GI Cancer Flashcards
what is the pre-invasive term for severe dysplasia in the breast
ductal carcinoma in situ lobular carcinoma in situ
What staging does M1 represent in the Dukes and AJCC staging
Stage 4/Dukes D
where do sessile serrated adenomas typically arise
proximal colon
what layer breach has to happen for metastasis of the prostate
basal cell layer
what is the pre-invasive term for severe dysplasia in the glans penis
Erythroplasia of Queyrat
high risk types of HPV
16 and 18
what is the pre-invasive term for severe dysplasia in the skin
Bowen’s disease
what layer breach has to happen for metastasis of the colon
muscularis mucosae
what are the differences in macroscopic growth patterns between colorectal cancer in the proximal and distal colon
proximal - bulky, polypoid, exophytic distal - annular, stenosing, ulcerated
what are the serology hallmarks of HPV infection
koliocytosis p16 upregulation
main two causes of familial colorectal cancer
- lynch syndrome - familial adenomatous polyposis
what is interchangeable with carcinoma in situ
intraepithelial neoplasia dysplasia
What staging does T1 represent in the Dukes and AJCC staging
T1
what is the pre-invasive term for severe dysplasia in the bladder
carcinoma in situ
what is the metaplastic result of chronic atrophic gastritis
intestinal metaplasia
what are the main histological features of sessile serrated adenoma
- complex branching - boot-leg angulation and dilatation at base of crypts - elongated, vesicular nuclei, prominent nucleoli - increased atypia
what is attenuated variation of FAP
when you have
Explain the stages of Dukes’ classification system of colorectal cancer
A - invades into, but not through bowel wall B - invades through bowel wall, but not involving lymph nodes C - lymph node metastases D - distant metastasis
how does APC mutation lead to FAP
decreased cell adhesion and increased cellular proliferation
what layer breach has to happen for metastasis of the oesophagus
basement membrane
which two oncogenes are the most common oncogene mutations in colorectal cancer
K-RAS, B-RAF
what are the precursor lesions for colorectal carcinoma
adenomatous polyps
what does lynch syndrome cause other than higher chance of getting colorectal cancer
- extracolonic cancers
morphology of the types of adenomatous polyps
- tubular adenoma - sessile or pedunculated - villous adenoma - often large and sessile - tubulovillous adenoma - mixed features
what kind of genetic pathway does Lynch syndrome fall in to cause colorectal cancer
microsatellite instability
which two TSG are most often associated with colorectal cancer
SMAD4, SMAD2 and p53
What are the 2 staging systems of colorectal cancer
Dukes’ classification Australian ClinicoPathological Staging system
what layer breach has to happen for metastasis of the breast
myoepithelial cell layer loss
what are the 3 types of genetic pathways that can lead to colorectal cancer
- chromosomal instability - microsatellite instability - CpG island methylator phenotype
what is the gene mutation that causes Familial adenomatous polyposis
APC mutation
what gene does HPV integrate into and effect
E2 gene
what is the metaplastic result of chronic reflux oesophagitis
Barrets oesophagus
difference between mild/low grade dysplasia and moderate dysplasia
moderate - abnormal cells go to full thickness
what layer breach has to happen for metastasis of the cervix
basement membrane
what types of cells are in the cervical transformation zone
squamous epithelium and glandular epithelium
what are the dysplastic features of adenomatous polyps
- crowded cells –> push up to become pseudostratified - enlarged, hyperchromatic, pseudostratified nuclei - abnormal complexity to glandular architecture - goblet cell depletion - increased mitotic count
what is aneuploidy
distorted number of chromosomes with lots of switching between chromosomes
Which TSG is implicated in breast cancer
Her 2
which mutation is commonly associated with sessile serrated adenoma
BRAF mutation
What staging does T3 represent in the Dukes and AJCC staging
Stage 2/Dukes B
what are the main mutations of DNA mismatch repair genes in colorectal cancer
- MSH2 or MLH1 - sporadic MLH1 hypermutation
what defines epithelial cancer
invasion of cells across the BM
what is the most common familial colorectal cancer syndrome
lynch syndrome
criteria for identifying dysplasia of the oesophagus
- surface maturation of glandular mucosa - architecture of glands –> crowding, change in shape and complexity. Glad fusion (feature of malignancy) - cytology of proliferating cells –> nuclear atypia, loss of polarity - response to inflammation and erosions/ulcers
how many polyps do you have to have to be classed as having familial adenomatous polyposis
100
where does dysplasia normally start in the epithelia
at the lower levels (near the stem cells)
Barretts oesophagus is a key precursor for what
oesophageal adenocarcinoma
diagnostic criteria for Barretts oesophagus
- endoscopic evidence of columnar lining in oesophagus above gastroesophageal junction AND - histological evidence of intestinal metaplasia (goblet cell) in biopsies from the columnar epithelium
what does the overexpression of genes E6 and E7 do (from HPV)
E6 binds p53 –> apoptotic resistant, loss of G1/S and G2/M phase cell cycle check points, genomic instability E7 binds Rb –> disrupts G1/S phase cell cycle checkpoint, compensatory upregulation of P16
what could be the reasons for early onset colorectal cancer
- familial syndromes - chronic inflammatory bowel disease
what is the pre-invasive term for severe dysplasia in the endocervix
adenocarcinoma in situ
predictors of increased malignant risk of adenomatous polyps
- polyp size (>1cm) - villous morphology - high grade dysplasia (severe crowding, loss of nuclear polarity, pleomorphism, gland fusion)
how is lynch syndrome inherited
autosomal dominant - inherited mutation in a DNA mismatch repair gene
What staging does N1 represent in the Dukes and AJCC staging
Stage 3/Dukes C
what does disruption of the E2 gene do on the viral plasmid
- overexpression of E6 and E7 oncoproteins - loss of p53 and Rb tumour suppressor function - cell cycle can proceed despite DNA damage - loss of p53 apoptosis function
what is the main genetic pathway that leads to sporadic colorectal cancer
chromosomal instability
Colorectal cancer high risk features
- high grade - T3 with localised perforation or T4 - close, indeterminate or positive margins - lymphovascular invasion -
what is the difference between diagnosis of barrett’s oesophagus from American college of gastroenterology and from the UK/Japan
presence of goblet cells no required for diagnosis for Japan/UK
where does HPV like to live
tropism for basal keratinocytes such as the cells of the transformation zone
what histology do the cells within adenomatous polyps show
- abnormal crypt architecture - dysplasia - no invasion beyond muscularis mucosae
explain the stages of the Australian clinciopathological staging system
A - invades beyond muscularis mucosa B - invades beyond muscularis propria C - lymph node metastases D - Distant metastasis
