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CancerGen > Tumour Classification > Flashcards

Tumour Classification Flashcards

1
Q

Clear Diagnosis is important for what?

A

Prognosis and treatment of the individual, as well as understanding causation and prevention

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2
Q

What do patients want to know about a cancer?

A

Their chance of cure.
Prognosis.
Treatment options.
Risk to family.
Risk of progression of something benign

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3
Q

What do clinicians want to know about a cancer from classification?

A

To weight the risks and benefits of treatment.
To know prognosis.
Treatment options.
The likelihood and impact of identifying an actionable driver.

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4
Q

What are the different types of classification?

A

Benign Vs Malign.
Tissue/Organ of origin.
Depth of invasion, spread. TNM (Tumour Node Metastasis).
Tumour Grade - how aggressive and differentiated.
Molecular identification using DNA/RNA.

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5
Q

What are some benign lesions?

A

Fibroma. Naevus. Metaplastic lesions (cell type has changed to another).

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6
Q

What are some malignant lesions?

A

Leiomyosarcoma, colorectal adenocarcinomas, melanomas.

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7
Q

Is it just a matter of benign vs malignant? Why?

A

No, because some benign lesions have a propensity to become malign in the future.

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8
Q

What feature of a benign lesion should make us more worried, and why?

A

Metaplastic (external stimuli cell turns cell to different type) -> Dysplastic (internal signal turns cell to abnormal version of itself). Because then the curative window before they become carcinomas is small.

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9
Q

To better identify malignant and benign lesions we need to better identify what else?

A

Normal tissue

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10
Q

What will clear biomarkers enable?

A

Identify drivers of transition, predict progression, detect early, prevent over diagnosis.

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11
Q

What are aspects of dysplastic tissue?

A

Crowding of cells, multilayer growth, nuclear atypia, disruption of normal architecture.

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12
Q

Why is looking for dysplasia not good enough to identify cancers early?

A

A tumour can transition too quick through dysplasia?

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13
Q

Which organs get the most cancers? (not specific organs)

A

Those exposed to the most carcinogens. Those affected by hormonal changes. Those with a high cell turn over.

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14
Q

Organ of origin may impact aggressiveness which is:

A

Rate of growth and metastasis. Impacts survival.

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15
Q

Organ of organ may cause local issues such as:

A

Glioblastoma - little space in brain, can cause significant symptoms.
Pancreatic cancer - Damages digestion ability, leads to muscle wasting

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16
Q

Organ of origin can largely impact therapy response, be it sarcoma, carcinoma, etc. Tell me about this with respect to CRC, gastric, esophageal and breast cancers.

A

CRC has a poor response to Taxol.
Anthracyclines have little benefit in gastric or esophageal cancer, but is the cornerstone of breast cancer treatment.

17
Q

Knowing the tissue of origin can guide genetic tests, how and why?

A

Certain tissues are exposed to certain mutagens, which tend to produce particular changes in specific oncogenes. So we know which tests to be running.

18
Q

Why is BRAF V600E often in melanomas?

A

UV causes C>T mutations at CT dinucleotides.

19
Q

What specific mutations do the carcinogens in smoking often cause?

A

KRAS G12C.

20
Q

How many different cell types might be in the lung?

A

50

21
Q

Sarcomas are rare tumours from what type of cells?

A

Connective Tissue cells

22
Q

Neuroendocrine cells in the lung are what type of cell?

A

Epithelial sub type.

23
Q

What are 3 types of tumour from neuroendocrine cells of the lung, each with a very different prognosis?

A

Carcinoid, Large Cell NEC, and Small Cell NEC.

24
Q

SCC oesophageal cancers respond much better with neoadjuvant chemoradiotherapy than AC oesophageal cancers. What are these two types in full?

A

Squamous Cell Carcinoma respond better than Adenocarcinomas.

25
Q

What are the 2 main ways we differentiate the tissue of origin of a tumour?

A

Histopathology - Tumours do de-differentiate but may retain some features of the original tissue (e.g. maybe a glandular structure in the colon, would be a likely adenocarcinoma).
IHC - For lineage specific proteins. E.g. Cytokeratins for Epithelial.

26
Q

In terms of Grade (Aggressiveness), why does degree of differentiation correlate with the outcomes?

A

Because its harder to classify when cells are de-differentiated. And because differentiation and proliferation are inversely related.

27
Q

Why are differentiation and proliferation inversely related from a cell signalling point of view?

A

Because cyclin-CDK complexes push the cell cycle, and phosphorylate (inactivate) the transcription factors for differentiation.

28
Q

What does TNM stand for for classification purposes?

A

Tumour, nodes, metastasis

29
Q

In terms of the T measurement, which grades the primary tumour, what does it look at?

A

How far through the layers towards the blood vessels it has infiltrated etc.
Size (Bigger is harder to resect without damaging healthy tissues).
Risk of fistula (connection between two organs that shouldn’t be) formation from radiotherapy.

30
Q

In terms of the N grading what does it look at?

A

The number of locally draining lymph nodes the cancer has spread to. More nodes = poorer outcomes

31
Q

When does a cancer become classed as metastasis?

A

When it’s spread to distant nodes or another site.

32
Q

What’s basically the only type of metastasis that can sometimes be cured at 20-30% rate?

A

CRC spread to liver.

33
Q

Fancy grids are used for what purpose with TNM?

A

Used to calculate a total stage to predict prognosis

34
Q

We’ve moved beyond histo and TNM with what 3 aspects are there to molecular classification?

A

DNA, RNA and epigenetics

35
Q

How does knowing a cancer is MMR deficient guide prognosis and treatment?

A

These cancers have good prognosis, but they should not be treated with adjuvant chemotherapy

36
Q

What percentage of lung cancers can be categorised purely by oncogenic driver mutations, which has a bigger impact on response than the TNM classification?

A

30%

37
Q

We’re particularly progressing in our breast cancer classification using microarrays and RNA seq. How many strong prognostic grouping do we see based on their expression?

A

We see 5 subtypes.

38
Q

What helped us move from 2 types of gastric cancer to 4 types?

A

Huge TCGA studies where info was pooled together, giving us more power to differentiate them

CancerGen (18 decks)

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