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PPI > Cancer > Flashcards

Cancer Flashcards

1
Q

Which factors contribute to cancer development?

A

Factors that contribute to cancer development:
* Exposure to cancer causing chemicals (carcinogens. e.g. smoking, environment)
* Viruses (HPV)
* Lifestyle
* Genetics (Mutations in: BRCA1, BRCA2 (breast cancer). TP53, PALB2, PTEN)

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2
Q

Cancer definition

A

Definition of cancer:
* uncontrolled cell division of abnormal cells

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3
Q

Characteristics of cancer cells

A

Characteristics of cancer cells
*

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4
Q

What are the 3 most common forms of cancer in the UK?

A

3 most common cancers in the UK:
* Lung
* Colorectal
* Breast

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5
Q

Eating ___g processed meat/day increased colorectal cancer risk by 18%

A

Eating **50g ** processed meat/day increased colorectal cancer risk by 18%

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6
Q

Red meat consumption increased cancer risk by what percentage?

A

Red meat consumption increased cancer risk by 6%

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7
Q

50g of unprocessed red meat eaten once a day increases cancer risk by how much?

A

50g of unprocessed red meat eaten once a day increases cancer risk by 20%

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8
Q

What can the haem in red meat do?

A

The haem in red meat can alkylate DNA

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9
Q

What is a carcinogen?

A

A carcinogen is a substance that can cause cancer

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10
Q

What are the two types of carcinogens?

A

Two types of carcinogens: Gentoxic and Epigenetic carcinogens

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11
Q

Genotoxic carcinogens

A

Genotoxic carcinogens:
* Damage or modify DNA
* E.g: Radiation, Alkylating agents (CH2CH2 double bond), Asbestos, Arsenic, Dimethylnitrosamine

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12
Q

Epigenetic carcinogens

A

Epigentetic carcinogens:
* Indirect mechanisms e.g. immunosuppression, hormonal imbalance, alter gene expression.
* May alter the rate of cell growth
* Doesn’t damage DNA
* Takes longer to develop
* Creates a favourable environment for cancer development
* E.g: Saccharin, Oestrogen, Bile acids

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13
Q

What are the 3 main types of malignancies?

A

3 main types of malignancies:
* Carcinomas (90 %, most common)
* Sarcomas (2%)
* Leukaemias (8%)

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14
Q

Do most cancers come from self renewing, essentially non-renewing or conditionally renewing cells?

A

Most cancers form from self-renewing and conditionally renewing cells.

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15
Q

What is tissue classification based on?

A

Tissue classification is based on the ability to replace cells.

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16
Q

3 types of tissue renewability REC

A

3 types of tissue renewability
R: Rapidly self-renewing tissues
E: Essentially non-renewing tissues
C: Conditionally renewing tissues

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17
Q

Rapidly self-renewing tissues

A

Rapidly self-renewing tissues
* Skin
* Intestinal epithelium
* Haematopoietic system (blood)
* Balance between damaged/aged cells and cell replacement required

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17
Q

Conditionally renewing tissues

A

Conditionally renewing tissues
* Little or no replacement under normal circumstance
* Regeneration can occur after damage. disease or hormonal influence
* E.g.: Liver, breast, prostate, uterus

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17
Q

Essentially non-renewing tissues

A

Essentially non-renewing tissues
* Have no capacity to replace cells
* E.g. ovum, Central Nervous System

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17
Q

Which type of tissue doesn’t usually have cancer formation?

A

Most cancers don’t form from essentially non-renewing tissues.

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18
Q

Where do cancers arise from?

A

Cancers arise from stem cells

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19
Q

What can pluripotent stem cells differentiate into?

A

Pluripotent stem cells can differentiate into lymphoid stem cells or myeloid stem cells.

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20
Q

Cancer is a ______ disease

A

Cancer is a clonal disease

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21
Q

How many forms do fibroids express in?

A

Fibroids only express in one form

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22
Q

Explain Carcinogenesis

A

Carcinogenesis
* Process of a normal cell transforming into a cancerous cell
* Takes time to occur (hence relation to age)
* Results in GENETIC ALTERATIONS (mutations)

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23
Q

50% of cancers are caused by a mutation in which gene?

A

50% of cancers are caused by P53 gene mutation

24
Q

What is hyperplasia?

A

Hyperplasia:
Increase in number of cells (cell proliferation)

25
Q

What is adenomatous polyposis coli protein (APC)?

A

Adenomatous polyposis coli protein (APC):
tumor suppressor gene

26
Q

If genes are mutated, what happens to hyperplasia cells?

A

If genes are mutated, hyperplasia cells develop into carcinoma

27
Q

Is cancer a genetic disease?

A

Yes, cancer is a genetic disease.

28
Q

What is Kirsten rat sarcoma viral oncogene (K-ras)?

A

Kirsten rat sarcoma viral oncogene (K-ras):
* a gene that provides instructions for making a protein called K-Ras
* The protein relays signals from outside the cell to the cell’s nucleus. These signals instruct the cell to grow and divide or to mature and take on specialized functions

29
Q

As we age what happens to DNA?

A

As we age, there is more damage done to DNA

30
Q

Describe carcinogenesis

A
  1. Carcinogenesis is the transformation of a normal cell to a cancerous cell.
  2. Normal cell> hyperplasia>carcinoma> metastasis (potentially)
  3. It occurs due to mutations in tumour suppressor genes or oncogenes (mutated proto onco genes)
  4. The mutation of these tumour suppressor genes may cause cancer: K-Ras, SMAD, APC, P53.
  5. It occurs under specific conditions (may be triggered by damage)
  6. DNA damage accumulation promotes cancer development
31
Q

Why is there a correlation between cancer formation and age?

A

There is a correlation between cancer development and age because damage accumulation of DNA takes time

32
Q

Carcinoma ______ respond to signalling to stop proliferating

A

Carcinoma don’t respond to signalling to stop proliferating

33
Q

Define hyperplasia

A

Hyperplasia:
* Increase in number of cells (cell proliferation)

34
Q

Define oncogene

A

Oncogene:
* Mutated protooncogene
* product is produced in higher quantity or has higher activity
* Instructs cell to divide
* drives carcinogenesis at a molecular level
* Synthesize growth factors that act as signals for uncontrolled proliferation which leads to cancer formation
* if highly expressed, cancer is formed
* maintains the cell cycle

35
Q

What is P53?

A

p53:
* Tumour suppresor gene
* Prevents excessive proliferation (increase in cell number)
* May cause: cell cycle arrest, apoptosis, DNA repair, inhibition of angiogenesis
* Induced by radiation, drug induced DNA damage, oncogenic and hypoxia

36
Q

What do tumour suppressor genes do?

A

Tumour suppressor genes code for proteins that can STOP the cell cycle

37
Q

What might P53 cause?

A

P53 may cause: cell cycle arrest, apoptosis, DNA repair, inhibition of angiogenesis

38
Q

What are CDKs?

A
  • CDKs are cyclin dependent kinases.
  • Enzymes that add phosphate groups.
  • They play a role in cell cycle regulation.
39
Q

Growth _______ and cyclins _________ cell growth

A

Growth factors and cyclins stimulate cell growth.

40
Q

What does P53 do to CDK?

A

P53 stops CDK (cyclin dependent kinase) from binding to cyclin via competitive inhibition by promotion of p21.

41
Q

Which p? does P53 promote to prevent CDK?

A

p53 promotes p21 to prevent CDK

42
Q

Oncogenes: Action?

A

Oncogenes:
* Initiate cell division
* Increase rate of transformation from a normal cell to a cancer cell

43
Q

Tumour-suppresor genes: Action?

A

Tumour-suppressor genes:
* Prevent excessive growth of a cell
* By controlling cell proliferation
OR
* By control of DNA repair rate

44
Q

DNA repair genes: Action?

A

DNA repair genes:
* Repair damaged DNA
* Work in different ways to repair damaged DNA e.g. correct mismatched bases, correct copying erros that distort the structure of DNA.

45
Q

Apoptosis genes: Action?

A

Apoptosis genes:
Control the cell’s self-destructive process

46
Q

What is lipid peroxidation?

A

Lipid peroxidation:
- Free radicals steal electrons from lipids in cell membranes leading to cell damage
- Chain of events that can lead to reactive oxygen species formation and oxidative stress

47
Q

What happens if apoptosis genes are switched off?

A

If apoptosis genes are switched off cancer development may be promoted

48
Q

What are free radicals?

A

Free radicals are highly reactive molecules with unbound electrons. They are dangerous.

49
Q

How can free radicals cause damage?

A

Free radicals can cause damage by attempt of stabilization by taking electrons from nearby molecules, causing cellular damage.

50
Q

How can the cell generate free radicals?

A

The cell can generate free radicals in the following ways:
* Absorption of energy (e.g. UV light, x-rays can hydrolyse H20 to OH- and H)
* Metabolisms of chemicals or drugs, ( e.g., CCL4 (carbon tetrachloride) to CCL3.)
* Transition metals e.g., Fe & Cu catalyse free radical formation reactions.
* Nitric oxide can be converted to highly reactive species e.g., peroxynitrite anion (NO3-).

51
Q

What can nitric oxide cause?

A

Nitric oxide can cause vasodilation of the blood vessels

52
Q

What do free radicals target?

A

Free radicals target various cellular components including lipids, proteins and DNA.

53
Q

Which areas have lipid bilayers?

A

The nucleus, mitochondria, and cell membrane have lipid bilayers.

54
Q

What is lipid peroxidation?

A

Lipid peroxidation:
* Breakage of a lipid by a free radical
* Free radical is generated (initiation), free radical attacks the lipid, lipid broken down into two forms, another free radical is generated.
* Two stages: initiation and propagation

55
Q

What are the cell injuries which can be caused by free radicals?

A

The cell injuries which can be caused by free radicals:
* Lipid bilayer
* Nucleus: DNA fragmentation
* Lysosomes (content can be released into cell), Nucleus, Mitochondria : Membrane lipid peroxidation
* Protein cross linking and fragmentation

56
Q

What mechanisms are there to try and reduce free radical cell injury?

A

Mechanisms to reduce free radical injury:
* Antioxidants: block initiation of free radical formation or inactivate them (E.g.: Vitamin E, Ascorbic acid, glutathione)
* Iron (ferritin= iron storage form)and copper bound to storage/transport proteins> minimize OH formation.
* Enzyme free radical scavengers. E.g. superoxide dismutases, catalase, glutathione peroxidase

57
Q

What creates oxidative stress?

A

Oxidative stress summary:
* Imbalance between production and removal of free radicals
* Cellular reactions may generate partially reduced reactive oxygen species (ROS) e.g.,
Alkoxyl radical from alcohol
Peroxynitrite (NO3-) from nitrite + H2O2
O-2 [superoxide] and H2O2,
All create: Oxidative Stress if not countered by antioxidants

58
Q

What happens if oxidative stress isn’t countered by antioxidants?

A

If oxidative stress isn’t countered by antioxidants:
* Cellular components may be damaged
* Cancer, diabetes, neurodegeneration, kidney disease, and CVDs may materialize

59
Q

Why is the ratio of reduced glutathione to oxidized glutathione important?

A

The reduced (GSH)-to-oxidized (GSSG) glutathione ratio represents a dynamic balance between oxidants and antioxidants.
It gives an indication of oxidative stress

60
Q

Why is the link between diet and cancer complex?

A

The link between diet and cancer is complex because our diet is made of lots of different foods and nutrients.

61
Q

What type of diet is likely to reduce the carcinogenic process?

A

A balanced diet is thought to reduce the carcinogenic process via:
* Maintaining high levels of antioxidants (fruit & veg)
* Healthy immune system
* Higher levels of fibre,
* Low red meat, salt and sugar

PPI (23 decks)

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