Cancer Flashcards

1
Q

What is the definition of cancer according to
the World Health Organization?

A

Large group of diseases, can start in almost
any organ or tissue of body when abnormal cells grow uncontrollably, go beyond their usual boundaries to invade adjoining parts of the body, and/or spread to other organs.

Second leading cause of death globally, accounting for an estimated 9.6 million deaths, or one in six
deaths, in 2018.

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2
Q

What are the most common types of cancer in males according to the World Health Organization?

A

Lung, prostate, colorectal, stomach, & liver cancer

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3
Q

What are the most common types of cancer in females according to the World Health Organization

A

Breast, colorectal, lung, cervical, & thyroid cancer

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4
Q

What is Parenchyma?

A

Functional tissue of tissue/structure/organ, i.e.,
group of cells that are performing the tissue’s work

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5
Q

What is Stroma?

A

Connective tissue or supporting tissue of a structure
or organ

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6
Q

What roles can the Stroma play?

A

˃ container role: outer membrane that encloses the
structure’s parenchyma)
˃ structural role: supports/reinforces the structure’s
shape and tissue integrity
˃ protective role: can help protect the tissue cells
˃ attachment role: component that attaches the structure to others (e.g., tendinous attachment to bone)
˃ term technically also includes all parts that do not perform functions of the structure (blood vessels, ducts, etc.)

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7
Q

(Stroma Roles) What is the container role?

A

Outer membrane that encloses the structure’s parenchyma)

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8
Q

(Stroma Roles) What is the structural role?

A

Supports/reinforces the structure’s shape & tissue integrity

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9
Q

(Stroma Roles) What is the protective role?

A

Can help protect the tissue cells

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10
Q

(Stroma Roles) What is the attachment role?

A

Component that attaches the structure to others (e.g., tendinous attachment to bone)

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11
Q

What is Cell Proliferation?

A

Process by which cell populations are maintained in tissue or structure. Most cells are produced, mature, do their work, & die from injury/disease, internal process, or age. With most cell types, dead cells are replaced by replication of neighbour cells.

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12
Q

What are Labile Cells?

A

Cells that continuously divide & regenerate, typically found in areas like skin, gut lining, & bone marrow. Their constant division helps maintain & repair tissues.

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13
Q

What are Stable Cells?

A

Cells that divide only when needed, typically during tissue repair after injury. Usually in resting state but can re-enter cell cycle if necessary. Eg. liver cells (hepatocytes) & kidney cells. Unlike labile cells, they don’t divide constantly but have potential to regenerate when required.

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14
Q

What are Permanent Cells?

A

Cells that don’t divide after they have fully matured. Once damaged, they cannot regenerate or be replaced by new cells. Eg. include neurons (nerve cells) & cardiac muscle cells. If injured, these tissues heal through scarring rather than cell regeneration.

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15
Q

When cells are lost, normal ways of maintaining cell population in a tissue or structure include?

A

Boundaries: Cells stop replicating when tissue-defining structures (e.g., basement membrane) are filled.
Cell-Cell Controls: Chemical signals regulate cell replication, growth, & apoptosis.

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16
Q

What role do boundaries play in cell population control?

A

Cells stop replicating when they reach physical boundaries like the basement membrane, preventing overgrowth.

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17
Q

How do cells communicate to maintain population size?

A

Cells send chemical signals to sense cell depletion or overpopulation, which either stimulate or suppress cell replication, growth, or trigger apoptosis.

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18
Q

How does the body prevent overpopulation of cells?

A

Chemical signals turn off once normal cell population is reached, mitigating against excess cell growth.

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19
Q

What factors are involved in controlling cell populations?

A

Chemical signals that can stimulate or suppress:
- Cell replication
- Cell growth
- Apoptosis (programmed cell death)

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20
Q

What does autophagy (autophagocytosis) mean?

A

It means “eating of self.”

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21
Q

What is the primary function of autophagy?

A

It’s a normal, orderly process that disassembles damaged, excess, or dysfunctional organelles, making their building blocks available for reuse.

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22
Q

How does autophagy contribute to cellular health?

A

It promotes cell health & function & recycles cellular components, acting as a homeostatic process.

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23
Q

What role does autophagy play in cellular housekeeping?

A

It eliminates poor-quality/damaged cellular components & intracellular toxins/pathogens.

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24
Q

When is autophagy increased?

A

It increases during cellular stress & starvation conditions to prune organelles & reduce energy expenditure.

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25
Q

How does autophagy occur within the cell?

A

Targeted elements are isolated into a double-membraned vesicle called an autophagosome, which fuses with a lysosome to degrade its contents. Useful components are recycled.

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26
Q

What are some complex roles of autophagy beyond its basic function?

A

It promotes cell surface antigen presentation, protects against genome instability, prevents necrosis, & promotes cellular senescence.

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27
Q

How does autophagy relate to disease prevention?

A

It is involved in preventing diseases such as cancer, neurodegenerative conditions, heart failure, diabetes, liver disease, autoimmune diseases, & infections.

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28
Q

What is known about the regulation of autophagy?

A

It is a highly regulated process that has received increasing attention for its complexity.

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29
Q

What happens when autophagic processes become abnormal?

A

They can promote cellular disorder & death, contributing to disease.

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30
Q

How does reduced autophagy affect aging?

A

Inefficient autophagy can lead to less healthy conditions within cells, allowing pathological changes & paving the way for disease states.

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31
Q

What is apoptosis?

A

Apoptosis is programmed cell death, triggered within the cell under certain conditions (e.g., old, unwanted, or unhealthy cells).

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32
Q

What happens to most cells regarding replication?

A

Most cells have a finite number of replications and undergo apoptosis when that limit is reached.

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33
Q

What are some examples of excess tissues eliminated by apoptosis?

A

Webbing between fingers in utero, excess neurons & synapses in the brain, & thymus tissue over time.

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34
Q

What types of internal cell damage can initiate apoptosis?

A

Damage from viral infections, oxidants/free radicals, UV light, cancer-causing factors, & some autoimmune processes.

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35
Q

How does apoptosis help prevent cancer?

A

It eliminates damaged cells, thereby reducing the risk of genetic mutations that could lead to cancer.

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36
Q

What happens once apoptosis is initiated?

A

Proteins called CASPASES break down DNA/chromatin, the nucleus deconstructs, & the cell shrinks, forming BLEBS & releasing chemicals to attract macrophages.

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37
Q

What are apoptotic bodies?

A

Remnants of the nucleus & cytoplasm that are bundled into membrane-bound blebs, which are later cleared by phagocytic cells.

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38
Q

What are the consequences of excessive apoptosis?

A

Too many cells are killed, leading to serious tissue damage/loss (e.g., in Alzheimer’s Disease & Parkinson’s Disease).

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39
Q

What happens when there is insufficient apoptosis?

A

Cells that should be eliminated become resistant to death, contributing to conditions like cancer.

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40
Q

How do genetic mutations affect apoptosis in cancer?

A

Many cancers have genes that block apoptosis initiation, making them treatment-resistant despite DNA damage.

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41
Q

What are scientists seeking to understand about apoptosis?

A

They aim to better understand the signals that initiate apoptosis for potential therapeutic applications.

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42
Q

What are blebs?

A

Outpouchings of the membrane

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43
Q

What is cell differentiation?

A

The process by which stem & progenitor cells evolve into mature, functioning tissue cells.

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44
Q

What are progenitor cells?

A

Cells that are a stage between stem cells & differentiated cells, essential for developing various tissue types.

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45
Q

What happens to cells once they are specialized (differentiated)?

A

They cannot revert to stem or progenitor status.

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46
Q

What role do stem cells play in adult tissues?

A

They act as a repair system, replenishing specialized cells & maintaining tissue populations.

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47
Q

Which tissues have a larger role for stem & progenitor cells?

A

Blood, skin, & endothelial lining membranes.

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48
Q

What is tissue dystrophy/atrophy?

A

A temporary or permanent decline in the number and size of cells in a tissue or structure.

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49
Q

What is hypertrophy?

A

Increased size of parenchymal cells in response to increased workload, e.g., in muscles or glands. It can reverse if conditions change.

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50
Q

What is hyperplasia?

A

Increased number of parenchymal cells in response to higher needs, such as in breast tissue during pregnancy or the formation of skin calluses.

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51
Q

What defines normal hyperplastic changes?

A

They remain under normal tissue proliferation guidelines, like breast tissue changes during lactation.

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52
Q

What are some examples of dysfunctional hyperplasia?

A

Unusual breast growth in males due to hormonal issues, prostate hyperplasia related to aging, & abnormal tissue accumulation from chronic inflammation.

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53
Q

What is metaplasia?

A

The replacement of a mature differentiated cell type with another mature, differentiated cell type that is more resilient under stress.

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54
Q

Why does metaplasia occur?

A

It occurs when cells in a tissue or structure are under stress that they cannot handle.

55
Q

What is an example of metaplasia in smokers?

A

Replacement of specialized mucociliary cells in the respiratory tract with simple squamous epithelium, which withstands stress better but leads to loss of mucociliary function & smoker’s cough.

56
Q

How does GERD cause metaplasia?

A

Changes in the esophagus lining occur due to chronic exposure to stomach acid, resulting in metaplastic changes.

57
Q

Can metaplastic changes be reversed?

A

Yes, if the irritant is removed within a reasonable time, metaplastic changes can revert; otherwise, the tissue may become degenerative.

58
Q

What is dysplasia?

A

A degenerative change in a cell population where cells deteriorate under chronic adverse conditions, leading to genetic damage & mutations.

59
Q

What are the characteristics of dysplastic cells?

A

They become smaller, misshapen, have fewer organelles, & may exhibit PLEOMORPHISM (variation in cell shapes).

60
Q

What happens to tissue structure in dysplasia?

A

There is increasing disarray, & the cells perform their functions less effectively, with impaired autophagy & apoptosis.

61
Q

Does dysplasia always lead to cancer?

A

No, dysplasia does not inevitably lead to cancer development, but it can. Some low-grade cases may never progress beyond dysplasia.

62
Q

What is Grade III dysplasia?

A

It is considered precancerous, indicating significant changes that require treatment, although the cells are not yet cancerous.

63
Q

What is pleomorphism?

A

Presence of variations of the same cell type.

64
Q

What is anaplasia?

A

Anaplasia refers to a set of cell changes used to diagnose whether a growth is malignant, observed only in cancerous tissue.

65
Q

What causes anaplasia?

A

It results from a series of genetic mutations that lead to de-differentiation of cells.

66
Q

How can an anaplastic cell be described?

A

An anaplastic cell can be said to have “regressed” to a stem-cell-like state, losing structural & functional features of mature cells.

67
Q

What happens to anaplastic cells regarding tissue controls?

A

Anaplastic cells become non-responsive to normal tissue controls & take on multipotent qualities.

68
Q

What is the capacity of anaplastic cells?

A

They can launch new populations of renegade cells like themselves.

69
Q

How does the presence of anaplastic cells affect tissue?

A

The more anaplastic cells present, the less the tissue resembles and functions like its original form.

70
Q

What can occur in highly malignant growths regarding tissue identification?

A

In highly malignant growths, it may not be possible to identify any characteristics of the tissue of origin.

71
Q

What is metastasis?

A

Metastasis is the ability of cancer cells to leave their tissue of origin & invade other tissues to establish new cell populations.

72
Q

How many genetic mutations are required for anaplastic cells to become capable of metastasis?

A

A minimum of 10 additional genetic mutations.

73
Q

What is a key characteristic of metastatic cells?

A

They have lost all adhesion mechanisms that keep tissue cells grouped together.

74
Q

What are the four pathways through which metastasis occurs?

A
  1. Progressive direct local invasion of neighboring structures.
  2. Movement through body cavities.
  3. Via the bloodstream (hematogenous metastasis).
  4. Via the lymphatic system (lymphogenous metastasis).
75
Q

Why is metastasis considered the most dangerous aspect of cancer?

A

It is responsible for 90% of cancer deaths.

76
Q

What happens to cancers that remain localized?

A

They are usually very treatable, especially if they are early-stage or slow to metastasize.

77
Q

How do cancer cells behave in relation to normal tissue controls?

A

They move beyond the regulatory signals for cell size, shape, alignment, quantity, & functionality, acting parasitically on neighboring tissues.

78
Q

What vulnerabilities do cancer cells possess?

A

They do not work together, fail to form purposeful tissues, & can be identified as abnormal by the body’s immune system, particularly specialized killer & helper T-cells.

79
Q

What is carcinoma-in-situ (CIS)?

A

A pre-tumor condition defined by the presence of anaplastic cells contained within the tissue of origin, without invasion beyond the basement membrane.

80
Q

What differentiates carcinoma-in-situ from severe dysplasia?

A

The presence of anaplastic cells is the key determining factor.

81
Q

How is carcinoma-in-situ staged?

A

It is given a stage of 0, while invasive cancers are staged from 1 to 4.

82
Q

What is the debate surrounding the CIS classification?

A

Some prefer to label a growth as cancer only once it becomes invasive, while others recognize CIS as an early-stage cancer, with the latter view being minority.

83
Q

What is carcinoma?

A

Carcinoma refers to cancers that arise from epithelial or endothelial tissue origins, accounting for 85% or more of cancers.

84
Q

What is sarcoma?

A

Sarcoma refers to cancers that arise in tissues without basement membrane structures, such as bone (osteosarcoma), muscle (myosarcoma), bone marrow, cartilage, & fat tissue.

85
Q

What is unique about carcinoma regarding the in-situ stage?

A

Only cancers that arise in tissues with basement membrane structures go through an in-situ stage; therefore, there is no sarcoma-in-situ.

86
Q

Do blood cell cancers have an in-situ phase?

A

No, blood cell cancers like leukemia do not have an in-situ phase.

87
Q

What does neoplasia mean?

A

Neoplasia means “new growth,” where cells reproduce outside of normal controls, resulting in an uncoordinated mass of cells (neoplasm or tumor).

88
Q

How do neoplasms interact with host tissue?

A

Neoplasms are parasitic on the nutrition & hormone supplies of the host tissue.

89
Q

Can neoplasms be benign or malignant?

A

Yes, neoplasms can be either benign or malignant; only cancerous tumors are considered malignant.

90
Q

What determines if a tumor is malignant?

A

The determination of malignancy is based on the presence of anaplasia.

91
Q

What is the rate of growth of benign neoplasms?

A

Progressive but slow turnover; mitoses are paced & normal; may stop or regress. Tumours generally oval or spherical in shape, usually symmetrical in presentation. Often stop growing at a certain point

92
Q

What is the differentiation of benign neoplasms?

A

Well differentiated; abnormalities to some degree, but cellular
characteristics like tissue of origin

93
Q

What is the cellular appearance of benign neoplasms?

A

Well-differentiated cells

94
Q

What is the local invasion of benign neoplasms?

A

Local growth that crowds but does not infiltrate or invade surrounding normal tissues. Benign tumours expand in the
place they started. Typically have an encapsulating membrane

95
Q

What is the metastasis of benign neoplasms?

A

Absent – no spread

96
Q

What are the complications of benign neoplasms?

A

Pressure on adjacent structures may cause uncomfortable S/S & require surgical removal. Some types of benign tumors are judged to be precancerous & are removed preventively

97
Q

What is the rate of growth of malignant neoplasms?

A

Cell division without control. Erratic, variable, typically rapid turnover with frequent, often abnormal mitoses. Tumours usually irregular in shape, poorly circumscribed, & extend into adjacent tissues. Angioneogenesis (formation of new blood vessel networks) to service their cells

98
Q

What is Angioneogenesis?

A

Formation of new blood vessel networks

99
Q

What is the differentiation of malignant neoplasms?

A

Irreversible DNA damage causing autonomous growth of an array of abnormal cells. Varying degrees of anaplasia present

100
Q

What is the cellular appearance of malignant neoplasms?

A

Nuclei larger, darker, irregularly shaped (the
nuclei of cancer cells contain excess DNA,
generally with an abnormal number of
disorganized chromosomes)

101
Q

What is the local invasion of malignant neoplasms?

A

Poor cohesion of cells within tumour, & invasive growth pattern (can overrun host
stroma). Penetration of the basal membranes
of origin & invaded tissues. Sending out of
“fingers” into adjacent tissue

102
Q

What is the metastasis of malignant neoplasms?

A

Increasingly likely with cells that exhibit a progressed stage of anaplasia

103
Q

What are the complications of malignant neoplasms?

A

Effects of invasive damage to local/distant
tissues. Can secrete substances that cause
effects throughout the body, e.g., fatigue,
fever, weight loss

104
Q

What is a key characteristic of cancer cells related to genetics?

A

Cancer cells demonstrate genetic instability, indicated by a high frequency of DNA mutations.

105
Q

What does pleomorphism mean in the context of cancer cells?

A

Pleomorphism refers to the presence of multiple variations of cell types within a cancer.

106
Q

How do cancer cells behave in relation to growth factors?

A

Cancer cells are growth factor independent; they can proliferate without tissue growth signals & do not stop based on cell density.

107
Q

What does the loss of intercellular cohesiveness imply for cancer cells?

A

Cancer cells lose their ability to adhere to each other & their tissue of origin, allowing them to disconnect & spread.

108
Q

What type of behavior do cancer cells exhibit towards other cells & tissues?

A

Cancer cells display aggressive & parasitic behaviors.

109
Q

What characteristics of stem cells do cancer cells exhibit?

A

Cancer cells can exhibit characteristics of pre-differentiated ancestor/stem cells, enabling them to produce large clonal populations of abnormal cells.

110
Q

What is the replication ability of cancer cells?

A

Cancer cells have unlimited replication potential due to the ability to renew telomeres.

111
Q

How do cancer cells evade the immune system?

A

Cancer cells develop strategies to evade the immune response, particularly during the tumor-forming stage.

112
Q

What do cancer cells induce to support their growth?

A

Cancer cells cause the formation of new blood vessel networks to supply nutrients.

113
Q

What is a notable metabolic feature of cancer cells?

A

Cancer cells have considerable anaerobic capacity, allowing them to thrive in low-oxygen environments.

114
Q

What can cancer cells produce independently?

A

Cancer cells can independently produce hormones, enzymes, & lytic substances to break down tissues for nutrition and invasion.

115
Q

How has the understanding of cancer cell production changed since before the 1940s?

A

It is now understood that all bodies regularly produce precancerous & cancerous cells, which are typically managed by the immune system.

116
Q

What contributes to cancer prevention by the immune system?

A

A robust immune response, including processes like autophagy & apoptosis, helps prevent and eliminate cell abnormalities.

117
Q

What are some local immune responses against cancer cells?

A

Local cell-mediated immune policing by glial cells, Kupffer cells, dendritic cells, & tissue-based macrophages.

118
Q

What role do specialized helper & killer T-cells play in combating cancer?

A

They identify & eliminate “self cells gone bad,” including those infected by viruses & cancer cells, & are particularly active in the blood & lymph.

119
Q

What does Stage 0 in cancer staging indicate?

A

Stage 0 is carcinoma-in-situ, characterized by anaplastic cells but no invasive behavior.

120
Q

What is Stage 1 in cancer staging?

A

Stage 1 involves local intra-tissue invasion, but the tumor is restricted to the primary site.

121
Q

What does Stage 2 signify in cancer staging?

A

Stage 2 indicates regional invasion, such as into local lymph nodes or neighboring structures, & may involve more than one tumor.

122
Q

What is described in Stage 3 of cancer staging?

A

Stage 3 involves larger-sized and/or multiple tumors that are spreading well outside the tissue of origin & beginning distant metastasis behaviors.

123
Q

What does Stage 4 indicate in cancer staging?

A

Stage 4 is characterized by established distant metastases.

124
Q

Is there usually a single cause of cancer?

A

It is extremely rare for cancer to have a single cause; most cases involve multiple interacting risk factors.

125
Q

What percentage of cancers in North America are estimated to be preventable?

A

Approximately 75-80% of cancers in North America are estimated to be preventable through human action.

126
Q

How do hereditary factors influence cancer?

A

Hereditary factors can play a significant role, with their impact varying by cancer type.

127
Q

What types of exposures are associated with cancer?

A

Exposure to toxins and pollutants, such as smoking (25-30% of cancer deaths), occupational chemicals, pesticides, and food-related pollutants.

128
Q

How does lifestyle relate to cancer risk?

A

Overuse of alcohol and overconsumption of processed foods can contribute to cancer development.

129
Q

What role do hormones play in cancer development?

A

Hormones that influence tissue growth, such as high estrogen from birth control or HRT, can be involved in cancer development.

130
Q

What are other causes of cancer?

A

Radiation exposure & certain infections, including viruses (e.g., Epstein-Barr, HIV) & some oncogenic bacteria (e.g., salmonella).

131
Q

How can immune response be linked to cancer?

A

Causes of damage, depletion, or impairment of immune responses can contribute to cancer development.

132
Q

What lifestyle factors may increase cancer risk?

A

Chronic sleep impairment, emotional trauma, chronic stress, & poor lifestyle choices can increase the risk of cancer.

133
Q

How is “lack of sunshine” related to cancer?

A

“Lack of sunshine” is linked to Vitamin D deficiency & emotional health, both of which can influence cancer risk.