Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

214.201 > Cancer > Flashcards

Cancer Flashcards

1
Q

Cancer characterised by?

A
  • Loss of growth control leading to an unregulated increase in cell number
  • Metastasis and invasion of other tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cancer is caused by what?

A

Mutations in genes controlling cell growth after exposure to carcinogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cancer differ in what?

A
  • Tissue of origin
  • Causal factor(s)
  • Molecular mechanisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is cancer incidence in NZ and worldwide?

A

Leading cause of death in NZ and second worldwide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do tumours develop?

A
  • Cells lose growth control causing them to proliferate and form new growth - neoplasia
  • Cells do not die via apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Difference between benign and malignant tumours?

A
  • Tumour is benign if the neoplastic cells are clustered in a single mass
  • Tumour becomes malignant once cells have undergone metastasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Characteristics of benign tumour?

A
  • Cells are well differentiated and look like normal cells
  • May perform the normal function of the tissue
    e. g. secrete hormones, although may over-secrete - insulinoma
  • Cells grow relatively slowly but this is not suppressed by apoptosis or contact inhibition
  • Size may be limited to just a few mm by lack of blood supply Surrounded by a fibrous capsule & confined to original location
  • Do not infiltrate, invade, or metastasize
  • Can damage nearby organs by compressing them
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Characteristics of of malignant tumour?

A
  • Cells are less differentiated and do not look like normal cells
  • Do not perform the normal function of the tissue -May secrete new signalling molecules, enzymes or toxins etc.
  • Cells grow rapidly since they have lost the ability to control proliferation and differentiation
  • No fibrous capsule
  • Cells infiltrate & invade surrounding tissues and metastasize to form new tumours at distant sites
    • Tumour sends “legs” into surrounding tissue
  • Can compress and/or destroy surrounding tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are tumours classified?

A

According to tissue of origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How are benign tumours named by?

A

Tissue name + -oma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are malignant tumours names derived?

A
  • Carcinomas are derived from epithelial cells
  • Adenocarcinomas are derived from glandular epithelial cells
  • Sarcomas are derived from mesenchymal cells
  • Leukaemias are derived from haemopoietic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the most common type of cancer?

A

Carcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are examples of Adenocarcinomas?

A

Lung, colon, breast, pancreas, stomach, oesophagus, prostate, ovary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are examples of Squamous cell carcinoma?

A

Skin, oropharynx, larynx, lung, oesophagus, cervix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are examples of other types of carcinomas?

A

Small-cell lung-, large- cell lung-, haptic-, renal- and bladder- carcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some examples of Sarcomas & Leukaemias?

A

Osteosarcomas (from bone), Liposarcoma (from adipose tissue), Rhabdomyosarcoma (from muscle), Acute Lymphotic Leukaemia, Acute Myelogenous Leukaemia, Multiple Myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How are most adult cells characterised?

A

Terminally differentiated and quiescent (non-dividing)

exceptions include; hair follicles, blood and gut stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How are cell numbers remained constant?

A

Within each tissue, cell death, by apoptosis or necrosis, is balanced by cell division, often of stem cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is cell division regulated?

A

By growth factors which allow quiescent cells to enter the cell cycle and divide.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the Hallmarks of Cancer

A
  • Self-sufficiency in growth signals
  • Insensitivity to anti-growth signals
  • Evading apoptosis
  • Sustained angiogenesis
  • Limitless replicative potential
  • Tissue invasion and metastasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does telomere length control lifespan?

A
  • Cells contain telomerase, an enzyme which can elongate telomeres
  • Telomerase activity is essential for allowing cells to keep proliferating
  • As cells age, telomerase becomes inactive and hence telomeres shorten & cells lose the ability to divide – limits lifespan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does increased telomerase affect cells?

A

Increased telomerase activity allows cells to proliferate indefinitely and leads to cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the normal cell cycle?

A

There are four phases:

  • G1 – gap between M & S phase
  • S phase – DNA synthesis/replication
  • G2 – gap between S & M phase
  • M phase – mitosis, cytokinesis/division
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why does the cell cycle prevent uncontrolled cell proliferation?

A

The cell cycle regulates cell proliferation.
If differentiated cells start dividing again or cycling cells lose control then this can lead to uncontrolled proliferation & cancer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the cell cycle checkpoints?

A

1) G1/S transition checkpoint
- Are growth factors present?
- Are nutrients available?
- Is DNA damaged?
- Is the cell big enough?
2) G2/M transition checkpoint
- Has DNA replicated?
- Is DNA damaged?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What happens if these needs are not met?

A

Cell cycle arrest which can lead to cell death by apoptosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the tumour suppressors and what do they do?

A

p53, p21 & p27

They inhibit cell division.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What active complex is needed to pass through G1/S checkpoint?

A

Cdk4/6-cyclinD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What happens when DNA repair genes are mutated?

A

Genome instability and increased likelihood of further mutation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are some germline mutations?

A
  • Rb – retinoblastoma

- BRCA1/2 – breast cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How many mutations are need for cancer to develop? In particular colon and lung?

A

2-20
Colon - 4-5
Lung - 10-15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is it beneficial to identify molecular fingerprints of cancers?

A
  • Screening
  • Diagnosis and targeted treatments
  • Understanding mechanism and development of new therapies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the two main mutations types affecting cell proliferation?

A
  • Oncogenes

- Tumour suppressor genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are proto-oncogenes and how do oncogenes vary?

A

Proto-oncogenes normally stimulate cell proliferation allowing progression from G1 to S phase. Oncogenes are mutations that allow this progression in the absence of growth factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are TSGs and how do mutations of these cause cancer?

A

Tumour suppressor genes negatively regulate cell division, preventing
abnormal proliferation, suppressing tumorigenesis.
Mutations cause a loss of function, allowing DNA that is damager or not fully replicated to progress through cell cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the Ras-MAPK pathway and how do mutations affect it?

A

Growth factors activate the pathway, activating Cdk4/6 and allows progression through the G1/S checkpoint and cell division. Activating mutations enable the pathway to always be active, enabling cell division independently of growth factors (oncogene).

37
Q

What is p53 and how do mutations affect it?

A

p53 senses DNA damage.

Inactivating mutations of p53 disables its ability to cause cell apoptosis when damage has occurred.

38
Q

What are the stages of cancer development?

A

1) Initiation
- Exposure to carcinogen
- Damage to DNA
2) Promotion
- Altered cell divide via tumour promoter
- Altered cells remain dormant or removed
3) Progression
- More mutations
- Uncontrolled cell replication and loss of specialisation
- Cells are aggressive and invasive

39
Q

What is intravasation?

A

The ability for cells in primary tumour to escape into the circulation

  • Loss of adhesion
  • Secretion of proteases to degrade basement membrane
40
Q

How does cancer complete invasion and metastasis?

A

Cells develop intravasation, survive in blood or lymphatic system, complete extravasation, develop into secondary tumour, angiogenesis, metastasis of multiple distant sites

41
Q

What are host risk factors?

A
  • Hereditary
  • Reproductive hormones - can act as tumour promoters
  • Obesity - insulin promotes tumour growth
    Immune surveillance of tumour antigens
42
Q

What are environmental risk factors?

A
  • Chemical carcinogens (Smoking, alcohol, occupational exposure)
  • Viruses and bacteria (Hepatitis, HPV)
  • Radiation (UV exposure, radioactivity)
43
Q

Benefits of fruit and vegetables?

A

May protect by blocking effects of carcinogens or suppressing growth of tumour cells.

44
Q

What are some local effect - clinical manifestations from tumours?

A
  • Compression or blockage of structures close by
  • Blood vessels - bleeding or blockage
  • Effusions - build up of fluid (pleural effusion, ascites)
45
Q

What are some systemic effect - clinical manifestations from tumours?

A
  • Malnutrition (Malabsorption, anaemia, anorexia & Cachexia)
  • Fluid and electrolyte imbalances
  • Fatigue and sleep disturbances
  • Paraneoplastic syndromes
  • Pain in later stages
46
Q

What is anorexia-cachexia syndrome?

A

Protein/energy malnutrition due to:

  • Increased energy demand
  • Reduced energy intake & malabsorption
47
Q

What are the seven warning signs of cancer

A
  • Change in bowel or bladder habits
  • A sore that does not heal
  • Unusual bleeding or discharge from any body orifice
  • Thickening or a lump in the breast or elsewhere
  • Indigestion or difficulty swallowing
  • Obvious change in a wart or mole
  • Nagging cough or hoarseness
48
Q

How do you screen and diagnose cancer?

A
  • Indirect, non-specific tests (blood count, abnormal hormones)
  • Cytology (pap smear, tissue biopsy)
  • Diagnostic imaging (x-ray, MRO, ultrasound)
  • Tumour markers (prostate-specific antigen PSA)
  • Microarray technology (gene chips measure mRNAs)
49
Q

What is the tumour grading?

A
  • Grade l - Cells differ slightly from normal cells and are well differentiated
  • Grade ll - Cells are more abnormal and moderately differentiated
  • Grade lll - Cells are very abnormal and poorly differentiated
  • Grade lV - Cells are immature and undifferentiated
50
Q

What is the overall tumour staging?

A
  • Stage 0 - Cancer in situ
  • Stage l - Tumour limited to the tissue of origin
  • Stage ll - Limited local spread
  • Stage lll - Extensive local and regional spread
  • Stage lV – Metastasis to distant sites
51
Q

What is the TNM staging?

A
  • T 1 – 4 = tumour size
  • N 0 – 3 = lymph node involvement
  • M 0 – 1 = metastasis
52
Q

What involves prevention of cancer?

A
  • Avoiding environmental exposure
  • Diet, smoking alcohol, obesity
  • Products e.g sunscreen
  • Vaccination HPV
  • Routine screening (Smear)
  • Education
53
Q

Cancer treatment?

A
  • Surgery (if no metastasis)
  • Radiation therapy (apoptosis)
  • Chemotherapy (targets rapidly dividing cells)
  • Hormone and anti-hormone therapy
  • Immunotherapy (stimulate immune system to kill cancer cells)
  • Targeted therapies
54
Q

What are the most prevalent cancers in NZ?

A

1) Lung
2) Bowel
3) Breast

55
Q

Lung cancer incidence and risk factors?

A
  • Adults 40 - 70 yrs old
  • Usually diagnosed late & after metastasis
  • 80-90% due to long term exposure to carcinogens in tobacco smoke
  • Occupational exposure
56
Q

Lung cancer signs and symptoms?

A
  • Persistent, worsening cough
  • Coughing up excessive phlegm with blood
  • Chest pain with coughing or breathing
  • Recurring chest infections
57
Q

Lung cancer diagnosis?

A
  • Symptoms
  • Chest x-ray, CT scan
  • Sputum cytology
58
Q

Lung cancer prevention & treatment?

A
  • Cessation of smoking
  • Surgery
  • Radiation
  • Chemotherapy
59
Q

Bowel cancer incidence and risk factors?

A
  • Adults 50+ yrs old, slightly more prevalent in men
  • Early detection and treatment gives 90% chance of long term survival
  • Increasing age & low fibre, high fat diet
  • Inflammatory bowel
  • Hereditary nonpolyposis colorectal cancer
60
Q

Bowel cancer signs and symptoms?

A
  • Blood in bowel motions or change in bowel habits for several weeks
  • Abdominal discomfort e.g. bloating, cramps etc
  • Unexplained weight loss, tiredness, anaemia
61
Q

What is the multistep progression of bowel cancer?

A

1) Normal colon epithelium
2) Hyper proliferating epithelium
3) Benign adenoma (polyp)
4) Intermediate adenoma
5) Late adenoma with villi
6) Adeno- carcinoma
7) Metastatic colon cancer

62
Q

Bowel cancer diagnosis?

A
  • Rectal and abdominal exam
  • Blood tests
  • Colonoscopy; CT colonography
63
Q

Bowel cancer prevention?

A
  • Maintain a healthy diet & weight
  • Regular exercise
  • Quit smoking & cut back on alcohol
  • Bowel screening helps earlier detection
64
Q

Bowel cancer treatment?

A
  • Surgery
  • Radiation
  • Chemotherapy
65
Q

Breast cancer incidence?

A
  • Most common cancer in women (1 in 9 will be affected)

- Most will have no family history

66
Q

Breast cancer signs and symptoms?

A
  • Change in breast shape or lumps in breast
  • Thickening of tissue
  • Nipple changes e.g. skin dimpling
  • Blood stained discharge from nipple
  • Rash
  • Painful area
67
Q

Breast cancer host risk factors?

A
  • Being female
  • 50+ years old
  • Previously having breast cancer
  • Increased number of abnormal cells in milk ducts
  • Affected first degree relative (risk doubles)
  • Mutation of BRCA1 (Chr 17) and BRCA2 (Chr 13) genes
68
Q

Breast cancer environmental risk factors?

A
  • Nulliparity – not having given birth
  • First child after 30
  • High fat diet, alcohol use
  • Oestrogen replacement therapy
69
Q

Breast cancer hormone & growth factor effects?

A
  • Circulating oestrogen and progesterone (can act as tumour promoter)
  • Amplification of HER2 (acts as oncogene)
70
Q

Breast cancer diagnosis?

A

Medical history; physical exam; mammogram/ultrasound; biopsy and lab testing on tissue

71
Q

Breast cancer prevention?

A
  • Regular mammogram
  • Self examination
  • Good lifestyle
72
Q

Breast cancer treatment?

A
  • Surgery, radiation, chemotherapy

- Hormone treatment (block hormone receptors or lower hormone levels)

73
Q

Skin cancer incidence?

A

NZ has highest rate in the world

74
Q

Skin cancer risk factors?

A
  • Family history
  • Skin that burns easily
  • Cumulative sun exposure (age) or episodes of severe sunburn, esp. as a child
  • Sunbeds
75
Q

Skin cancer signs and symptoms?

A

Red, scaly, rough skin lesions on sun-exposed areas; hands, head, neck, lips and ears

76
Q

Skin cancer diagnosis?

A
  • Skin checks, mole maps

- Biopsy

77
Q

Skin cancer prevention?

A
  • Cover skin

- Check skin

78
Q

Skin cancer treatment?

A
  • Surgery
  • Radiation
  • Photodynamic therapy - photosensitiser drug and light or laser treatment kills tumour cells with reactive oxygen species (ROS)
79
Q

Prostate cancer incidence and risk factors?

A
  • Second most frequently diagnosed cancer
  • Male > 50 yrs
  • Poor diet – obesity, link with red meat?
  • Family history, BRCA1/2
  • Elevated testosterone
80
Q

Prostate cancer signs and symptoms?

A
  • Initially asymptomatic

- Frequent urination, pain or difficulty with urination, blood in urine

81
Q

Prostate cancer diagnosis?

A
  • Digital rectal examination (DRE), ultrasound, MRI, biopsy

- Screening for prostate-specific antigen (PSA) useful

82
Q

Prostate cancer prevention?

A

Diet/exercise?

83
Q

Prostate cancer treatment?

A
  • Most are slow growing - managed with drugs to ↓ testosterone (Finasteride)
  • For aggressive tumours - surgery, radiation / brachytherapy, chemotherapy
84
Q

Cervical cancer incidence?

A

4th most common cancer in women worldwide

85
Q

Cervical cancer risk factors?

A
  • HPV greatest risk factor (mostly subtypes 16 & 18)
  • Number of sexual partners
  • Family history, smoking, poor diet
86
Q

Cervical cancer signs and symptoms?

A
  • Abnormal vaginal bleeding or discharge

- Tiredness, pain in pelvic area, legs or lower back

87
Q

Cervical cancer prevention?

A
  • Cervical screening using Papanicolaou (Pap) or smear test – every 3 years
  • HPV vaccination
  • Barrier protection during intercourse
88
Q

Cervical cancer diagnosis?

A
  • Pap test, visual inspection (colposcopy), and biopsy

- Also imaging (ultrasound, CT, MRI, PET, bone scan)

89
Q

Cervical cancer treatment?

A

Surgery, radiation / brachytherapy, chemotherapy

214.201 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions