Introduction to Cancer Flashcards
(115 cards)
1
Q
What is the term cancer used to describe?
A
A large group of diseases that are characterised by cellular malfunction.
2
Q
What is different between healthy and cancerous cells?
A
Healthy cells are programmed to respond to their local environment – life (and death) signals are continually received; without positive signals, most cells are programmed to die by apoptosis.
Cancerous cells have lost this programming and therefore grow and replicate “out of control”.
3
Q
What is the technical term for cancer cells?
A
Neoplasm.
4
Q
What is a neoplasm?
A
The technical term for a cancer cell.
5
Q
What is a group of neoplasmic cells called?
A
A tumour.
6
Q
What is a tumour made of?
A
Neoplasm cells.
7
Q
There are over how many forms of cancer?
A
200.
8
Q
What are the symptoms of cancer related to?
A
The size, location, and cells making up a tumour.
9
Q
How many new cases of cancer are diagnosed in the UK per annum?
A
300,000.
10
Q
What proportion of people develops cancer?
A
1 in 3.
11
Q
What proportion of deaths are attributed to cancer?
A
1 in 4.
12
Q
Describe benign tumours.
A
Benign tumours are non-cancerous growths of cells enclosed in a fibrous shell or capsule. They take up space and can interfere with surrounding tissues or vessels, impeding the function of the body. They also look unpleasant. They may secrete excess hormones and other factors.
13
Q
How are benign tumours treated?
A
Surgery.
14
Q
Describe malignant tumours.
A
Malignant tumours are cancerous growths of cells which invade surrounding tissues. They can become uncontained and move around the body, this is known as metastasis. These cells lose their function through de-differentiation.
15
Q
Carcinomas are cancers of what cells?
A
Epithelial cells.
16
Q
Sarcomas are cancers of which cells?
A
Mesenchymal cells (soft tissue, muscle).
17
Q
Leukaemias are cancers of which cells?
A
Blood and bone marrow cells.
18
Q
Lymphomas are cancers of which cells?
A
Lymphocytes.
19
Q
Germ cell cancers are cancers of which cells?
A
Sexual cells.
20
Q
Blastomas are cancers of which cells?
A
Precursor cells, those not terminally differentiated.
21
Q
What are the stages of cancer?
A
Stages 0-4.
22
Q
Describe stage 0 cancer.
A
No evidence, non-invasive.
23
Q
Describe stage 1 cancer.
A
Small spread with no spread to local lymph node.
24
Q
Describe stage 2 cancer.
A
Based on size or spread to local lymph node.
25
Describe stage 3 cancer.
Based on size or spread to local or more distant lymph nodes.
26
Describe stage 4 cancer.
Fully metastatic spread to distant parts of the body.
27
What proportion of women develops breast cancer?
One in eight.
28
How can breast cancer be screened for?
Through self-examination and mammography.
29
How many cases of skin cancer are there per year?
1.3 million.
30
What is the 3rd most common cancer in men and women?
Colon and rectal cancer.
31
Give some warning signals for colon and rectal cancer.
Blood in the stool, rectal bleeding.
32
What is the most common cancer in males today?
Prostate cancer.
33
Which cancer type is describes as a silent disease?
Pancreatic cancer.
34
What percentage of people survive pancreatic cancer?
4%.
35
Give some contributors to the development of pancreatic cancer.
Inflammation, diabetes, high-fat diet.
36
What age range is at the greatest risk of testicular cancer?
17-34.
37
Which type of testicles presents a greater risk?
Undescended.
38
Which form of cancer is the 4th leading cause of death in young women?
Ovarian cancer.
39
What is a common sign of ovarian cancer?
Enlargement of the abdomen.
40
What can be carried out to screen for ovarian cancer?
Annual pelvic exams.
41
How many different types of ovarian cancer is there?
31.
42
What are the 4 main classes of leukaemia?
ALL, AML, CLL, CML.
43
How many main classes of leukaemia?
4.
44
What does leukaemia lead to?
The formation if immature white blood cells.
45
What percentage of leukaemia cases are in children?
50%.
46
What is the survival rate of leukaemia?
90%.
47
What activity can lead to an increased risk of endometrial/uterine cancer?
Early sexual intercourse.
48
Give a warning sign for endometrial/uterine cancer.
Abdominal bleeding.
49
What causes cancer?
Oncogenes, mutated tumour suppressors, mutated DNA repair genes, biological factors, chemicals in food, viral factors, medical factors, occupational and environmental factors, social and psychological factors.
50
What are oncogenes?
These are genes (proto-oncogenes) that promote cell growth. When mutated or altered they can enhance tumour formation and growth. Oncogenes often encode proteins that are involved in cell signalling.
51
How are oncogene mutations acquired?
These mutations are usually acquired through DNA damage however they can also be somatic (from one’s parents).
52
Are oncogenes dominant or recessive?
Dominant.
53
How were oncogenes discovered?
Oncogenes were discovered as a result of virus-induced tumours (vRas, vSrc).
54
Give some important oncogenes.
Src, Ras.
55
How many classes of oncogenes are there?
4.
56
Describe oncogenes class 1.
Growth factors e.g. sis B chain of PDGF (platelet-derived growth factor).
57
Describe oncogenes class 2.
Growth factor receptors e.g. erbB membrane receptor for EGF (epidermal growth factor).
58
Describe oncogenes class 3.
Intracellular transducers – e.g. abl tyrosine protein kinase, ras-G protein.
59
Describe oncogenes class 4.
Nuclear transcription factors – e.g. fos, myc, myb.
60
How are oncogenes activated?
* Chromosomal translocation.
* Excessive production of protein.
* Point mutation – a change in a single base changing a whole protein.
61
Describe ras.
Ras is a G-protein that signals on the ras-MAPK (kinase) pathway. Its activity is regulated by guanosine nucleotides (GDP and GTP).
62
How does ras work and become activated?
Active ras is bound to GTP – control of ras achieved by control of GTP. Ras has an intrinsic phosphatase activity – inactive GDP – ras is switched off most of the time. A point mutation causes constitutive activity; A single mutation can remove the phosphatase function – GTP remains as GTP – ras remains active.
63
How does src work?
Src is a cellular tyrosine kinase involved in signalling from EGF and PDGF receptors. A truncated (shortened) form has constitutive activity and causes sarcoma in chickens (Rous sarcoma virus).
64
Unmutated, what do tumour suppressors do?
Unmutated, these genes control growth and death (apoptosis) of cells by suppressing tumour formation.
65
Are oncogenes for tumour suppressors recessive or dominant genes?
Recessive.
66
How are mutations in tumour suppressor oncogenes acquired?
Mutations are usually acquired through DNA damage. They can also be acquired (usually one allele – second is acquired).
67
What is P53?
P53 is a tumour-suppressor gene (regulates cell division); mutations of this gene are associated with many types of a tumour (~ 50% of human tumours lack a functional P53 gene).
68
How many tumours lack a functional P53 gene?
~ 50% of human tumours lack a functional P53 gene.
69
What happens when P53 mutates?
When P53 mutates the cell cannot control cell division. Cancer cells lacking P53 initially are more resistant to DNA damage; they stay alive and reproduce anyway. With continuing treatment, the DNA damage accumulates to the point of non-viability.
70
What does functional P53 do?
The expressed P53 protein is a transcriptional regulator that is activated in response to DNA damage. Wild-type P53 prevents progression of the cell cycle until DNA damage is repaired.
71
Which anti-cancer drug restores P53 activity?
The anticancer drug, adriamycin restores p53 activity.
72
What are thymine dimers and how are they formed?
Thymine dimers can form when one goes into the sun (the joining of two thymine bases) and these dimers can cause an incorrect base to be introduced when the DNA is replicated.
73
What biologic factors are implicated in cancer?
Genetic predispositions, reproductive and hormonal risks.
74
What chemicals in food are implicated in cancer?
* Sodium nitrate – generated by soil bacteria - mutates the amine group on bases to oxygens – kills H. Pylori.
* Clostridium botulinum.
75
What viral factors and implicated in cancer?
* Herpes-related virus.
| * Human papillomavirus (HPV).
76
What medical factors are implicated in cancer?
* Diethylstilbestrol (DES).
| * Chemotherapy – modifies DNA.
77
What occupational and environmental factors are implicated in cancer?
* Asbestos, nickel, chromate.
| * Radioactive substances.
78
What social and psychological factors are implicated in cancer?
* Stress.
| * Negative emotions.
79
What is the mainstay of cancer treatment?
Surgery.
80
How can surgery to remove cancer sometimes be difficult?
Defining boundaries can be difficult – need to remove as much as possible without causing excessive damage. Cancers of epithelial cells and blood cells can’t be cut out.
81
What is radiotherapy?
This is the use of radiation to destroy cancerous cells.
82
In what ways are drugs used in cancer treatment?
* To prevent a tumour developing, e.g. tamoxifen for healthy women at a high risk of breast cancer.
* Before surgery to shrink the tumour (neoadjuvant).
* To kill any cancer cells remaining after surgery and radiotherapy (adjuvant).
* To treat inoperable cancer (e.g. brain), disseminated cancers (e.g. Leukaemia) or metastasis.
83
What are the potentially exploitable characteristics of cancer cells?
* More rapid growth and division than corresponding normal cells (though probably slower than GI and blood cells).
* Disrupted metabolism of cancer cells may lead to specific metabolic or nutritional requirements.
* Chromosome ends are stabilized by the repetitive sequence at the end – Telomeres.
* Cancer cells often display different surface proteins /antigens.
* Hormone dependence.
84
What is the difference in growth rates between cancerous and healthy cells?
Cancer cells have more rapid growth and division than corresponding normal cells (though probably slower than GI and blood cells).
85
What are the specific targets when targeting cancer cell growth and division?
* DNA synthesis with anti-metabolites.
* DNA replication and processing with alkylating agents.
* Blocking of metabolic pathways.
* Altering the stability of microtubules to inhibit cell division (mitosis).
* Inhibition of angiogenesis.
86
What compounds prevent the assembly of tubulin dimers?
Vinca alkaloids.
87
What compounds prevent the disassembly of tubulin dimers?
Taxanes.
88
What nutrient is required for some leukaemic cells?
Asparagine.
89
What drug can be used to inhibit pyruvate kinase M2?
Resveratrol.
90
Why does the use of asparaginase have little effect on healthy cells?
Healthy cells can produce their own asparagine.
91
What is the Warburg effect?
Enhanced glucose uptake, lactate production, and anabolism.
92
How does asparaginase work?
Asparaginase is injected for treatment of leukaemia’s which are highly-dependent on dietary asparagine. Injected asparaginase metabolises blood asparagine, withdrawing it from tumour cells, and causing asparagine-dependent tumour cells to die.
93
How does photodynamic therapy work?
Cancer cells have rapid metabolism so lactic acid builds up, acidifying the cells and their environment – differentiation. Light-absorbing compounds are administered to the tissue or whole body (some are selectively retained by tumours as they are acidified by lactic acid). Light is shone on the area and induces oxygen free radial oxygen formation: Photodynamic Therapy (PDT). Radicals damage tissue and induce an immune response.
94
Why is photodynamic therapy not as easy as it sounds?
This isn’t as simple as it sounds however as the light might not be able to get to the area of the body where it is needed, so surgery may be required.
95
How are chromosomes stabilised?
Chromosome ends are stabilized by the repetitive sequence at the end called telomeres.
96
How are telomeres affected by cell division?
Telomeres shorten with each cell division until a critical length reached; cells then undergo cell cycle arrest (senescence) or apoptosis.
97
What happens to unprotected chromosome ends?
The unprotected chromosome ends cause chromosome fusions, breakage, and rearrangements and tumour development.
98
What is a chromosome crisis?
Somatic mutations block senescence induction, cells continue to divide, and telomere erosion continues until cells stop dividing again -- this second block is called "chromosome crisis."
99
How is telomere length maintained?
Telomere length is maintained by a ribonucleoprotein called telomerase, which adds new DNA ends to chromosomes.
100
During development, where is telomerase detected?
During development, telomerase activity is detected in almost all tissues.
101
In adults, where is telomerase significantly expressed?
In adults, telomerase is significantly expressed in germline and stem cells of renewable tissues such as bone marrow, skin, and the gastrointestinal tract.
102
What happens when some cancer cells express active telomerase?
Some cancer cells express active telomerase avoiding senescence (or apoptosis); becoming “immortal”.
103
Give some examples of surface proteins/antigens expressed by cancer cells?
* Overproduction of HER2 in ~25% of metastatic breast cancers.
* Abnormal Bcr-Abl tyrosine kinase encoded by the Philadelphia chromosome in chronic myeloid leukaemia.
* Cancer cell specific cell surface antigens.
104
What are the treatment strategies for hormone-dependent cancerous cells?
* Block the hormone receptors with anti-hormones (e.g. tamoxifen, cyproterone acetate).
* Swamp cells with excessive doses of hormones (downregulate receptors).
105
What is prednisolone and what is it used for?
A synthetic corticosteroid used in the treatment of blood cell cancers (leukemias), and lymph gland cancers (lymphomas).
106
What is stilboestrol and what is it used for?
(artificial oestrogen) - Effective against prostate cancer and surprisingly effective against breast cancer in post-menopausal women.
107
What is tamoxifen?
Partial anti-oestrogen.
108
What is flutamide and that is it used for?
Antiandrogen: palliative hormonal treatment of advanced prostate cancer and sometimes in the adjuvant and neoadjuvant hormonal treatment of earlier stages of prostate cancer.
109
What is goserelin and what is it used for?
Gonadotropin-releasing hormone analogues and used to block hormone production in the ovaries or testicles. Used to treat hormone-sensitive cancers of the prostate and breast.
110
Give some examples of third-generation aromatase inhibitors/inactivators.
Letrozole (Femara) and Exemestane (Aromasin).
111
How does anastrozole (Arimidex) work?
This drug blocks conversion of aromatizable steroids to oestrogen by inhibiting the enzyme aromatase. It is compared to anti-oestrogens like tamoxifen and has no oestrogen agonist effects.
112
Clinically, what is anastrozole used to treat?
Clinically anastrozole is used to treat hormone-dependent breast cancer in post-menopausal women.
113
How di anti-hormones work?
These are antagonists of steroid hormone action. They interact with the ligand-binding domains of steroid hormone receptors and competitively inhibit the action of receptors by mechanisms (not understood). Therefore, target the hormone receptors with anti-hormones, or swamp the cells with excessive doses of hormones.
114
What is an angiogenic inhibitor?
An angiogenic inhibitor is a drug or dietary component that inhibits angiogenesis i.e. the growth of new blood vessels.
115
One example of an angiogenesis inhibitor is bevacizumab, how does it work?
Inhibitors include bevacizumab which binds vascular endothelial growth factor (VEGF), inhibiting its binding to the receptors that promote angiogenesis.
