Molecular Mechanisms of Cancer

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Questions and Answers

Which of the following is NOT a typical function of tumor suppressor genes?

  • Repairing DNA mistakes
  • Controlling cell cycling
  • Stimulating cell growth (correct)
  • Encouraging apoptosis

Activating invasion and metastasis refers to cancer cells' ability to repair damaged DNA more efficiently than healthy cells.

False (B)

What is the primary goal of precision medicine in cancer treatment?

To use a patient's genetic profile to guide treatment decisions

__________ are normal genes that encourage cell growth when spurred; however, when mutated, they can cause constant activity, leading to cancerous growth.

<p>Proto-oncogenes</p> Signup and view all the answers

Match the following hallmarks of cancer with their descriptions:

<p>Sustaining proliferative signaling = Cancer cells stimulate their own growth. Evading growth suppressors = Cancer cells ignore signals to stop growing. Inducing angiogenesis = Cancer cells promote blood vessel formation to nourish tumors. Resisting cell death = Cancer cells avoid apoptosis.</p> Signup and view all the answers

Which of the following is a major challenge in cancer therapy, referring to the genetic diversity within a tumor?

<p>Tumor heterogeneity (B)</p> Signup and view all the answers

Immunotherapies work by directly attacking cancer cells using synthetic drugs.

<p>False (B)</p> Signup and view all the answers

A mutation in which of the following genes, responsible for fixing DNA or inducing apoptosis, can lead to cancer if it loses function?

<p>p53 (A)</p> Signup and view all the answers

Flashcards

Proto-oncogenes

Genes that promote cell growth; when mutated, they can cause constant activity, leading to cancerous growth.

Tumor suppressor genes

Genes that control cell cycling, repair DNA, and induce apoptosis; when mutated, cells grow uncontrollably, potentially leading to cancer.

p53 Gene

A gene that normally fixes DNA or induces apoptosis. Mutations can cause cancer if the gene loses function.

Precision medicine

Using a patient's genetic profile to guide treatment decisions, increasing effectiveness and reducing side effects.

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Targeted therapies

Therapies that act on cancer-specific molecules, such as EGFR inhibitors.

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Immunotherapies

Therapies that boost the immune system to fight cancer cells.

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Sustaining proliferative signaling

The ability of cancer cells to stimulate their own growth.

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Activating invasion and metastasis

The process where cancer cells spread to other parts of the body.

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Study Notes

  • Focus is given to the intricate molecular mechanisms of diseases, particularly cancer, and the strategies for devising effective treatments.

Understanding Cancer at the Molecular Level

  • Cancer arises from accumulated mutations in proto-oncogenes and tumor suppressor genes, disrupting normal cell functions.
  • Proto-oncogenes encourage cell growth when spurred; when mutated can cause constant activity, leading to cancerous growth.
  • Tumor suppressor genes control cell cycling, repair DNA mistakes, and encourage apoptosis (“cell suicide”); when these genes mutate, cells grow uncontrollably which can lead to cancer.
  • Mutations in genes such as p53, which usually fixes DNA or induces apoptosis, can cause cancer if the gene loses function.
  • Cancer genome sequencing detects molecular abnormalities and helps personalize cancer treatments.
  • Understanding these mechanisms is vital for creating effective cancer therapies.

Hallmarks of Cancer

  • Sustaining proliferative signaling means cancer cells stimulate their own growth.
  • Evading growth suppressors means cancer cells ignore signals to stop growing.
  • Activating invasion and metastasis means cancer cells can spread to other body parts.
  • Enabling replicative immortality means cancer cells can divide endlessly.
  • Inducing angiogenesis means cancer cells promote blood vessel formation to nourish tumors.
  • Resisting cell death means cancer cells avoid apoptosis.
  • Deregulating cellular energetics means cancer cells change how they produce energy.
  • Avoiding immune destruction means cancer cells hide from the immune system.
  • Genome instability and mutation means cancer cells acquire more mutations, speeding up their growth.
  • Tumor-promoting inflammation means cancer cells cause inflammation that helps them grow and spread.

Precision Medicine and Targeted Therapies

  • Precision medicine uses a patient's genetic profile to guide treatment decisions, increasing treatment effectiveness and reducing side effects.
  • Targeted therapies act on cancer-specific molecules, such as EGFR inhibitors for tumors with EGFR mutations.
  • Immunotherapies boost the immune system to fight cancer cells, like checkpoint inhibitors that block proteins hindering immune responses.
  • Success depends on correctly identifying drug targets and understanding resistance mechanisms.

Challenges and Future Directions

  • Overcoming drug resistance, where cancer cells evolve to resist therapies, is a major challenge.
  • Addressing tumor heterogeneity, the genetic diversity within a tumor, is crucial for effective treatment.
  • Developing personalized combination therapies to tackle multiple cancer pathways simultaneously is a promising approach.
  • Liquid biopsies, analyzing cancer cells or DNA in blood samples, allow real-time monitoring of treatment response and disease progression.

Conclusion

  • Tackling cancer requires understanding its complexity and using the latest discoveries to create personalized, targeted treatments. Continuous research and technological advancements are essential for improving patient outcomes.

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