Cancer Flashcards

• Overview of cancer burden • Pathophysiology • Risk factors • Exercise/PA and prevention of cancer • Mechanisms underlying PA and cancer risk • Prescribing exercise for those with cancer

1
Q

What is the proposed origin of the term ‘cancer’?

A

Around 400 B.C., Hippocrates is said to have named masses of cancerous cells karkinos — Greek for crab. Science and medical historian Howard Markel discusses a few hypotheses on why Hippocrates named the disease after a crab, and how well cancer was understood in the ancient world.

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2
Q

What are the primary characteristics of cancer cells?

A

o Self-sufficiency in growth signals: cancer cells acquire an autonomous drive to proliferate - pathological mitosis - by virtue of the activation of oncogenes such as ras or myc.
o Insensitivity to growth-inhibitory (antigrowth) signals: cancer cells inactivate tumor suppressor genes, such as Rb, that normally inhibit growth.
o Evasion of programmed cell death (apoptosis): cancer cells suppress and inactivate genes and pathways that normally enable cells to die.
o Limitless replication potential: cancer cells activate specific gene pathways that render them immortal even after generations of growth.
o Sustained angiogenesis: cancer cells acquire the capacity to draw out their own supply of blood and blood vessels - tumor angiogenesis.
o Tissue invasion and metastasis: cancer cells acquire the capacity to migrate to other organs, invade other tissues, and colonize these organs, resulting in their spread throughout the body.

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3
Q

What are the primary differences between benign and malignant tumours?

A

o B: Cells tend not to spread; M: Cells can spread
o B: Most grow slowly; M: Usually grow fairly rapidly
o B: Do not invade nearby tissue; M: Often invade basal membrane that surrounds nearby healthy tissue
o B: Tend to have clear boundaries; M: Can spread via bloodstream or lymphatic system, or by sending ‘fingers’ into nearby tissue
o B: Under a pathologist’s microscope, shape, chromosomes, and DNA of cells appear normal; M: May recur after removal, sometimes in areas other the original site
o B: Do not secrete hormones or other substances (an exception: pheochromocytomas of the adrenal gland); M: Cells have abnormal chromosomes and DNA characterized by large, dark nuclei; may have abnormal shape
o B: May not require treatment if not health-threatening; M: Can secrete substances that cause fatigue and weight loss (paraneoplastic syndrome)
o B: Unlikely to recur if removed or require further treatment such as radiation or chemotherapy; M: May require aggressive treatment, including surgery, radiation, chemotherapy, and immunotherapy medications

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4
Q

Describe how exercise can play a role in cancer prevention; what are the proposed mechanisms?

A

o Perhaps the best illustration of the role that exercise has in disease management is cardiac rehabilitation. Heart disease encompasses a cluster of pathophysiologic states that increase the risk of an adverse cardiac event, such as a heart attack or stroke.
o Sustained rhythmic exercise stimulates the cardiorespiratory system and results in neurologic and cellular adaptations that improve the efficiency of the heart and circulation. These structural and functional improvements ultimately reduce the workload on the heart, thereby improving functional capacity of the patient and reducing the risk of cardiac events.
o Likewise, exercise adaptations to regular exercise training could alleviate or reverse the physiologic insults resulting from cancer treatment and possibly alter disease progression.

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5
Q

Do exercise based interventions in cancer patients prolong survival and improve quality of life?

A

Continuing to monitor patients beyond the end of the structured intervention is essential for establishing the long-term effects of interventions in promoting sustained physical activity, increasing survival, preventing recurrence and enhancing quality of life.

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6
Q

Which types of cancer does physical activity play a role in?

A
o	Bowel Cancer 
	Strong effect
	30-60 min d-1 mod/vig PA = 30-40% reduction in risk
o	Rectal Cancer 
	No effect
o	Breast Cancer 
	Probable effect
	30-60 min d-1 mod/vig PA = 20-30% reduction in risk
o	Prostate Cancer 
	Unclear/inconsistent
	10-30% reduction in risk
o	Lung Cancer 
	Possible effect
	20% reduction
o	Testicular Cancer 
	Unclear/inconsistent
o	Ovarian Cancer 
	Unclear/inconsistent
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7
Q

How many mutated genes/genetic changes does it take for a human cell to become cancerous?

A

Five or six

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