tumour pathology 1-5 Flashcards
what is a benign glandular epithelium called
adenoma
what is a malignant glandular epithelium called
adeno-carcinoma
what is a benign squamous epithelium called
squamous
papilloma
what is a malignant squamous epiyhelium called
squamous carcinoma
what is a benign bone cancer called
osteoma
what is a malignant bone cancer called
osteo-sarcoma
what is a benign fat tumour called
lipoma
what is a malignant fat tumour called
lipo-sarcoma
what is a benign fiborous tumour called
fibroma
what is a malignant fibtous tissue called
fibro-sarcoma
is there a benign white blood cell tumour
no
what’s the name of a malignant WBCs cancer (more specificly bone marrow)
leukaemia
what are the types of tumour in lymphoid tissue
no Benign
malignant = lymphoma
what are the cancers associated with melanocytes
naevus - benign
melanoma - malignant
what are the tumours in the central nervous system
Astrocytoma
what are the tumours in the peripheral nervous system
Schwannoma
what are germ cell tumours called
Teratomas
what are teratomas made off
what is the difference between ovarian and testicular
various tissue
ovarina teratoma is benign
testicular teratoma is usually malignant
what are the features and ‘‘break out’’ of a malignant tumour
invasive
can have the presence of a capsule however BREACHING will ocur
poorly differentiated
loss of normal function
what are the type of tumours that are well differntiated
benign
what is the top 3 cancers overall
breast then lung then prostate
what are the top - 5yr survivable cancers
melanoma - 90
breast - 85
prostate - 85
uterus - 80
what are the properties of cancer cells releated to genes
loss of suppressor genes
gain of function of oncogenes
what are some of the suppressor genes
APC
Retinoblastoma
RAC1
what are some of the oncogenes
B-raft
Cyclin D1
what are the other properties of cancer
altered function
independent/unregulated growth
tumour biomarkers
what is important to remember about cancer cell properties
no single feature is unique to cancer cells
how is cell function altered
loss of cell to cell adhesion
cell to extracellular matrix is lost
production of tumour biomarkers
what are tumour bio markers used for
Screening
Diagnosis
Prognostic
Predictive - response to therapy
what dose the biomarker kras detect
colorectal cancer
what dose braf detect
melanoma
‘bra your skins messed up’
what dose EGFR detect
lung cancer
EGs Fucking Resps
what dose Her 2 detect
BREAST CANCER, gastric cancer
what dose a Carcino-embryonic antigen (CEA)
suggest
colorectal cancer
what dose the presence Alpha-fetoprotein
Hepatocellular carcinoma
Teratoma of testis(malignant)
what happens to the morphology of a cancer cell
cellular and nuclear pleomorphism
variation in shape and size
what are the two factors that control tumour growth
angiogenesis
apoptosis
what is tumour angiogenesis
new blood vessel formation by tumour
why is tumour angiogenesis important
required to sustain tumour growth
route of metastasis
more blood vessel = poorer prognosis
what is apoptosis
Mechanism of programmed single cell death
what dose it regulate and what is it involved in
regulates tumour growth
involved in chemotherapy and radiotherapy
what is the basic out line of tumour spread
normal tissue – tumour – metastasis
what is trans-coelomic spread
type of local spread
across body cavities
pleural/peritoneal cavities
what are the modes of spread
local
lymphatic
blood
trans-coelomic
what is local spread
invasion into the connective tissue
they site of metastasis is..
not related to tissue blood flow
what is a metastatic niche
the role played by a tumour depending on its characteristics and tissue
what are the most common metastasis locations
Liver
Lung
Brain
where are the least like spread
Spleen
Kidney
Skeletal muscle
where dose breast and prostate canner commonly metastasise
in the bone
what are the local effects of a benign tumours
pressure and obstruction
what dose a benign tumour usually put pressure on
the GI tract
blood vessels
what are the local effects of malignant tumours
pressure
obstruction
tissue destruction
bleeding
Pain
what dose the bleeding caused by malignant tumours do
lead to haemorrhage
lead to anaemia
what does the tissue destruction caused by malignant tumours lead to
ulceration and infection
what can the pain of a malignant tumour be down to
pressure on nerves
perineural infiltration bone fractures
what tumours have systemic effects
malignant tumours
what are the systemic effects of a malignant tumour
weight loss
secretion of hormones
paraneoplastic syndromes
EFFECTS CAUSED BY TREATMENT
how dose cancer effect hormone secretion
normal hormones produced - however volume is all over the place (endocrine)
abnormal - a hormone that usually isn’t produce from the organ
what are the two hormones that are abnormal for lung cancer
ACTH
ADH
what are Paraneoplastic Syndromes
no one really knows
symptoms in tissues nowhere near the tumour site
immune mechanism
why is it important to detect cancer early
Reduce/prevent morbidity/mortality
what has been identified when a caner is detected at a pre-invasive stage
dysplasia
intraepithelial neoplasia
what is Dysplasia
how is it graded
a pre-malignant change (earliest pin of detection)
high grade - develop into cancer sooner
low grade - develop into cancer later
where is it identified and
Identified in epithelium
No invasion
But can progress to cancer
what are its features
disorganisation of cells
Increased nuclear size
Increased mitotic activity
Abnormal mitoses
what is a intra-epithelial neoplasia
is the development of a HIGH GRADE dysplasia
what dose early detection require
Requires effective test Sensitive/specific Acceptable cheap political backing
what is an example of early detection
Cervical Cancer Screening
reduce incidence of squamous carcinoma of cervix
detects dysplastic cells in that region
what is the basic process of the cell cycle
inter phases
mitosis
cytokinesis
m1, s, m2 P M A T cytokinesis
what is G0
a stage of dormancy
how do CDKs work
cyclin binds and lets them phosphorylate subunit which allows the cycle to continue
what are CKIs
inhibitor molecules that bind to the cyclin/CDK complexes
what are some examples p16/p21
what is the Retinoblastoma gene
Encodes a phosphoprotein (pRb) expressed in almost every human cell
the breaks
what happens when pRB is hypophosporlyated
it becomes active and
cell stays at G1
how are the breaks turned off
when the cDK/cyclin complexes pRB
what happens when pRB is phosphorylated
it looses affinity to E2F
what is E2F
powerful signal for cell cycle activation
what is the process of carcinogenesis
Uncontrolled proliferation of cells forms tumours
what are the two frequently disrupted pathways in carcinogenesis
the cyclin/CDK complex—pRB–E2F pathway
p53 pathway
what dose p53 detect
DNA damage
what dose NORMAL p53 do
detects damage
and either repairs
activates p21 (CDK inhibitor)
or kills the cell
what dose BAX do
cause cell death apoptosis
what happens if p53 is mutated
leads to the DEREGULATED proliferation of cells that have damaged DNA
how is the cyclin/CDK–pRB- E2F pathway stopped
the tumour suppressor gene turns off the production of pRB
what do cells with mutated p53 proliferate to form
malignant neoplasms
what factors can cause carcinogenesis
Environmental agents
Chemicals
Radiation
Oncogenic viruses
Inherited factors
what are proto-oncogenes
a normal gene that codes for normal growth regulation
growth factors and their receptors
what is the two hit hypothesis
in a video game everyone has two lives but some people only have one
its the hypothesis that certain mutations occur more often if people who have been given a copy of a mutated gene
an example of the two hit hypothesis
inherited retinoblastoma
what are tumour suppressor genes
how will cancer occur
example
anti-oncogenes
act as the emergency elevator breaks
Loss of both normal allelic copies
p53
how may people inherit cancer
what will it look like
5-10%
early onset of multiple tumours
what do p16s do
what cancer occurs if they mutate
inhibits CDKs
malignant melanoma
what are oncogenes
Derived from proto-oncogenes with gain of function
alteration of structure - point mutation or translocation
overexpression
what is BRAC1/2
a tumour suppressor gene
what is an example of a proto-oncogene
what dose it do
how is it activated
Her2 -
EGF receptor
VEGF
amplification
lead to breast ovarian and gut
how dose chemical carcinogenesis occur
DNA is critically damaged by oxidizing and alkylating agents - it binds to the DNA (adducts)
leading to the loss of anti-oncogenes and the mutation of proto-oncogenes
what is Radiation carcinogenesis
as it says on the tin
DNA damage
what are Viral carcinogenesis
examples
viruses insert genome with a oncogene
or something that mutates a proto-oncogene
HPV - genital
HEP B - liver
how is tumour formation is a multi-step process
what is needed
sporadic cancers need
several oncogenes
loss of anti-oncogenes
happens with mutations over time
what are examples of anti oncogenes
p16, cyclin D, CDK4, Rb
