Chapter 5 Flashcards
cancer
uncontrolled cell growth
probabilities of developing cancer
50% in women
33% in men
most prevalent type of cancer
males= prostate
females= breast
most prevalent death rates for certain cancer
lung cancer for both male and female
what is the cancer incidence trend
downwards
are poor countries at higher or lower risk for cancer deaths
higher
are blacks at higher or lower risk for cancer deaths
higher
neoplasm
new uncontrolled cell growth
unsure if benign or malignant
tumor
non-specific term meaning lump or swelling
hypertrophy of cells
metastasis
discontinuous spread of malignant neoplasm to distant sites
how does cancer metastasize
through blood or lymphatics
malignant
capable of metastasis
cancer
any malignant neoplasm or tumor
how are metaplasia and neoplasia similar
both are increased cell proliferation
how are metaplasia and neoplasia different
neoplasia does not have a stimulus for cell proliferation
how can you tell the difference of different masses
biopsy and fine needle aspiration
hyperplasia treatment
remove stimulus
may need to remove hyperplastic tissue if it interrupts other tissues
what are the factors of neoplasm treatment
depends on benign or malignant and site
malignant neoplasm treatment
curative therapy (chemotherapy, radiation, surgery)
palliative therapy
how are neoplasms distinguished
benign vs malignant
how they differentiate
benign neoplasm
grows slowly, does NOT metastasize
well differentiated
looks like normal cell
malignant neoplasm
grows rapidly, can metastasize
less differentiated
-oma
naming of neoplasms
does NOT distinguish between benign or malignant
hematoma
big bruise
carcinoma
malignancy of epithelial cells
sarcoma
malignancy of connective tissue
what is the most common form of cancer w/age
carcinoma
melanoma
cancer of melanocytes
lymphoma
cancer of lymphoid tissue (lymphocytes)
what causes cancer
loss of genomic integrity
what leads to a loss of genomic integrity
damaged DNA from mutations
what cells are involved in loss of genomic integrity
germline cells (can be passed on)
somatic cells (can NOT be passed on)
how are mutations acquired
carcinogens, inherited, spontaneous
carcinogens
environmental factors
inherited mutations
BRCA1 and BRCA2
type of environmental carcinogens
ionizing radiation, virus (Hepatitis, HPV), UV rays, dietary (alcohol, smoked meats), chronic inflammation
hallmarks of cancer
- self sufficiency in growth signals
- insensitivity to growth-inhibitory signals
- evasion of apoptosis
- limitless replicative capacity
- sustained angiogenesis
- tissue invasion and metastasis
- evade immune surveillance
what drives changes of cancer hallmarks
gene mutations
gene mutations
oncogenes, tumor suppressor genes, DNA repair genes
proto-oncogene
involved in cell growth and division
NORMAL CELLS
oncogene
proto-oncogene that was activated by mutations
examples of oncogenes
HER2, RAS
HER2 gene
encodes growth factor receptor
RAS gene
relays signals from cell surface
when is RAS active
GTP bound
when is RAS inactive
GDP bound
what does mutating do to RAS gene
leaves RAS permanently on
tumor suppressor genes
stop cell cycle
p53
guardian of genome
regulates transcription of genes
when are p53 levels high vs low
high in damaged cells
low in healthy cells
is cancer resistant to apoptosis
yes
why is cancer resistant to apoptosis
inactivate pro-apoptotic proteins
activate anti-apoptotic proteins
upregulate telomerase
DNA repair genes
correct errors from DNA replication
chromosomal instability
chromosome arrangement is altered
imbalance of chromosomes
increases inflammation
is inflammation a hallmark of cancer
yes
immune system in tumorigenesis
immune system protects host against tumor growth while promoting it by releasing reactive oxygen species
what are hits
mutations
multiple hits =?
multiple mutations
when do malignancies develop
through premalignancy
dysplasia
premalignant state but does not always progress to malignancy
tissue is atypical, usually epithelial
carcinoma in situ (CIS)
cancer in place (does NOT move)
not invasive
can cure by removing all of tumor
invasion
release of proteases
how does neoplastic growth start
monoclonal
monoclonal
all the same type of cell
how does neoplastic growth end
tumor cell heterogeneity
heterogeneity
cells will have different mutations
tumor growth fraction
ratio of proliferating cells to total cells
malignant neoplasms invasion
must secrete proteases to digest and break down collagen
malignant neoplasms metastasis
seeding, spread to another organ
moves via blood vessels and lymphatics
seeding
spreading to another organ
angiogenic growth factors
needs glycolysis to spread
paraneoplastic tumor
cancer cells mediated by humoral factors released into blood
non-metastatic manifestations of malignancies
examples of paraneoplastic tumors
hormones (cushing syndrom)
cross-reacting antibodies (reacting to self)
where are paraneoplastic tumors common
lung, breast, ovaries, lymphatics
immune surveillance
immune system surveys host cells to identify abnormalities
what cells are involved in immune surveillance
natural killer cells
cytotoxic T cells
why are immunodeficient patients more at risk for cancer
loss of t cell ability
cytology
looking at cells
ways to obtain cells
biopsy, resection, fine needle aspiration
grading
microscopic assessment
how abnormal do de-differentiated cells look
staging
behavioral assessment
size & extent of metastasis
how big/aggressive tumor is
can cancer cells differentiate to greater or lesser degree
yes
well-differentiated neoplasms
grow slowly, benign or malignant, slow to invade and metastasize
poorly-differentiated neoplasms
grows rapidly, malignant, high number mitotic figures (how many cells are going through mitosis), aggressive invaders and metastasize early
anaplastic
looks different than what it should
tumor grading
TMN
stage 0
CIS
stage I
cancer is not spread into surrounding tissues
larger than stage 0
stage II
may extend to nearby tissues
stage III
spreads to nearby lymph nodes, but not other parts of body
stage IV
spreads to distant tissues and organs
most diagnoses, hard to treat
tumor markers
substances appear in blood, not used for early cancer detection
what are tumor markers useful for
confirmation of diagnosis
monitor therapy
examples of tumor markers
prostate specific antigen (PSA)
breast cancer-CA-15-3
