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Bio 360 - Cell Biology > Topic 9 - Cancer > Flashcards

Topic 9 - Cancer Flashcards

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1
Q

What does cancer immunotherapy refer to? microbes have an affect?

A
  • that cancers cells will produce specific antigens that they present on their surface
  • these antigens are targeted by the immune system, particularly antibodies
  • a recent study examined how specific members of the gut microbiota influence the efficacy of this type of immunotherapy
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2
Q

What percentage of deaths are due to cancer? heart disease?

A
  • 29.9% deaths due to cancer (the most)

- 19.7% deaths due to cancer

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3
Q

Examining a spread of cancer deaths throughout the Canadian provinces/ territories, what is the trend

A
  • higher rates of cancer deaths in the territories compared to the 10 provinces
  • population gap however* OR the effect of light on breast cancer
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4
Q

What effect does Light at Night have on the risks of Breast Cancer?

A
  • too much light at night decreases the melatonin levels in the body
  • this lack of melatonin now fails to suppress ESTROGEN which is linked to increases in Breast Cancer risk
  • particularly shift workers affected
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5
Q

What is the correlation between Cancer Risk and Age/Gender? ASIR?

A
  • increased risk of cancer with an increase in age
  • Age-standardized incidence rates
  • across the board, females have a lower risk of cancer? - due to higher inclination of seeing a doctor
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6
Q

What does Canada’s future look like regarding population within 10 years

A
  • there will be a growth between 55-65

- while any age below that will only grow due to increase in population size naturally

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7
Q

What does Canada’s future look like in regards to NEW CANCER CASES within 10 years?

A
  • a significant increase in cancer cases begining at age 45-49, maxing at 65-750, tapering off beyond 85+
  • Notably significantly more Male cancer cases compared to females
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8
Q

What are particular cancer prevalences that will increase significantly in the next 10 years? (4)

A
  • Colorectal
  • Lung
  • Prostate
  • Breast
  • 4 major cancers
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9
Q

What is the trend like for cancer deaths AVOIDED? 1. All Cancers 2. Lung Cancer
3. Breast Cancer

A
      1. will have projected decreased rates cancer deaths – due in part to improvements in Cancer treatments
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10
Q

Explain the Relative Survival Rates (RSR) of the 4 cancers: prostate, breast, colorectal, lung - 1, 3, 5, 10 years

A

this point examines the survival rate after having treatment to the cancer

  • high chances of survival from BREAST and COLORECTAL cancer, PROSTATE
  • less RSR from treatment for LUNG cancers after treatment
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11
Q

What can we infer from tumour cell population doublings and identifying breast cancer?

A
  • after 25 tumour cell population doublings, it will first be visible on an Xray (10^8 cells)
  • after 28 tumour cell population doublings, the tumour is first palpable (10^9 cells)
  • after >35 tumour cell population doublings, the patient will die (10^12 cells)
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12
Q

Explain the relative trends of Cancer events for Females from 1930 onwards.

A
  • consistent cancers: pancreas, ovary, breast
  • consistent decrease in cancers: colon & rectum, uterus, stomach
  • Increase in CANCER cases: lung cancer 1965 (not as significant as male lung cancer)
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13
Q

Explain the relative trends of Cancer events for Males from 1930 onwards.

A
  • consistent cancers: leukemia, liver, pancreas, colon rectum, prostate
  • consistent decrease in cancers: stomach
  • increase in CANCER cases: lung cancer (significantly more than females)
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14
Q

Explain the Global Events that lead to the increase in lung cancers among the population?

A
  • global consumption of cancer skyrockets - 1920-1980s
  • global lung cancer deaths caused by smoking (estimate) skyrockets 1950-present
  • small portion of lung cancer UNRELATED to tobacco
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15
Q

What was the Heliobacter Pylori Experiment

A
  • Barry Marshall and Robin Warren, working on a treatment for H. pylori infections
  • stomach cancer was that to arise from ulcers in the stomach
  • Marshall produced an antibiotic for H. pylori, consumed it got sick and treated himself with the antibiotics
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16
Q

Explain the Cancer Screening story, should we all be screened?

A
  • Paper published 2 million people develop preventable cancers each year which are caused by viruses, bacteria, and infectious agents
  • it is not politically exciting to save lives this way… saving the lives could not justify the EXTREME cost of such screen
  • over-treatment (common in breast and prostate cancer - increase in antibiotic resistance)
  • screen for all cancers?
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17
Q

Where are PAP tests used?

A
  • for the papilomavirus - HPV vaccines
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18
Q

Carcinomas

A
  • cancers of the epithelial cells, ex. the skin or lining of internal organs
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19
Q

Sarcomas

A
  • cancers of connective tissues or NON-epithelial tissues, ex. muscles
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20
Q

Leukemia & Lymphomas

A
  • cancers of White Blood Cells and Lymphocytes (lymph nodes)

- malignant progressive disease where bone marrow and blood-forming organs produce immature/abnormal blood cells

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21
Q

Carcinogenesis

A
  • the initiation of cancer forming chemical compounds are linked to mutagenesis (causing mutation in DNA which will produce mutant cells which can take ahold in tissues)
  • can be chemical or radiation, ex the sun which cause the thymine dimers
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22
Q

What is the Thymine Dimer?

A
  • a simple mutation caused by the Carcinogen UV-light that will form a dimer between two thymine subunits
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23
Q

Explain the 3 cases of balancing proliferation and apoptosis.

A
  • Homeostasis: normal cell division and normal apoptosis
  • Tumour: increased cell division and normal apoptosis
  • Tumour: normal cell division and decreased apoptosis
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24
Q

What makes Cancer so dangerous?

A
  • reproduce without the normal constraints on growth and division
  • invade and colonize other tissues
25
Q

Define a Benign Tumour

A
  • cell growth that is not invasive, localized

- the tumour has not invaded other tissue yet since it has not broken through the basal lamina

26
Q

Define a Malignant Tumour

A
  • tumour has broken through the basal lamina and has started spreading to other tissues
27
Q

Define Tumour Metastasis

A
  • in a normal epithelium cell a mutation occurs which cause a benign tumour to grow
  • cells become invasive and enter a capillary where they travel through the blood and attempt to adhere to blood vessels walls and break through this membrane
  • micrometastasis will occur where the cells take up shop as a secondary growth
    NOTE: one in a million cells will actually establish itself in a new tissue environment - majority of cells will not be able to take up a new site
28
Q

Define the barriers to metastasis

A
  • DIFFICULT: to escape from parent tissue (which would cause entry into new vessels)
  • EASY: traveling through circulation (survival in circulation, arrest in a capilary, exit into remote tissue/organ)
  • DIFFICULT: Colonization of remote sites (survival of cells in foreign tissue, initial growth of these cells, persistence of growth)
29
Q

Explain how the cell hierarchy affects tumour growth

A
  • upon cell differentiation from Stem cells, in normal tissue this process is slow and rare where daughter cells consist of stem cells & differentiatiating specialized cells
  • compared in cancer tissues, a cancer stem cell is rare, and cells will need to overcome limited renewal capacity
30
Q

What are two hurdles cancer cells must overcome?

A
  • limited self renewal capacity

- rare stem cells become cancerous so differentiation of a cancer cell to perform a different action in a cell is rare

31
Q

What is the origin of a mutation, is a single mutation enough, and a tumour only has one cell type?

A
  • it will originate from a signal cell which had a mutation persist through a number of replication cycles which extends to daughter cells
  • requires multiple mutations of a number of cellular functions (a gradual accumulation of mutations) – at least 5 different genes will need to mutate to lead to TUMOUR PROGRESSION - consider the tumour graph
  • a tumour consists of many cells (cancer cells are genetically unstable)
32
Q

In the cancer founder cell, what 3 heritable changes may lead to cancer arising?

A

point mutation

  • a mutation in the promoter OR coding region OR difference in the sequence will cause this mutation to persist during cell division if not fixed – leads to gene inactivation
  • an epigenetic mutation causes gene inactivation; different regulation of the gene, ex. heterochromatins form around the packed DNA meaning the gene is inactive and cannot be expressed
  • an accident causes DNA methylation itself and inactivation of the sequence itself
33
Q

Are epigenetic changes also heritable over generations?

A

YES; epigenetic inheritance may allow an organism to continually adjust its gene expression to fit its environment - without changing its DNA code.
- however in case of mutation this will be detrimental to the cell

34
Q

What results from the accumulation of somatic mutations?

A
  • this accumulation results when a mutation is able to persist within the cell, “survival of the fittest” - where the cell is now better adapted to out grow the other cells
35
Q

Define a “Driver Mutation”

A
  • mutation within a gene that confers a selective growth advantage (thus promoting cancer development)
  • cancer critical genes which will compromise cellular function
36
Q

Define a “Passenger Mutation”

A
  • mutations that don’t contribute to the development of cancer but have occurred during the growth of the cancer
37
Q

Two factors that may lead to cancer development?

A
  • lifestyle and environmental factors
  • constitutional mutations (genetic inheritance)
  • interesting point: with a change in lifestyle up to 50% of cancer can be avoided
38
Q

Name a few examples of Carcinogens.

A
  • vinyl chloride
  • Benzene
  • Aresenic
  • Asbestos
  • Radium
39
Q

Explain the Ames Test and its limitations

A
  • The Ames Test is used to test the potential mutagenic factor of a test compound
  • ex. potential mutagen is mixed with a culture of histidine-dependent salmonella and homogenized liver extract
  • mixed and cultured on a plate
  • the addition of the liver extract helps i trying to get a mutation to survive
40
Q

Why is the liver extract aded in the Ames test?

A
  • contains cytochrome P450 enzyme which is able to break down molecules or convert mutagenic molecules to make them into a harmful chemical
  • if the mutagen is strong enough it will be able to breakdown the p450 and cause the mutation
41
Q

Given an example in detecting cancer?

A

ex. the Philadelphia chromosomes in chronic myloid leukemia (CML)
- a rearrangement between two chromosomes 22 and chromosome 9 occur
- chromosome becomes longer, while chromosome 22 shorter
- this rearrangement/random duplication occurs all over the place

42
Q

What is the difference between INTERchromosomal rearrangement and INTRAchromosomal rearrangement

A
  • rearrangement between two chromosomes: typically between the homologous maternal and paternal chromosomes
  • rearrangment within a single chromsome
43
Q

Where would a GOF occur and what effect would it have?

A
  • Gain of Function mutation (typically in oncogenes)
  • results in an overactivity mutation
  • one mutation in one of the alleles that activate the mutation which promotes cell transformation
  • dominant
44
Q

Where would a LOF occur and what effect would it have?

A
  • Loss of Function mutation (typically in tumour suppressors)
  • a mutation event results in an inactivation of one allele of a tumour suppressor, which is still active due to a functional gene copy
  • a second mutation in the second allele of the tumour suppressor results in the elimination of the tumour suppressor gene completely
  • recessive
45
Q

How does a proto-oncogene go to an oncogene?

A
  • a point mutation in the coding sequence: produces a hyperactive protein in a signalling pathway
  • regulatory mutation: over expression of a normal protein (hypersensitivity)
  • gene amplification: normal protein is over expressed, ex. signal protein or a receptor causing hyper-phosphorylation or hyperactivity
  • Chromosome rearrangment: (2) a nearby regulatory DNA sequence causes a normal proteins over production OR fusion of a actively transcribed gene produces hyperactive proteins
46
Q

How do you identify an oncogene? definition? example?

A
  • gene that has the potential to cause cancer, that when mutated becomes an oncogene
  • oncogene may result in the “loss of contact inhibition by cancer cells
  • meaning normal cells will only grow in a monolayer attached to a plate, while cancer cells will grow on top of each other
  • Ras as an oncogene: functions in signal transduction pathway of MAP kinase kinase kinase
47
Q

How do you identify Cancer Cells?

A
  • Cancer cells will switch from cellular respiration (oxidative phosphorylation and Oxygen with high energy ATP) instead using GLYCOLYSIS to produce ATP via NADPH
  • this is known as the Warburg Effect
48
Q

Examine hereditary cancers of the retinoblastoma genes (3 cases)

A
  1. a normal healthy cell with two health chromosomes - a mutation may inactivate on of the Rb genes but it does not persist - so NO TUMOUR formation
  2. in NON-hereditary Rb, where an occasional cell mutates an Rb gene, the second copy is still RARELY inactivated; BUT excessive proliferation if both mutate - excessive proliferation leads to the rare Rb tumour in ONE eye
  3. hereditary Rb where one gene is mutant; occassionally only one mutant with one good copy of the Rb gene – excessive cel proliferation of a double mutant now results in tumours in BOTH eyes
49
Q

Name the 6 ways a normal Rb gene can be lost?

A
  • chromosome loss
  • chromosome loss followed by chromosome duplication
  • mitotic recombination event
  • gene conversion during mitotic event
  • deletion
  • point mutation
50
Q

Compare a genetic change and an epigenetic change?

A
  • genetic mutation will be required in both genes to lead to cancer
  • epigenetic change also required in both genes to lead to cancer
  • or a combination of the two will lead to cancer
51
Q

Name two methods of identifying Cancer Genes? as old techniques.

A
  • Microarrays
  • Sequencing; amplify and sequence the coding exons, then sequencing the cancer genome (whole gene families and coding exons), then sequencing of transcription
52
Q

What is a sequencing technique we complete now a days?

A
  • sequence RNA and compare the healthy RNA vs tumour RNA
53
Q

What is the purpose of Cancer Genome Sequencing? - where are tumour suppressors most active?

A
  • to identify new oncogenes or tumour suppressor genes
  • ex. IDH1 in the Kreb cycle or FOXL2: tissue-specific TF
  • many tumour suppressors are involved in chromatin modification and remodelling
54
Q

What is a future ambition for Cancer genome sequencing?

A
  • to sequence the individuals cancer genome and healthy genome
55
Q

Expain IMATINIB and CML

A
  • CML: chronic myeloid lymphoma
  • a hyperactive oncogeneic kinase (ATP bound) will phosphorylate a phosphatase which leads to: signal for cell proliferation and survival
  • GLEEVEC will instead bind to the oncogenic kinase at the same site as ATP thus inactivating the oncogenic kinases activity
56
Q

Why are multi-drug treatment important in cancer?

A
  • single treatment on a tumour, may have a rare mutant emerge to drug A which breaks off forming a tumour B – drug B also becomes resisted against by a rare mutation where these mutants are now UNCONTROLLABLY CANCER RESISTANT TO BOTH DRUGS
  • simultaneously treat cancer with both drugs prevent any resistance to the drugs & cures cancer
57
Q

Immunological Therapy will examine what?

A
  • Antibodies designed for specific antigens on the target cancer cells will bind to them and inject poisons
  • this will attack the immunosuppressive environment where cells can prevent interactions between immune cell receptors and the cancer cells antigens
58
Q

Is Ras an oncogene? and Rb a tumour suppressor gene?

A
  • Ras is a monomeric GTPase responsible for functions in signal transduction pathway of MAP kinase kinase kinase which activates gene transcription
  • Rb functions as a tumour suppressor since it will inhibit the activation of E2F (this protein when free will active cell cycle advances and promote DNA synthesis and proliferation)

Bio 360 - Cell Biology (10 decks)

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