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CAN > Renal Cell Carcinoma And Colon Cancer > Flashcards

Renal Cell Carcinoma And Colon Cancer Flashcards

1
Q

Types of RCC

A

Clear cell carcinoma
Papillary
Chromophobe

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2
Q

Features of RCC

A 
Kidneys are retroperitoneal present late 
Haematuria 
Flank pain 
Abdominal mass
Those are triad of features 
More common but less specific features include 
Weight loss 
anaemia 
Fever symptoms related to metastasis
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3
Q

Clear cell carcinoma why is it called this

A

Small masses of cells separated by capillaries
Clear cytoplasm - cytoplasm originally contained lipid this was dissolved when being processed
Cells not processed are yellow due to lipid presence
Some cells black due to haemorrhage

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4
Q

Types of clear cell carcinoma

A

Familial - Von hippel lindau syndrome
Sporadic
Metastatic carcinoma with unknown primary

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5
Q

Von hippel lindau

A

Autosomal dominant
Occurs 1 in 36000
Mean age of presentation 37years
Haemangioblastomas of CNS and retina, pancreatic and renal cysts and renal tumors
Germ line mutation of the VHL tumour suppressor gene

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6
Q

What is the VHL protein involved in

A

HIF

Hypoxia inducible factor pathway

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7
Q

Do VHL tumours form just at the kidneys

A 
No 
Brain spinal cord
Retinal haemangioblastoma and cysts 
Adrenal - phaechromocytoma
Renal cysts 
Pancreatic cysts and cystadenomas 
Epididymal cystadenomas
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8
Q

VHL mutation causes

A

Accumulation of HIF alpha
VEGF
PDGF
TGF alpha

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9
Q

Sporadic clear cell RCC

A

Commonest type
Mean age 61years
Abhorrent VHL gene - found in 75% of sporadic cases
Loss of VHL function important during RCC pathogenesis

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10
Q

RCC common infiltrates

A

Renal vein

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11
Q

Treatment

A 
Radical nephrectomy 
Remove kidney 
Perinephric fat 
Adrenal glands and blood vessel 
Done because primary tumour can extend to the adrenals not a met just grew that far
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12
Q

Happens when tumour becomes high grade?

A

Change in morphology
-> sarcomatoid clear cell
Spindle like

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13
Q

Histology report on nephrectomy specimen

A 
Type of renal cell carcinoma 
Fuhrman nuclear grading
Tumour necrosis 
Local spread- insinus or perinephric fat 
Vascular main renal vein invasion 
Completeness of resection 
Final TNM staging - pTNM
Prognostic indicators
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14
Q

Staging stage 1

A

<4 cm partial nephrectomy

>4cm or multiple - radical nephrectomy

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15
Q

Stage 2,3

A

Normal contralateral kidney -> radical nephrectomy

Solitary kidney -> partial nephrectomy

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16
Q

Stage 4

A

Immunotherapy -> clinical response -> nephrectomy?

17
Q

RCC in adults

A

Mortality rate 40-50%
20% patients present with locally advanced or metastatic disease
30% who undergo surgery will develop mets
Currently available for advanced RCC is immunotherapy with IL 2 and INF alpha with small survival benefit at the price of significant toxicity

18
Q

Colon cancer clinical signs and investigations

A

Malaise
Weakness
Weight loss
Altered bowel habits
Anaemia
Upper GI endoscopy -normal if no oesophageal or stomach lesion
Colonoscopy exam- exophytic ulcerative mass in the colon
Exophytic - proliferating on the exterior or surface epithelium of an organ or other structure in which the growth originated
Lesion is partially obstructing the lumen of the bowel

19
Q

Tissue biopsy results

A

Abnormal tortuous colonic glands
Glands are arranged haphazardly around the tissue
Fibrotic stroma - pink
Cells look blue - nuclei stained blue -> enough to diagnose colon cancer

20
Q

CT exam results

A

Bulky circumferential tumour in colon
Tumour shows pericolic streaking
Haziness around wall of colon tumour is in = tumour is perforating the fat around the colon

21
Q

Treatment

A

Remove diseased part of the colon right hemicolectomy

Tumour is analysed when removed from the patient

22
Q

Analysis

A

Reaches the outer bowel wall surface
Polyps present - pre neoplastic benign but may become cancerous
Enlarged lymph nodes - tumour metastasised to regions lymph nodes
Abnormal glands - larger nuclei
Highly differentiated glands - can be clearly seen well defined
Moderately diff - not as easy to see les well defined
Poor diff - diff to see poorly defined

23
Q

TNM staging T

A 
PT1 tumour invades submucosa 
PT2 tumour invades muscularis propria
PT3 tumour invades through the muscle into subserosa 
PT4a tumour invades adjacent organs 
PT4b tumour invades visceral peritoneum
24
Q

N stage

A

PN0 no lumps nose metastasis
PN1 metastasis in up to 3 nodes
PN2 metastasis in 4 or more nodes

25
Q

M stage

A

PM0 no distant metastasis

PM1 distant metastasis present

26
Q

Dukes classification

A

A tumour confined to bowel wall node neg
B tumour spread beyond muscle node neg
C1 tumour lymph node pos highest node spared
C2 highest node involved

27
Q

Histology

A

Invasive adenocarcinoma poorly differentiated
Invading through the wall reaching serosal surface, pT4
Lymphovascular and perineural invasion
12/25 met nodes pN2
Apical node positive dukes C2

28
Q

Molecular prognostic factors

A

Micro satellite stable/in stable
Majority MSS (micro satellite stable) tumour show chromosomal instability
Aneuploidy, allelic losses, amplification, translocation, mutation of APC, KRas, TP53

29
Q

Mismatch repair genes

A

Indications
Young age multiple colonic tumours, cancer in other organs, family history
Immunohistochemistry
-MLH1, MSH2, MSH6, PMS2

30
Q

MSI-H tumour

A

Proximal colon
Poorly differentiated
Mucinous histology
Increased lymphocytic infiltration

31
Q

What is the clinical importance of MSI-H tumours

A

Sporadic 15%, less aggressive tumours
Microsatellite status should be assessed in all pT3N0 tumours to decide on adjuvant chemotherapy

Lynch syndrome alert patient and blood relatives
Healthy relatives tested - clinically /direct
DNA sequencing of MMR genes
Monitor patients for other cancers

32
Q

Lynch syndrome -

A

Autosomal dominant
Germline mutations of one of the MMR genes
Germline mutations identified by sequencing - genetic test requires patients consent
Young age
Right colon
Assciated with cancers in endometrium, ovary, renal pelvis, ureter, small bowel, stomach and pancreas

33
Q

Loss of MSH2 and MSH6 what is diagnosed

A

Lynch syndrome

Refer to geneticist

34
Q

Loss of MLH1
BRAF not mutated
No MLH1 promoter methylation
Diagnoses ?

A

Lynch syndrome

Refer to geneticist

35
Q

Loss of MLH1
BRAF mutated
MLH1 promoter methylated

A

Sporadic

Not genetics referall

36
Q

Mutations involved ? Can they be targeted with immunotherapy

A

RAS and BRAF

Mab can be used

37
Q

Ras mutations

A

KRas NRAS
Found in 40-45% of colorectal tumours
Mutations occur in codon 12, 13, 61, 117, 146.
Result in constructive activation of the protein
Unlikely to benefit from EGFR mab treatment

38
Q

BRAF mutation

A

8% colorectal cancers
Commonest p.V600E mutation within the kinase activation domain
Poor prognosis if not associated with MSI H status
Not regarded as a negative predictive marker for anti EGFR1 therapy currently

CAN (21 decks)

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