of the growing tumor (ANGIOGENESIS)
- malignant tumour may OUTGROW its blood supply; the part of the tumour with the POOREST blood supply undergoes NECROSIS

  • often, small blood vessels are exposed in ULCERATED parts of a tumor, leading to ANEMIA from chronic blood loss
  • an ulcerated tumor may be the source of a SEVERE HEMORRHAGE

anything not fed properly goes through necrosis - metastasis can occur much easier!

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17
Q

central necrosis

A

blood supply is best the the periphery of the tumor and poorest at the center (lung tumors)
- necrotic area in the middle

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18
Q

peripheral necrosis

A

if tumor is growing outward from an epithelial surface (colon)… blood supply is best at the base and poorest at the surface
- necrotic area peripheral/ surface

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19
Q

genetic change in neoplastic disease

A

alteration of genes so cell no longer responds to normal control mechanisms (uncontrolled proliferation)
-in genes governing cell cycle (growth/ death - inhibition or promotion) and DNA repair

  • can be caused by: radiation, carcinogens, viruses - failure of DNA repair/ fidelity mechanisms
  • failure of immune defenses
  • over time these can accumulate (age development)
  • can also be inherited susceptibilities to developing cancer

*usually before cancer, genetic change can impair ability to control cell proliferation and make you more susceptible to cancers
- you can also INHERIT genes with genetic mutations that make you more susceptible (ex. BRCA1/2)

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20
Q

cancer PROMOTING genes associated with carcinogens (3 groups)

A

proto-oncogenes
tumor-suppressor genes
DNA repair genes

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21
Q

genetic change: proto-oncogenes

A

promote normal cell growth
malfunction: point mutation, amplification, or translocation forms an oncogene, resulting in UNRESTRAINED CELL GROWTH

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22
Q

genetic change: tumor-suppressor genes

A

inhibit (or control) cell proliferation (and division)
malfunction: BOTH genes INACTIVATED in same cell, PROMOTES CELL PROLIFERATION

  • genes expressed in a pair of HOMOLOGOUS CHROMOSOMES
  • BOTH (one from each parent) need to be deactivated for things to happen (PREDOMINATES in cases where ONE defective gene is INHERITED)
  • they BLOCK mitosis completion and DNA replication to suppress cell proliferation
  • loss of function by mutation –>unrestrained cell growth
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23
Q

2 ways mutations can happen to tumour-suppressor genes

A

HEREDITARY:
- infant inherits nonfunctional RB gene from parent
- functional one keeps division controlled unless acquired mutation
- higher risk!! need only 1 mutation

SPORATIC:
- all body cells have two normal RB genes
- 2 random mutations happen
- lower risk!!! need 2 mutations

ex. retinoblastoma gene (RB)

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24
Q

genetic change: DNA repair genes

A

controls errors in DNA duplication
malfunction: gene inactivation INCREASES MUTATION RATE

  • BOTH must be DEACTIVATED (similar to tumor-suppressor genes)
  • replication ongoing repair can be compromised!!

*they should be able to help repair DNA, if this gene is messed up then you can’t fix DNA

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25
Q

proto-oncogene (Philadelphia chromosome)

A
  • seen in chronic granulocytic leukemia (translocation of pieces of chromosome 9 and 22) - Philadelphia chromosome
  • proto-oncogene abl (22) becomes fused with bcl (9) results in UNCONTROLLED and OVERACTIVE tyrosine kinase that stimulates rampant cell growth (very aggressive cancer)
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26
Q

genes regulating apoptosis

A

programmed cell death
- influence survival time of cells
- cells have pro and antiapoptotic proteins (genes to control)
- if gene fails or over regulated -LOSS OF APOPTOTIC CONTROL!!!
- cells continue to accumulate
- cells eventually form a tumor

most commonly effects seen with genes that promote cell survival/ growth (BCL-2, Bcl xl, MCI-1)
- these genes are key regulators. If they are overactive, they encourage cell survival, which can disrupt normal apoptosis and contribute to tumor growth.

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27
Q

genetic changes leading to cancer: colon cancer

A

mostly, cancers do not result from a single mutation event, but MULTIPLE accumulated events over time
- INITIAL mutation DESTABILIZES GENOME and allows next event

  • accumulation in mutations in tumor-suppressor genes
  • activation of oncogenes (mutated oncogenes)
    *these can BOTH lead to cancer

ex. colon cancer develops after…
- accumulation of 3 tumor suppressor genes (mutated) - APC, DCC, p53
- activation of an oncogene (Ras) - a mutated protooncogene

  1. first mutation: normal colon cancer (loss of APC gene)
  2. second mutation: small polyp, benign (oncogenic mutation in Ras gene)
  3. third mutation: large polyp, benign (mutation or loss of p53 function)
  4. invasive colon cancer, malignant
    throughout, tumour suppressor genes are lost/ mutated, and protooncogenes are activated to oncogenes
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28
Q

cancer causing viruses (oncogenic viruses)

A

leukemia/ lymphoma: T cell leukemia-lymphoma virus (HTLV-1) related to HIV virus (tax oncogene)

kaposi sarcoma: human herpesvirus 8 (HHV-8)

condylomas (warts): papilloma virus (HPV), predisposed to cervical carcinoma

chronic viral hepatitis: hep B and C viruses (chronic inflammation/ repair)

nasopharyngeal carcinoma: ebstein-barr virus (EBV aka HHV-4) also causes infectious mononucleosis (infects B cells and epithelial cells)

cancers caused by viruses can be a targeted EFFECT of VIRAL INFECTION (HTLV) or a random side effect from CHRONIC INFLAMMATION (HCV) or DNA INSERTION (HIV - retrovirus)

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29
Q

hereditary and tumors

A
  • most mutations that cause cancer are NOT directly inherited
  • predisposition results from multifactorial inheritance pattern
  • at risk individual has inherited SET OF GENES that influence hormonal or enzyme-regulated biochemical process in the body that can INCREASE SUSCEPTIBILITY to a specific cancer
    (you can inherit a set of genes that make you more susceptible)

ex. breast cancer (autosomal dominant)
- 80-90% of cases: no family history of the disease
- 10% of cases linked to gene mutation
- abnormal BRCA 1/2 DNA REPAIR GENES - 80% risk of breast cancer by age 90

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30
Q

inheritance of certain genetic alterations that have increased cancer risk (generally account for small amount of cancers)

*these are rare, most aren’t inherited directly

A
  • breast cancer susceptibility genes BCRA1/2
  • Ph1 chromosome
  • multiple polyposis of colon - prone to development of COLON POLYPS that are prone to malignancy (autosomal dominant)
  • neurofibromatosis - increased production of benign tumors of the NERVES that have increased risk of malignancy (autosomal dominant)
  • multiple endocrine adenomatosis - formation of multiple ENDOCRINE ADENOMAS (autosomal dominant)
31
Q

diagnosis of tumors (2 considerations)

A

early recognition - symptoms/ screening (age dependent)

precancerous conditions
- change in bowel or bladder habits
- sore throat not healing
- unusual bleeding/ discharge
- thickening or lump in breast or elsewhere
- indigestion or difficulty swallowing
- change in wart or mole
- nagging cough or hoarseness

32
Q

precancerous conditions

A

NONMALIGNANT condition with a tendency to become malignant - visual/ physical exam

precancerous conditions should always be treated appropriately to PREVENT MALIGNANT change, which occurs in many, but not all, cases

33
Q

precancerous conditions: actinic keratoses

A

small, CRUSTED SCALY patches that develop on sun-exposed skin

34
Q

precancerous conditions: lentigo maligna

A

FRECKLE-like proliferation of MELANIN-producing cells, may develop on sun-exposed skin and transform into melanoma

35
Q

precancerous conditions: leukoplakia

A

thick, WHITE patches in MUCOUS membranes of the MOUTH from exposure to tobacco tars from pipe or cigar smoking or smokeless tobacco (snuff or chewing)
- may give rise to SQUAMOUS cell cancers of the oral cavity

erythroplakia - RED patches, associated with higher than leukoplakia

36
Q

diagnosis of tumors (2 steps, and what screening programs need to consider)

A
  1. recognize early warning signs/ symptoms
  2. complete medical history and physical exam

screening programs need to consider INVASIVENESS/ SEVERITY, COST/ BENEFITS
- surface - visual
- orifice (holes) - endoscopy
- internal - CT scan/ MRI

37
Q

cancer screening (A,B,C,D,E)
(melanomas- skin cancer)

A

Asymmetry
(if you draw a line through middle of mole, halves of melanoma won’t match in size)

Border
(the edges of an early melanoma tend to be uneven, crusty, or notched)

Colour
(a variety of colours (especially white and blue) is bad. healthy moles are uniform in colour)

Diameter
(melanomas are usually larger in diameter than a pencil eraser, but they can be smaller)

Evolving
(when a mole changes in size, shape, or colour, or begins to bleed or scab, this points to danger)

38
Q

screening programs in Ontario

A

there are a lot of cancers that need screening because you can’t see them right on the skin

BREAST CANCER: 50-74, mammography every 2 years
- high risk: mammography and MRI every 2 years (personal or family history or positive genetic testing BRCA1/2, TP52, PALB2)

CERVICAL CANCER: 21-70, sexually active
- regular pap test (HPV) every 3 years

COLON CANCER: 50-74, high risk (fam history) any age
- fecal immunochemical test (blood in stool) every 2y (low risk)
- colonoscopy every 5-10y (high risk)

LUNG CANCER: high risk only, 55-74, smoked 20+ years (at any time)
- CT scan (annual for 3 years)

39
Q

lab procedures for diagnosis of tumors

A
  1. examination of rectum and colon, stomach esophagus (ENDOSCOPY)
  2. CBC (complete blood count) - elevated WBC in ABSENCE of infection
  3. x-ray/ CT/ MRI studies
  4. abnormal smear: slides of abnormal cells shed from surface of tumors (pap)
    - Pap smear: a cluster of abnormal cells from in situ carcinoma of the cervix (cells look different than surrounding squamous epithelial ones)
  5. biopsy: endoscopic procedures
  6. cytologic diagnosis: fine needle aspiration, biopsy (many organs - precise location of tumor by CT, x-ray, or ultrasound)
  7. histology: frozen section slides prepared and stained - rapid histological diagnosis in minutes
  8. determine primary (where it starts)/ secondary (where it spreads to)
    - secondary brain tumor 4x more common than primary brain tumor (secondary from lung/ breast)
    - important to know where the tumor started
40
Q

diagnosis of tumors: tumor-associated antigen test

A

some cancers secrete substances that can be detected in the blood with lab tests

41
Q

diagnosis of tumors: tumor-associated antigen test
CARCINOEMBRYONIC ANTIGEN (CEA)

A
  • present in amounts related to size of tumor and possible spread
  • produced by most malignant tumors of the GI tract, pancreas, breast
  • CEA level falls after resection of colon cancer but then rises when tumor recurs, indicating need for more tx
42
Q

diagnosis of tumors: tumor-associated antigen test
ALPHA FETOPROTEIN

A
  • normally produced by fetal tissues in placenta but not adult cells
  • elevated in primary carcinoma of liver
43
Q

diagnosis of tumors: tumor-associated antigen test
HUMAN CHORIONIC GONADOTROPIN

A
  • normally elevates by placenta in pregnancy
  • elevated in testicular carcinoma
44
Q

diagnosis of tumors: tumor-associated antigen test
PSA TEST (acid phosphatase)

A
  • normally produced by prostate epithelial cells
  • may be elevated in prostate cancer
  • only 1 in 4 positive tests are from cancer (23-42% of those may never require tx, so is it useful?
  • misses 15% of cancers (sensitivity of 85%)
45
Q

TNM classification

A

T (size 1-4)
N (spread to regional LN 1-3)
M (distant metastasis 0-2)

useful for tx and px!!

46
Q

staging I-IV

A

depending on spread

I - early
II - localized
III - regional spread
IV - distant spread

47
Q

treatment: surgery

A

better success when benign (non-invasive), decreases with malignancy/ metastasis (tumor and surrounding tissues)

48
Q

treatment: radiotherapy

A

cancer is radiosensitive
- can be used to shrink tumor/ remove remaining cells

49
Q

treatment: hormones

A

corticosteroids can inhibit growth; some tumours are hormone-dependent (prostate, breast - testosterone/ estrogen)

50
Q

treatment: anticancer drugs (chemo)

A

variety of drugs: goal is to interfere (preferentially) with cancer cell growth and have acceptable damage to non-cancerous cells
- work best against FAST growing cancers

51
Q

treatment: adjuvant chemo

A

used in combination with surgery to remove residual cells that may not be removed/ detected

other:
- can have precise targets in some cases - but usually broad effects leading to a number of side effects
- philadelphia mutation (BCR-ABL cr 22 abnormality) - susceptible to tyrosine kinase inhibitors

52
Q

treatment of tumors: considerations

A

need to consider age/ health/ success

53
Q

chemotherapy

A
  1. can be BROAD OR TARGETED
  2. 3-6 months with 4-8 cycles of 3-4 weeks (pulsing/ recovery)
  3. induction (1 month intensive), consolidation (few months), maintenance (2-3 years)
  4. alkylating agents: INHIBIT DNA synthesis, structure or function (DNA replication)
  5. ELIMINATES cells that divide quickly, INHIBIT protein synthesis, mitotic spindle (cell division)
  6. Target GLYCOLYSIS (cancer specific property)
    - normal cells use oxidative phosphorylation for energy metabolism (70) but cancer cells use glycolysis
    - 70/30, cancer = almost all glycolysis
  7. susceptible cells and rapidly dividing cells found in:
    - mouth, skin, hair, bone marrow, digestive tract, kidneys, bladder
    - lungs, nervous system! (not all), reproductive system
    - lymphoid cells particularly vulnerable
  8. normal cells recover quickly, side effects dissapear gradually
  9. how soon the patient will feel better depends on overall health, types of anticancer drugs used
54
Q

side effects of chemotherapy

A
  1. ANEMIA
    (extreme fatigue, weakness, tiredness, paleness, dizziness experienced by MORE than half of patients REDUCES BONE MARROW’s ability to make RBCs)
  2. CONSTIPATION/ DIARRHEA
    (drugs, decrease in physical activity, unbalanced diet)
  3. DEPRESSION
    (physical and emotional stress)
  4. HAIR LOSS
    (alopecia)
  5. INFECTION
    (due to reduced ability of bone marrow to produce WBC)
  6. LOSS OF APPETITE
    (ANOREXIA, nausea, vomiting)
  7. MOUTH, GUM, AND THROAT PROBLEMS
    (sores)
55
Q

sexual/ reproductive side effects of chemo

A

men: affects sperm cells, temporary or permanent INFERTILITY

women: irregular periods, vaginal infections, menopause-like symptoms, INFERTILITY

56
Q

radiation therapy and its side effects

A

DAMAGES DNA to disrupt growth of cancer (shrinks cancer)

side effects:
- nausea
- fatigueness
- soreness
- lymphedema
- hair loss
- irritation and damage (specific to region treated)
- cancer

57
Q

radiation therapy: external beam

A

(most common)
- 15 min/ week, 5x/ week for 3-9 weeks
- more targeted, but tissue around tumor can be damages

58
Q

radiation therapy: internal radiation

A
  • tablet, liquid IV, or brachytherapy
  • implant to deliver radioactive dose DIRECTLY to tumor
  • LESS SIDE EFFECTS compared to external
    (implants can be in place for days, or permanent. to treat smaller tumors: prostate, cervical, womb cancers)
59
Q

surgery: things to consider…

A
  • patient health/ survivability (risks)
  • resectability (get it all out)
  • operability (access)
  • other tx options
  • organ transplant/ bone marrow transplant (for bloodborne cancers you need to replace stem cells)

goal is to remove tumor and surrounding tissue
- often used WITH CHEMOTHERAPY (surgery x chemo) - often need multiple treatments

60
Q

failure of immunologic defenses

A
  • failure to control viral replication and/or recognize tumor cells as foreign (they are self after all!)
  • immune checkpoint inhibitors (control immune response) inhibit development of autoimmunity (also interfere with attacking cancer cells - have to overcome reaction to self)
  • severe immunocompromised = increased risk for blood and skin cancer (Kaposi sarcoma - HIV, aging, chemo, drugs)
  • CANCER CELLS have many defenses to protect themselves from immune attack (decreased MHC expression or exhibit immune suppressing functions)
  • IMMUNE SYSTEM can detect and destroy cancerous cells (CD8 T CELLS, NK CELLS)!!!
  • SUPPRESSION OF IMMUNE SYSTEM = HIGH RISK/ PROGRESSION OF CANCER
61
Q

immune system’s methods of controlling cancer

A

CD8 (CYTOTOXIC) T CELLS: destroy cancer antigens presented by MHC1

NK CELLS: destroy cells expressing stress signals, deficient MHC1 expression

MACROPHAGES: destroy tumor cells by phagocytosis

ANTIBODIES TO TUMOR ANTIGENS: tag tumour cells for destruction by macrophages/complement

62
Q

immunotherapy

A

stimulating the body’s immune response to ATTACK CANCER

NONSPECIFIC:
- cytokines

SPECIFIC:
- tumor-infiltrating lymphocyte therapy
- tumor vaccines
- tumor antibody therapy

63
Q

non-specific immunotherapy

A
  • use of CYTOKINES to stimulate immune system and/ or inhibit tumor cells (get rid of cancer cells)
  • less toxic (flu symptoms)
  • promote antiviral effects or promote immune system

IFN ALPHA
- general antiviral effects
- inhibition of tumor growth
- useful in leukemia, multiple myeloma

IL-2
- stimulates NK cells and CD8 (cytotoxic) T cells
- used in metastatic melanoma, renal cell carcinoma

but, stimulating the immune system can be very dangerous - cytokine storm

64
Q

specific immunotherapy

A

immunotherapy targets: (specific to tumor itself)

65
Q

specific immunotherapy: administration of CD8(CTL) directed against tumor

A

pt cells are removed and primed/ reprogrammed to attack tumor - then reintroduced

66
Q

specific immunotherapy: CAR-T therapy

A

genetic TCR alteration (specifically modify T cells)

67
Q

specific immunotherapy: dendritic cell therapy

A

activation of dendritic cells in presence of tumor antigens

68
Q

specific immunotherapy: anti-tumor vaccines

A

tumor antigens from patient used to immunize patient against recurring disease after resection

69
Q

specific immunotherapy: anti-tumor antibodies

A

specific antibodies directed against tumor, sometimes linked with antitumor drug (chemo) or toxin (radioactive)

70
Q

specific immunotherapy: drugs to remove blockades that are inhibiting immune function

A

prevents tumor immune suppression functions (CTLA-4, PD1, PD-L1)

71
Q

specific immunotherapy: oncolytic viruses

A

(vaccinia, vesicular stomatitis virus)
- preferentially infects and kills cancer cells, stimulate anti tumor immunity
- attenuation (only grows in cancerous cells, tumor targeting by direct destruction or flagging immune system)

(engineering a virus that can only divide in cancerous cells and destroy them)

72
Q

survival rates in cancer

A

1 in 4 people will eventually develop cancer
- lung cancer: most common for males (smoking)
- breast cancer: most common for females

varies widely (4% to more than 99%)
- prostate/ thyroid cancer: 98-99% 5-year survival rate
- PANCREATIC cancer: 7% 5-year survival rate (WORST)

  • 5-year survival does not indicate cure; sometimes types RECUR, prove fatal (breast cancer, malignant melanoma)
  • 5-year survival rate reflects treatment/ screening success - NOT CURE

early diagnosis and treatment may enhance survival rate
chances for survival significantly REDUCED after tumor METASTASIZES to regional lymph nodes or distant sites

MAIN GOAL: detect cancer before metastasis

*pancreatic cancer is low 5-year survival but breast, prostate, and thyroid are all relatively high!

73
Q

neoplasm

A

abnormal mass of tissue that forms when cells grow and divide more than they should or do not die when they should

74
Q
A

pathophysiology (10 decks)

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