Day 3- Cancer (Patho) Flashcards Preview

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Flashcards in Day 3- Cancer (Patho) Deck (68)
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What are 3 modes/ mechanisms that cancer can travel?

~Bloodstream (hematogenous or vascular)
~Direct extension into neighboring tissues


How can the cancer grow to the neighboring tissues?

*The cells will just keep growing/ dividing until it gets to the neighboring tissues

~Local invasion and tumor angiogenesis
~Venous drainage and further spread via metastatic cascade
~“skip metastasis” – bypass local lymph and form distant nodal mets


Are there normal patterns that metastatic of cancer will follow?



What determines the normal metastatic pattern of cancer?

Patterns of regional venous drainage, blood flow, and lymphatics determine common metastatic patterns

**there's a huge table in the book on the primary cancer, mode of dissemination, and location of mets (just if you are interested- Table 13-4)


What is an example of metastatic patterns of cancer?

~breast cancer spreads via lymphatics and vertebral venous system to bones in shoulder, hip, ribs, vertebrae, lungs, liver


Why should the doctor be careful when resecting a tumor?

If the tumor does not have clear margins when resected, mets can occur. new blood vessels with form during the healing process from resection


What is benign mechanical transport?

~lymphatic transport of epithelial cells displaced by biopsy of basic tumor

*breast massage-assisted sentinel lymph node (SLN) localization can cause the tumor to dislodge- resulting in benign mechanical transport


What are all cancers characterized by?

~Unregulated growth

~Invasion and spread of cells from the original site to other sites - metastasis


Up to 70% of autopsies of patients who died of cancer showed....

spinal metastases



~replacement of one differentiated cell type with another mature differentiated cell type.
~Not malignant
~the basal cells (epithelium stem cells) switch to making another cell type, usually in response to some stress (think metaplasia of bronchial epithelium in a smoker)
~dysplasia can easily follow



~expansion of immature cells with decrease in the number and location of mature cells
~usually signals a pre-cancerous process



~increased number of cells, which may or may not signal a pre-cancerous or cancerous process
~may be very benign, such as a callous



~“new growth”
~may be benign or malignant


What are the 3 basic processes in which our body regulates cells?

~Cell division
~Cell differentiation


Where in the normal processes can a problem occur?


Cellular mutations can affect any of these processes, producing abnormalities in cell numbers


What are the steps for metastasis of cancer cells?

~Primary tumor
~Localized invasion
~Transportation thru the Circulatory System
~Arrest in microvasculature of organs


What does Intravasation mean?

the entrance of foreign matter into a vessel of the body and especially a blood vessel


What does Extravasation mean?

the escape from a vessel into a tissue


More details on the steps for metastasis of cancer cells

~Spread of tumor within the tissue of origin through local invasion of tissue

~Spread into micro-vascular by intravasation

~Circulates through the vascular before being trapped in the microvasculature of other organs

~Tumor cells then extravasate into the other organs to form a secondary tumor


What are the 6 hallmarks of cancer?

~Evading apoptosis
~Self-sufficiency in growth signals
~Insensitivity to anti-growth signals
~Tissue invasion & metastasis
~Limitless replicative potential
~Sustained angiogenesis


growth and division requires

*Nice to know- not on exam

external growth factors (GFs)

**I will put- "nice to know- not on exam" in the parts where she said it; I'm guessing she meant it for a good bit of this section, but I will put it in where she said it.


Growth Factors (GFs)

*Nice to know- not on exam

~Diffusible, produced by other cells & bind to cell receptors
~Trigger intracellular kinases which in turn triggers cell division


Abnormality of growth in cancer cells occurs when:

*Nice to know- not on exam

~Too many receptors & over-stimulation of growth
~Self production & release of GFs which stimulate growth
~Trigger may be genetic, environmental

*she wants us to know that a trigger makes the growth increase


What are oncogenes?

~Small segments of DNA which can transform normal cells into malignant ones
~Activated from “normal” proto-oncogenes by a mutation


What happens when cells stop listening to each other?

*Nice to know- not on exam

Cancer cells don't respond to signals and keep dividing over normal cells that have stopped growing


In normal growth and division, cells are signaled to stop with ....

*Nice to know- not on exam

anti-growth signals from other cells which include:

~Soluble growth factors
~Immobilized inhibitors embedded in the extracellular matrix
~Immobilized inhibitors on the surfaces of nearby cells


In normal cells, how is the growth checked?

*Nice to know- not on exam

the cell responds to antigrowth signals associated with the G1 checkpoint of the cell growth cycle


What are the phases in the cell cycle?

*Nice to know- not on exam



What is G0 phase

*Nice to know- not on exam

resting phase where the cell has left the cycle and has stopped dividing


What is G1 phase

*Nice to know- not on exam

cell growth in preparation for increased DNA synthesis

**G1 checkpoint is a regulatory step preventing move into DNA synthesis phase thus preventing cell division