TUMOR PATHOLOGY Flashcards
neoplasia
abnormal tissue growth and it persists even after a stimuli
hyperplasia
increase in the number of cells
hypertrophy
increase in the size of the cell
difference between a malignant and a benign
malignant is invasive while benign is non invasive
benign neoplasm
slow growing encapsulated and smooth well circumscribed.
atrophy
decrease in the organ due to the reduction of the size and or the number of cells
could be physiological or pathological .
arrangement of a tissue
the epithelium
mucosa + connective tissue
glands
metaplasia
complete change of the form of a cell that is from stratified to squamous
which tumor is inflammtory
malignant
characteristics of benign neoplasm
may compress organs
in some cases may cause pain if they are in the brain or if they compress a nerve.
examples of benign tumors
osteoma
shwannoma
angioma
fibroma
adenoma
papilloma
adenocarcinoma
invasive cancer of the glandular tissue
type of malignant cancer
Breast adenocarcinoma
Prostate adenocarcinoma
Lung adenocarcinoma
Lung squamous cell carcinoma
Colorectal adenocarcinoma
Melanoma
Lymphoma
leukamia
sarcoma
all neoplasms are tumors
true
carcinoma and sarcoma
types of malignant tumors
apoptosis
regulated cell death
oncogenes
from mutated proto-oncogenes that can now cause cancer
physical characteristics of cancer cells
1.hyperchromatic that is more DNA inside
2.coarse chromatin because they are ready to divide
3.pleomorphic - they are not of the same size
4.disorganised structure.
5.highly mitotic and abnormal forms.
6.bigger nucleus
behaviour of cancer cells
have unregulated growth
loss of cohesion
there is immaturity
immortality
replicative immortality
fully functioning telomerase that keeps on adding the telomeres .
they replicate and never die
activation of invasion and metastasis
ability to invade the connective tissue and cause metastasis
ability of cancer cells to gain oxygen and nutrients
through angiogenesis
angiogenesis growth factors are switched on while inhibitors are switched off.
ability to resist cell death
apoptosis caspaces are altered
cancer cells effect on cellular energetics
they use glycolytic metabolism
there is intake of alot of nutrients with production of less ATP.
Ability to increase in number
proliferative growth factors that alters the cell cycle
the growth receptors are also altered
ability to evade growth suppressors
that is tumor suppressor genes
alteration of p53
some tumor cells mediate a tumor associated inflammatory response
yes or no
carcinogenic and necrosis
there is release of cellular contents into the interstitium
this causes an inflammatory response
metastasis
spread of cancer cells through loss of cell to cell adhesion ,
loss of cell to ECM adhesion molecules
metastasis methods
Local spread
Lymphatic spread
Haematogenous spread
Trans-coelomic spread
metastasis through the lymph nodes
invasion of the connective tissue
entry to lymphatics
travel through lymphatics
exit of the lymphatics
entry to the lymph node
growth in the lymph node
trans - coelomic spread
-spread through the body cavity
in the peritoneal ; gastric , colonic , ovarian
-pleural that is the lung
local effects of cancer
pain
haemorrhage
loss of function
local effect on the brain
confusion
coma
seizure
local effect of tumor on the lungs
dyspnoea
haemoptysis
local effects of tumors on the liver
jaundice blockage of the gall bladder.
coagulopathy that is because of the blockage of the proteins that are used in coagulation.
local effects of cancer in the colon
diarrhoea
constipation
haemorrhage
local effect of the tumors on bone
anaemia
pain
fracture
systemic effects of cancer
cachexia
DVT
paraneoplastic syndrome
cachexia characteristics
weakness and wasting due to chronic illness
loss of muscle is greater and faster than fat loss.
paraneoplastic syndrome
abnormal production of hormones the hormones have systemic effects.
examples of hormone production that is altered by cancer
PTH
ACTH
ADH
DVT
deep vein thrombosis
tumor pressing on the blood vessel makes the diameter smaller and the flow of blood is altered making the blood more stickier.
what is pre cancer
dysplasia
that is disordered cell growth and doesnt involve spread
what is neoplasma
Abnormal growth of cells, uncoordinated with normal tissue and continuing even after cessation of stimulus
wilson and junger principles of screening
look at the photo
molecules involved in signal trasduction in a cell
the receptor for growth factor
the growth factors as ligands
the amplification system that is the messenger molecule and other molecules involved.
example of a signal transduction molecule
BRAF
cell cycle inhibitors
p53
retinoblastoma
factors that cause inhibition of a molecule
change in the structure
change in the molecule that is attached
retinoblasma
normal molecule that causes inhibition past the checkpoint
addition of a phosphate group by CDKs causes a change that inhibits Rb form being an inhibitor.
longest phase of the cell cycle
G1 phase
how does growth factor cause progression past the G1 phase restrictor
the growth factors eg amino acid levels and glucose levels.
role of the growth factors
they ellicit a pathway that cause the amplification of molecules leading to phosphorylation of the RB molecule.
cells that have inactive growth factor receptors that come together to form the active receptor when the growth factor binds
HER2
molecule responsible for damaged DNA repair
p53
rationale of p53
1.blocks the formation of phosphorylated Retinoblastoma
2.damaged DNA repair.
location of action of p53
both G1 and G2M
mismatch repair genes
they help recognise and replace DNA bases and induces p53 to stop the cell cycle .
oncogene
A mutated gene that can cause cancer
mutation of malignant melanoma
BRAF
sources of mutation
smoking
sunlight
inheritance
de novo mutations
sources of DNA damage
radiation
chemotherapy
example of a cancer caused by MLH1
colon cancer
how does smoking cause cancer
Numerous chemicals in cigarette smoke metabolised to carcinogens in liver released into circulation damage DNA numerous mutations eg mutations in p53
sunlight UV radiation and cancer
the UV radiation causes gene mutations in the p53 gene which causes increased risk in cancer.
human papilloma virus and cancer
produces the E6 protein that binds and inactivates p53 which causes increased risk of uncontrolled cell division.
Infection of cervix produces E6 protein which binds and inactivates p53. [Also produces E7 protein which binds and inactivates retinoblastoma gene product.] Increased risk of subsequent uncontrolled cell division precancer cancer
c myc protein
Increases proteins which push the cell towards cell division
Proteins produced which promote cell division
cymc and cancer
if cymc breaks off and joins an immunoglobulin regulatory sequence the cells are pushed forward in the cell cycle and the cells are stopped form dying and this promotes cancer.
cancers formed by translocation of the cymc sequence
lymphoma
name of the cymc translocation
This translocation is called t(8;14) [note that the left over bit of chromosome 8 joins the other left over bit of chromosome 14 as well.
how do environmental factors contribute to cancer
they cause the cell to be abnormal therefore increasing susceptibility to cancer.
how does alcohol cause cancer
large amounts of acetylaldehyde which goes to the systemic circulation and causes double stranded breaks of DNA in many genes which causes an increased risk of cancer.
they also cause damage of numerous genes such as p53
Human papilloma virus
Infection of cervix produces E6 protein which binds and inactivates p53. Also produces E7 protein which binds and inactivates retinoblastoma gene product. Increased risk of subsequent uncontrolled cell division precancer cancer
epstein barr virus
virus that infects B cells
causes B cells to proliferate
