Medical School Pathology: Hallmarks of Cancer Part 1: Growth

This video for medical students covers three of the eight hallmarks of cancer (listed below), as initially described by Hanahan and Weinberg in 2000. The material in this video is based on Robbins & Kumar Basic Pathology, 11th edition. These “hallmarks” are the functions and capabilities that cells must enquire in order to “succeed” as malignant tumors. In this video, I focus on the three that I associate with growth (in bold):

• Self-sufficiency in growth signals
• Insensitivity to growth-inhibitory signals
• Altered cellular metabolism
• Evasion of apoptosis
• Limitless replicative potential
• Sustained angiogenesis
• Invasion and metastasis
• Evasion of immune surveillance

I begin by reviewing regulation of the cell cycle and normal cell proliferation, then focus on two areas where they go awry. I finish with a discussion of the Warburg effect: how it benefits tumor cells and the steps they take to adopt this type of metabolism.

Good videos to watch ahead of time are the videos on p53 and RB

p53:

RB

[moshesadofsky]

Thanks again Dr. Deyrup for clarity and vision.
I have a couple of thoughts. You are absolutely right in including growth factor signaling as one of the essential early steps in getting cells to proliferate. You use as an example, cell surface receptors like kinases. Students should be made aware that this is one major class of signaling molecule, but not the only one. For example Estrogen is a growth factor, but it works through a different mechanism. And Notch pathways also work through different mechanisms, although they all can induce transcription. But the essential idea - that genes get activated - is crucial. Similarly there are several ways Inhibitors can be removed. Mutation, of course. But also epigenetic silencing turns out to be significant. And (as you showed elsewhere) shifting the balance of protein degradation. All heady to juggle. Thanks.

[mariodelemos]

Thank you Dr. Deyrup for such an engaging and clear presentation, particularly in pointing the relevance of various new information. As an oncology pharmacist, I find it challenging to remember the genes and proteins involved in carcinogenesis, many of which have become targets for drug therapy. Knowing what the do in normal cells give me a better framework to learn about them.

[mariodelemos]

I assume most cells in human body are dormant (permanently differentiated, senescent, quiescent) and therefore not taking up labelled glucose in PET scan?