Evolutionary Biology of Cancer: Tumour Heterogeneity and Treatment Options

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18 Questions

The article discusses both the punctuated equilibrium and gradualism models for clonal evolution in cancer.

True

The punctuated equilibrium model is considered a more accurate representation of cancer growth according to the article.

True

Cancer treatment options usually become more specific to clones that have undergone a selective sweep.

True

Clone-specific treatments may be ineffective if there are sub-clones lacking the mutant target.

True

Tumor heterogeneity is not an important factor to consider when looking at treatment options for cancer.

False

According to the article, cancer cells evolve solely through the gradualism model.

False

According to Nowell, there are six steps in the model of clonal evolution.

False

If a mutation is a driver mutation, it will lead to clonal expansion.

True

Most of the sub-clones formed due to genomic instability will survive in the tumour environment.

False

The dominant sub-clone in a tumour can be replaced when a newly generated sub-clone outcompetes it.

True

In the clonal evolution model, a selective sweep occurs when a sub-clone fails to survive due to metabolic disadvantage.

False

Punctuated equilibrium model is one of the five steps proposed by Nowell in the clonal evolution model.

False

Tumour heterogeneity does not play a role in conferring evolutionary advantages or disadvantages.

False

The Cancer Stem Cell Hypothesis and the Clonal Evolution Model are completely unrelated concepts.

False

The gradualism model suggests that evolution occurs in rapid, abrupt changes.

False

Tumour heterogeneity refers to the presence of only one type of cell in a tumor.

False

The punctuated equilibrium model proposes that evolution happens gradually over long periods of time.

False

Cancer growth is a simple and uniform process without any complexities.

False

Explore the impact of tumour heterogeneity on treatment options for cancer, emphasizing the importance of considering clone-specific treatments and sub-clones lacking mutant targets. Understand how advanced/metastatic cancer requires more specific treatments targeted at particular clones. Delve into the evolutionary biology of cancer and its implications for personalized medicine.

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