Exam 4 L4: Cribbs Cancer I Flashcards

1
Q

Cancer is ________

A

Cancer is basic cellular functions “gone wrong” :
Cell proliferation/cell cycle

Cell adhesion

Cell communication

DNA repair mechanisms

Apoptosis

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2
Q

Two conditions required for cancer are:

A

Two conditions required for cancer:

Uncontrolled cell divion —> tumor

(not all tumors are cancerous, if a tumor is confined its benign)

Tumors spread beyond tissues —-> malignant

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3
Q

Give the names for the following types of cancer:

Benign and malignant epithelial cancer

Benign and malignant muscle/cartilage cancer

A

Epithelial : Adenoma (benign)….. Carcinoma (malignant)

Muscle/Cartilage: Chondroma (benign)….. sarcoma (malignant)

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4
Q

What is the most prevalent type of cancer?

A

Carcinoma (malignant epithelial tumors)

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5
Q

Why are carcinoma’s the most prevalent type of cancer?

A

Epithelial cells undergo many cell divisions and are easily exposed to enviornmental factors in the enviornment

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6
Q

Cells become cancerous from ___________ or _______

A

Cell becomes cancerous from single genetic mutation or heritable epigenetic event (in order to pass it on to its progeny tumor cells)

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7
Q

Cancer arises from a combo of ___ and ___ changes

A

Cancer arises from a combination of GENETIC and EPIGENETIC changes

Genetic: Alteration of DNA sequence (low frequency, original event followed by sucessive events in same cell lineage)

Epigenetic: changes in pattern of gene expression without change in gene sequence (methylation, histone modification, etc)

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8
Q

Explain tumor progression

A

Tumor progression:

One cell gets mutated

Then there is cell proliferation of that mutated cell

Successive mutations create an invasive tumor—> Genetic Instability

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9
Q

Carcinogenesis is related to ______

A

CARCINOGENESIS is related to MUTAGENESIS

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10
Q

Tumor progression also involves impaired proliferation/apoptosis balance

Explain the two scenarios

A

Increased cell division with normal apoptosis will create a tumor

Normal cell division with decreased apoptosis will create a tumor

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11
Q

Explain how all of the checkpoints within the cell cycle can play a role in cancer

Also explain telomerase’s role in cancer

A

Cell cycle has multiple potential sites for abnormalities that lead to uncontrolled proliferation

Some cancers can also be caused to screwed up telomerase

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12
Q

Explain cancer stem cells:

Most cells in a tumor are called ______

Cancer stem cells have the ability to____

A

Most cells in a tumor are “transit amplifying cells”

Stem cells are self-renewing

Very few cells within a tumor are stem cells. The stems cells are the only ones that have the ability to make new tumors. THis is why radiation and chemo sometimes don’t always work, if they don’t kill stem cells. This is also why if you put a bunch of cancer in a petri dish, only some of them will make new tumors, because only a tiny fraction of the cells were stem cells and even have the ability to make new tumors

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13
Q

How can scientists see tumor cells?

A

Look at places with high glucose uptake (rapidly dividing cells)

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14
Q

Metastatic Process:

Cell grows as benign in epithelium, cells then become invasive and enter capillary…. (what happens next)

A

Cells can then travel through the blood stream (fewer than 1 in 1000 will survive to form metastases)

The ones that create new tumors have to be stem cells, and they have to find a good microenviornment

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15
Q

Colonization:
Only a ______ of tumor cells that reach a foreign enviornment are able to survive

Cancer cells that do survive carry mutations and thus are less dependent on intercellular signaling for cell division and survival, and they may also _____

As the tumor enlarges, _______ mechanisms set in

A

Only a small proportion of tumor cells that reach a foreign enviornment are able to survive

Cancer cells that do survive carry mutations and are thus less dependent on intercellular signaling for cell division and survival, and they may also escape apoptosis

As the tumor enlarges, self-perputuating mechanisms set in

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16
Q

Explain tumor angiogenesis

A

As a tumor enlarges, O2 demand increases

Internal cells become hypoxic

Hypoxic means there will be high levels of HIF (hypoxic inducing factor)

The tumor cells will then secrete VEGF in order for new capillaries to sprout and supply the tumor cell with more blood

17
Q

Signaling between cancer and stromal cells (which are _______) evolve to help tumor survival

A

Stromal cells are the structural cells within a tumor

Tumor microenviornment is very important

18
Q

Explain the three important genetic factors within cancer

A
  1. Oncogenes: “GOF”
  2. Tumor supressors: “LOF”
  3. Dna maintenance genes- maintain genomic stability
19
Q

Oncogene: expression is ______

Derived from a _______ that is present in normal cells but becomes an oncogene when activated

Explain the ways oncogenes can get activated

A

Oncogene expression is causative

Oncogenes are derived from protooncogenes that are normally inactive but become oncogenes when activated

Oncogenes can be activated by mutations, gene amplification, or chromosome rearrangement

20
Q

Explain the three scenarios:

Inserting Myc into a mouse strain

Inserting Ras into a mouse strain

Inserting Ras and Myc

A

Just myc: tumors will develop within about 100 days

Ras is more oncogenic, so it will start creating tumors more quickly

Ras and Myc together are very deletarious (activating more than one oncogene is very deadly)

They work together to become really cancerous

21
Q

Explain the different mutations that arise to give Gain of Function vs loss of function

A

Gain of function (overactivity mutation):
Single mutation event can create an oncogene

Loss of function (underactivity mutation):

mutation even inactivates the tumor supressor gene on one chromosome (no effect of mutation in the other copy), it isn’t until a second mutation even that creates the problem: two inactivating mutations functionally eliminate the tumor supressor gene, promoting cell transformation

22
Q

Loss of function: Tumor Supressor

Need to look for loss of gene

LOF is due to both ___ and ___ changes

Gene profiling is useful but complicated by ______

A

LOF: Tumor Supressor Genes

Need to look for loss of gene

LOF is due to both genetic and epigenetic changes

Gene profiling is useful but complicated by multiple contributing mutations

23
Q

___ is one of the INK proteins involved in many types of cancer (Ink stands for___)

A

p16 is one of the INK proteins involved in many types of cancer (INK stands for INhibitor of cdK’s)

24
Q

Explain how normally, active p16 is within a non-proliferating cell

And then how if p16 is inactive or absent, a cell can proliferate

Explain the mechanism

A

Normally, p16 is bound fo Cdk4, inhibiting it from becoming active and expressing S phase genes

When p16 is absent or inactive, Cdk4 can bind to its regulatory partner cyclinD, activating the Cdk4, allowing it to phosphorylated Rb, which then allows expression of S phase genes