null
US
Sign In
Sign Up for Free
Sign Up
We have detected that Javascript is not enabled in your browser. The dynamic nature of our site means that Javascript must be enabled to function properly. Please read our
terms and conditions
for more information.
Next up
Copy and Edit
You need to log in to complete this action!
Register for Free
61157
Characteristics of major tumour types
Description
Blood Science Mind Map on Characteristics of major tumour types, created by maisie_oj on 29/04/2013.
No tags specified
blood science
blood science
Mind Map by
maisie_oj
, updated more than 1 year ago
More
Less
Created by
maisie_oj
over 11 years ago
77
0
0
Resource summary
Characteristics of major tumour types
Commonest cancers
Males
Lung/bronchus
Prostate
Colorectal
Pancreas
Non-hodgkins lymphoma
Females
Breast
Lung/bronchus
Colorectal
Pancreas
Ovary
Lung cancer
Most common cause of cancer mortality
Major risk factor is smoking
Increasing in women (reflecting changing smoking patterns)
Outcome is uniformly poor - 5yr survival rate in ~15%
Aetiology and pathogenesis
Smoking!
Major carcinogens = polycyclic aromatic hydrocarbons, phenol derivatives and radioactive elements
Associated with other tumours: Mouth, larynx, oesophagus, pancreas, kidney, cervix and bladder
Classification
Squamous cell carcinoma - 25-40%
Adenocarcinoma - 25-40%
Small/"oat" cell carcinoma - 20-25%
Large cell carcinoma - 10-15%
Squamous cell carcinoma
Occurs in the proximal lung
Associated with precursor squamous metaplasia
Molecular changes
p53 mutation
EGFR over expression
Her2/neu over expression
Microscopically - Squamous cell mass often enclosing a keratin pearl
Adenocarcinoma
Occur in the distal lung
Increasing in frequency (particularly in women)
Related to low-tar cigarettes(?)
Metastasise widely
Less frequently associated with smoking than other types
Small cell (aka oat cell) carcinoma
Highly malignant neuroendocrine tumour
Frequently produce ectopic hormones - e.g. ACTH (= ectopic/paraneocrine Cushing's disease)
Proximal location - associated with smoking
Molecular changes
p53
RB
Surgery is ineffective - treated with chemotherapy
Breast cancer
Risk factors
Female
Age: 75% occur >50yrs, mean age is 64yrs
Pregnancy: protected if full term, however increased risk of pregnant <30yrs
Family histroy: Increases with each 1st degree relative
Race: lower incidence, but more aggressive disease in Africans
Aetiology
Uknnown
Genetic factors: 5% sue to inherited mutation: BRCA1, BRCA2 and p53
Estrogen exposure
Oophorectomy reduces risk
HRT increases risk - only if unopposed oestrogen
Lifestyle (diet, exercise, alcohol etc.)
Precursor lesions (progression of tumouregenesis)
Normal (non-proliferative changes)
Luminal cells, with myoepithelial cells
Germline mutation
Loss of apoptosis
Proliferative disease
Atypical hyperplasia
Sel sufficient growth
Carcinoma in situ
Limitless replication
Invasive carcinoma
Angiogenesis
Genome instability
Loss of growth inhibition
Classification of breast cancer
In-situ
Lobular (affects lobules)
Ductal (ducts)
High grade DCIS
Cells no longer resemble normal breast tissue
Extensive growth within the lumen of the duct
Fast proliferation!
Intermediate grade DCIS
Low grade DCIS
Cells appear somewhat normal, but abnormal growth noticeable
Calcification within the lumen
Diagnostic (seen with microscope)
Two forms
Cribiform
Micropapillary
Paget's disease
Malignant, irregular cells (Pagte cells) found in the areola and niple tissue that indicate an underlying breast cancer
Invasive
Lobular
Low frequency (15%), with 54% 10yr survival
Second most common brest tumour
Multifocality
Metastasises (to serous cavities and abdominal organs)
Lacks E-cadherin (next lecture)
Ductal
No special type
High frequency (47%) with 47% 10yr survival
Poorest prognosis
Special types
Tubular
Low frquency (2.3%), with good prognosis (90% 10yr survival)
Low grade tubules occupy >90% of the tumour
Sometimes with cribiform elements (<50%)
Excellent prognosis
Many others; with low frequency and mixed survival rates
Prognostic factors in breast cancer
Tumour type (invasive ductal vs. tubular form)
Tumour grade
Tubule formation - scored as: 1 (>75% tubules); 2 (50% tubules) and 3 (little-no tubules)
Nuclear pleomorphism - scored as: 1-3 (based on appearance and variation of cells)
Mitotic counts - scored as: 1-3 (depending on the mitotic activity)
Lower scores = better prognosis
Tumour size
1-9mm is best prognosis
>20mm significantly reduced prognosis
>50mm worst prognosis
Tumour spread (lymph node involvement)
Better prognosis if no involvement, worse the more lymph nodes involved and metastasis
Biologcial markers
HER2 / ER
Tested by IHC and FISH
Colorectal cancer
The majority of colorectal cancers are glandular
Arise from benign adenomas (polyps)
Well categorised, multistep progression
Adeonomas
Can be tubular or villous
Tubular = classic polyp form (brocoli)
Villous = hyperperplastic villous structure (finger-like)
Behaviour of adenomas
Precursor to carcinoma
Likelyhood of progression
Villous > tubular
Size
Degree of dysplasia (disorganised structure)
Familial adenomatous polyposis (FAP)
Germline mutation in APC (involved in beta-catenin signalling)
Causes dysregulated growth of colorectal glandualr tissue - results in hundreds of polp-adenomas by an early age
Develop invasive carcinoma by mid-20's
Progression of colorectal cancer
Normal colon
Germline (inherited)/somatic (acquired) mutation of supressor genes (first hit)
E.g. APC
Mucosa at risk
Methylation abnormalities and inactivation of normal alleles
Adenoma (benign) formation
Proto oncogene mutations (e.g. K-RAS)
Homozygous loss (LOH) of additional supressor genes, with overexpression of COX-2
E.g. p53
Adenocarcinoma
Additional mutations and gross chromosmal alterations (e.g. telomerase reactivation)
Invades the deeper layers (e.g. submucosa, muscularis propria) of the bowel wall
Staged using DUke's staging
Strong relationship to the outcome
T(IS) - adenocarcinoma restricted to mucosa
T(1) - Breaches muscularis mucosae and enters the submucosa
T(2) - Breaches the muscularis propria (external muscle layer of the bowel wall)
T(3) - Breaches the external serosa (membrane surrounding the bowel)
Second pathway
Microsatelite instability pathway (mutations in mismatch repair genes)
Causes hereditary non-polyposis coli carcinoma
Not preceeded by adenoma formation
Arises due to mutations in DNA mismatch repair genes
When DNA replicates mismatch repair genes act as 'spell checkers'
With mutated MMR genes - mistakes accumulate and results in numerous mutations to supressor genes and oncogenes
Genes affected
MSH2, MSH6, MLH1 and PMS2
Aetiology
Age of greatest risk: 60-79yrs
Dietary factors implicated (much lower incidence in South america and Africa
Low fibre and high red meat diets most at risk
Cervical carcinoma
Occurs at the endocervical transformation zone
Columnar epithelium of the vagina -> squamous epithelium of the cervix
Development
Normal
Cervical intraepithelial neoplasia (CIN) 1
Very mil/mild dysplasia (proliferative phase, with immunosupression)
CIN 2
Moderate dysplasia, with pro-angiogenic epithelial-stromal genomic signature
CIN 3
Severe dysplasia -> carcinoma in situ
Invasive carcinoma
Cause = HPV (see cancer lectures)
Skin tumours
Commonest cancer, but generally the lowest mortality (except melanoma)
Important types are
Squamous cell carcinoma
Cancer arising in the epithelial tissue of the skin
Microscopically
Lymphocyte infiltration of the epidermis
Reduced stromal tissue
Nests of squamous cells with keratin pearls
Abnormal cells (morphology, mitotic activity)
Basal cell carcinoma
Tumour arising from the basal layer of the epidermis
Microscopically
Clusters of tumour cells extending through the dermis
Reduced stroma
Normal appearance basal cells (in palisades at periphery of tumour cell nest) and spindle-shaped cells in the middle of tumour cell nests
(Malignant) melanoma
Benign = naevus (mole)
Pigmented lesions
Frequently asymptomatic
Change in size, colour or shape of a pigmented lesion may signal progression
The extent of the vertical growth phase dtermines the biological behaviour
Progression of melanocyte lesions
Normal skin
Spontaneous DNA mutation (UV exposure)
Naevus (benign)
Further mutations
PTEN, CDKN2A
Radical growth phase (RGP) of melanocytes
Further mutations
E.g. AKT
Vertical growth pahse (VGP), (through basement of epidermis -> into dermis)
Metastatic melanoma
E.g. N-RAS or BRAF
Or epigenetic mutation (e.g. in APC)
Aetiology of SCC and BCC
Both arise in sun-exposed skin
DNA damage through UV light exposure
Immunosupressed individuals have a higher incidence
Both tumours are invasive, but BCC is not metastatic
Show full summary
Hide full summary
Want to create your own
Mind Maps
for
free
with GoConqr?
Learn more
.
Similar
Cell adaptations
maisie_oj
Acute Inflammation
maisie_oj
Haemopoiesis
maisie_oj
Rheumatoid Arthritis
maisie_oj
Haemostasis (part 1: primary haemostasis)
maisie_oj
Haemostasis (part 2: secondary haemostasis)
maisie_oj
Blood transfusion and haematopoietic stem cell transplantation
maisie_oj
Anaemia
maisie_oj
Haemopoietic System Malignancies
maisie_oj
Thrombophilia (hypercoagulability)
maisie_oj
Bone marrow failure syndromes
maisie_oj
Browse Library