3.2 - Biology of Cancer Flashcards

1
Q

What is Cancer

A
  • cells divide uncontrollably and invade other tissues
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2
Q

Benign VS. Malignant Tumour

A

Benign
- grows slowly
- well-defined boundary (encapsulated; so don’t invade other tissues)
- not invasive
- well-differentiated
- low mitotic index (not many cells are dividing)
- does not metastasize

Malignant
- grows rapidly
- not ecapsulated (invades)
- poorly differentiated
- high mitotic index
- metastasizes

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3
Q

Types of Benign Tumours

A

1) Lipoma - fatty tissues

2) Leiomyoma - arises in smooth muscle tissue

3) Meningioma - arises from meninges

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4
Q

Types of Malignant Tumours

A

1) Carcinoma - epithelial tissue
2) Adenocarcinoma - glandular/ductal tissues
3) Sarcoma - mesenchymal tissues (supports bone, muscle, and fat)
4) Lymphoma - lymphatic tissues
5) Leukemia - blood forming cells

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5
Q

Carcinoma In Situ

A
  • originates in epithelial or glandular tissue
  • pre invasive (bc it has not yet invaded)
  • cancer cells that have not yet invaded surrounding tissue (has NOT broken through basement membrane)
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6
Q

Characteristics of Cancer Cells

A

1) Decreased need for growth factors
- normal cells require signals for when to grow and divide
- cancer cells just keep growing

2) Lack contact inhibition
- normal cells stop growing when they touch neighbouring cell
- cancer cells ignore this

3) Anchor dependence
- normal cells are attached to a surface
- cancer cells are not attached to anything

4) Immortality
- cancer cells can divide infinitely bc they have telomerase to maintain their chromosomes

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7
Q

Proto-Oncogenes VS. Oncogenes and Tumour-Suppressor Genes

A

Proto-Oncogenes
- normal genes
- regulate cell growth and protein production
- become oncogenes, when mutated

Oncogenes
- mutant gene that causes uncontrolled proliferation

Tumour-Suppressor Genes
- aka anti-oncogene
- help control cell growth

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8
Q

How are oncogenes activated

A
  • RAS regulates cell growth (acts a switch that turns growth signals on/off)
  • point mutation in RAS causes switch to get stuck on = uncontrolled proliferation
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9
Q

Types of Translocation that Sustain Proliferative Signalling

A

1) Burkitt Lymphoma

2) Chronic Myeloid Leukemia

3) Gene Amplification

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10
Q

gggg

A
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11
Q

What is Genomic Instability

A
  • increased tendency for cells to accumulate mutations
  • genetic errors can lead to activation of oncogenes or de-activation of tumour-suppressor genes

Caretaker Proteins: encodes for proteins involved in DNA repair

Chromosomal Instability - changes in chromosome # and structure
- results in chromosome loss, loss of heterozygosity (2nd copy provides protection)n
- chromosomal amplification (extra copies can lead to overexpression of oncogenes)

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12
Q

Telomeres

A

telomeres: caps at the end of chromosomes
- everytime a cell divides, telomeres shrink
- when it becomes too short cell is signalled to stop dividing
- cancer cells have an enzyme - telomerase - which extends telomeres and allows cells to continue dividing

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13
Q

What is Angiogenesis

A

angiogenesis: formation of new blood vessels
- they need more blood vessels to be supplied with nutrients and oxygen to continue growing
- cancers secrete angiogenic factors that support blood vessels and help endothelial cells migrate to tumour

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14
Q

How cancer cells support their own growth

A

1) Warburg Effect
- cancer cells prefer to use glycolysis instead of oxygen
- cancer cells us by products of glycolysis to help them build new cell structures and continue growing
- warburg effect is driven by inactivation of tumour-suppressor genes

Reverse Warburg
- cancer cells influence surrounding cells to witch to glycolysis so they can increase their energy supply from the byproducts

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15
Q

Resisting Apoptosis

A
  • defects in intrinsic and extrinsic pathways provide resistance to apoptosis

Intrinsic Path
- triggered by internal signals (DNA damage)
- normally activates apoptosis
- mutations (p53) disable this pathway

Extrinsic Path
- activated by external signals from other cells or receptors
- cancer cells can block receptors from receiving apoptotic signals

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16
Q

Inflammation and Cancer

A
  • chronic inflammation causes release of cytokines
  • cytokines promote cell growth and survival
  • excessive cytokine release promote tumour growth and development

ex. H pylori can cause chronic inflammation = cancer

  • H. pylori led to the discovery that antibiotics can reduce risk of cancer bc: if you remove inflammation, you stop excessive cytokine release = controlled cell growth
17
Q

What is a Tumour-Associated Macrophage

A
  • key cell that promote tumour survival
  • blocks t-cytotoxic cells and natural killer cells which kill abnormal cells and release cytokines which promote tumour growth and spread
18
Q

Which 2 conditions cause immunosuppression which can cause cancer?

A

1) Non-Hodgkins lymphoma
2) Kaposi Sarcoma

19
Q

Viruses that can cause cancer

A

1) Hep B and C Viruses
- cause chronic liver infection and inflammation = cancer

2) EBV
- associated w many types of cancers

3) Kaposi Sarcoma
- causes immunosuppression = cancer

4) HPV
- associated with oral, anal, and cervical cancers

5) Human T cell Lymphotrophic virus
- linked to T cell leukemia

20
Q

What is Metastasis?

A
  • spread of cancer from primary site to a distant site

Occurs through 2 routes:
1) Direct Invasion
- cancer directly invades neighbouring cells

2) Metastasis to distant organs
- cancer cells travel through lymphatic system or bloodstream

21
Q

What is the Epithelial-Mesenchymal Transition

A
  • process where epithelial cells transform into mesenchymal cells which is needed for metastasis

During EMT, epithelial cells
1) lose cell adhesion - allows them to be more mobile ad invasive

2) increased migratory capacity
- cells can move and spread to diff locations

3) resistant to apoptosis

4) causes stem-cell state
- less specialized
- allows them to adapt and thrive in diff environments

22
Q

How does release of lytic enzymes contribute to cancer spread

A
  • lytic enzyme release breaks down the extracellular matrix and decreases cell adhesion
  • cells can break off from primary tumour and migrate to distant sites
23
Q

What are paraneoplastic Syndromes?

A
  • health issues triggered by substances released by the tumour
    ex. lung cancer can release hormones that affect Ca levels and cause hypercalcemia
  • serves as the earliest indicator of cancer
24
Q

Clinical Manifestations of Tumours

A
  • little to no pain

Mechanisms
1) pressure - tumours put pressure on tissues

2) blocks ducts - tumours can obstruct ducts = accumulation of fluid = pain

3) Invasion - can invade sensitive areas or nerve tissues

4) Stretching of surface - bc tumours keep growing

5) Tissue destruction

25
Q

Other Clinical Manifestations

A

1) Fatigue
- most reported symptom

2) Cachexia
- severe form of malnutrition
- includes: weight loss, altered metabolism, early satiety, taste alterations, anemia

3) Anemia
- decrease in hemoglobin in blood

4) Infection
- when leukocyte and neutrophils counts fall, our ability to fight infections decreases

5) Leukopenia and thrombocytopenia
- direct tumour invasion of bone marrow cause leukopenia (decrease in white blood cells) and thrombocytopenia (decrease in platelets)

6) GI
- oral ulcers develop due to decreased cell turnover
- malabsorption - treatment affects digestive systems ability to absorb nutrients
- nausea - from chemo

7) Hair and skin
- alopecia - from chemo
- skin breakdown

26
Q

Stages of Cancer

A

Stage 1 - Early stage
- no spread to lymph nodes or tissues
- localized to OG site

Stage 2 - Localized
- starts growing into nearby tissues

Stage 3 - Regional Spread
- affects surrounding tissue
- spreads to distant lymph nodes

Stage 4 - Distant spread
- cancer has spread to distant organs and tissues

27
Q

TNM System

A

T - Tumour Size
T-1: 0-2 cm
T-2: 3-5cm
T-3: >5cm
T-4: tumour has broken through skin

N - Lymph Node
N-0: can not feel noded
N-1: swollen nodes
N-2: swollen and lumpy nodes
N-3: swollen nodes near collarbone

M-metastasis
M-0: nodes are cancer free
M-1: nodes show cancer cells or metastasis

28
Q

What are Tumour Markers

A
  • substances produced by cancer cells that are found on or in tumour cells, blood, CSF, or urine
  • help to diagnose specific types of tumours

Hormones
- ex. Certain breast cancer produces estrogen

Enzymes
-ex. Elevated levels of alkaline phosphates can be a sign of liver or bone cancer

Genes (mutations)
- ex. Mutations in BRCA 1 - which are linked to breast

Antigens
- trigger an immune response
ex. Prostate specific antigen (PSA) indicates prostate cancer

Antibodies
- some tumours produce specific antibodies

29
Q

What is the problem with tumour markers?

A

1) False positives
- tumour markers can be elevated in other cases that are not cancer
ex. Elevated prostate antigen levels can occur due to benign prostate hyperplasia

2) False Negative
- some cancer do not produce detectable levels of tumour markers

30
Q

What is an Immunohistochemical analysis?

A
  • staining a tissue sample with antibodies that bind to specific proteins
  • identifies presence and quantity of proteins in cancer cells
31
Q

How does radiation work?

A
  • kills cancer cells DNA
  • minimizes damage to surrounding tissue bec it is more targeted
32
Q

How does chemotherapy work?

A
  • targets rapidly dividing cells (but healthy cells can also be rapidly dividing)
  • interferes with processes that a cell requires for growth and survival
33
Q

Types of Chemo

A

1) Induction
- used to shrink or eliminate tumours

2) Adjuvant
- given after surgery
- used to kill remaining cells that may have not been removed during surgery

3) Neoadjuvant
- given BEFORE surgery
- tried to reduce size of the tumour; making it easier to remove in surgery

34
Q

What is targeted disruption cancer treatment?

A
  • aims to interfere with pathways crucial to cell growth and survival

Mechanisms:
- inactivating oncogenes
- blocking angiogenesis
- inducing apoptosis
- neutralizing cytokines