Tumour Pathology Flashcards
1
Q
How are tumours classified?
A
Location and wether or not its benign or malignant.
2
Q
Why are tumours classified?
A
To aid understanding of tumour behaviour .
3
Q
What does the name of a tumour convey?
A
It’s behaviour.
4
Q
What does tumour nomenclature depend on?
A
Tissue type where it is found.
5
Q
What is tumour nomenclature used for?
A
Identifies what therapy should be considered.
6
Q
What are the two types of epithelial tissue where tumours are found?
A
Glandular and Squamous.
7
Q
What is the benign and malignant tumour found in glandular tissue?
A
Benign= adenoma Malignant= adeno-carcinoma
8
Q
What is the benign and malignant tumour found in Squamous tissue?
A
Benign= squamous papilloma Malignant= squamous carcinoma
9
Q
What are the tumours found in bone?
A
Benign= osteoma Malignant= osteo-sarcoma
10
Q
What are the tumours found in fat?
A
Benign= Lipoma Malignant= Lipo-sarcoma
11
Q
What are the tumours found in fibrous tissue?
A
Benign= Fibroma Malignant= Fibro-sarcoma
12
Q
What are the tumours found in WBCs?
A
Malignant= leukaemia
13
Q
What are the tumours found in lymphoid tissue?
A
Malignant= lymphoma
14
Q
Where are tumours found in germ cells?
A
Teratomas
15
Q
What are the tumours found in teratomas?
A
Benign= ovarian Malignant= testicular
16
Q
What type of tumour has an invasive growth pattern?
A
Malignant
17
Q
What type of tumour is encapsulated?
A
Benign
18
Q
What type of tumour has no metastases?
A
Benign
19
Q
What type of tumour has cells that are normal and well-differentiated?
A
Benign
20
Q
What tumour is more lethal?
A
Malignant
21
Q
What type of tumour loses it’s normal function?
A
Malignant
22
Q
In what type of tissue is there evidence of spread?
A
Malignant
23
Q
What are the 4 features of cancer cells?
A
Altered genetics, altered cellular function, abnormal structure and independent growth
24
Q
What are altered genetics?
A
Gain of oncogenes and loss of suppressor genes
25
How are cellular functions altered?
Change in tumour-related proteins.
26
What does the abnormal structure of cancer cells allow?
Diagnosis
27
What are the affects of independent growth?
Failure to respond to cell-cycle regulations and uncontrollable division
28
What is the process in which cancer spread?
Metastasis
29
What is Metastasis?
The formation of secondary tumours
30
What is local spread?
Malignant tumour invasion in surrounding connective tissue into lymph and BVs
31
What is lymphatic spread?
Tumours attach and invade lymph vessels and form secondary tumours in the lymph nodes
32
What can lymphatic spread be used for?
Clinical evidence
33
What is blood spread?
Tumour cells invading blood cells and forming secondary tumours in tissues
34
What is trans-coelomic spread?
Spread of tumours across body cavities
35
Where are trans-coelomic tumours shown?
Stomach, ovaries, colon and lungs
36
What are the common sites for tumour formation?
Liver, lung, brain, bone and adrenal glands
37
What are the uncommon sites for skeletal muscle?
Spleen, kidneys, skeletal muscle and heart
38
What are the local effects of benign tumours?
Pressure and obstruction
39
What are the local effects of malignant tumours?
Pressure, obstruction, pain, tissue destruction and bleeding
40
How are tissues destroyed?
Ulceration and infection
41
How do tumours cause bleeding?
Anaemia and haemorrhage
42
How do tumours cause pain?
Pressure on nerves and bone fractures
43
What are the 3 systematic effects of tumours?
Hormone secretion, weight loss and treatment effects
44
What are the 2 types of hormones secreted?
Normal and Abnormal
45
How are normal hormones secreted?
Tumours produced in the endocrine organ
46
What is the function of normal hormones?
Abnormal control of production and secretion
47
How are abnormal hormones secreted?
Tumour produced in an organ that does not normally produce hormones
48
What type of hormone is most commonly secreted?
Abnormal
49
What causes weight loss?
Cachexia
50
What is the earliest stage of detecting cancer?
Pre-invasive stage
51
What is detected at the pre-invasive stage?
Dysplasia
52
What is dysplasia the same as?
Intraepithelial neoplasia
53
What is dysplasia 1?
Pre-malignant change and the earliest visualised change
54
What is dysplasia 2?
No invasion and can progress to cancer
55
Where is dysplasia 2 located?
Epithelium
56
What is meant by a high grade of dysplasia?
Higher chance of progressing to cancer
57
What can't occur if there is no invasion?
Detection of spred
58
What is a cell cycle?
Time interval between mitotic divisions
59
What is the normal cell cycle?
Mechanism of cellular replication
60
Cellular replication is also known as?
Proliferation
61
Is the normal cell cycle reversible?
No
62
What are the 4 steps of the normal cell cycle?
G1, S, G2, M
63
What happens in G1?
Cells can respond to external signals and components required for DNA synthesis are synthesised
64
What happens in S?
DNA is synthesised and replicated
65
What happens in G2?
Mitosis is prepared
66
What happens in M?
Mitosis and cell division
67
How does DNA synthesis an mitosis occur?
Sequentially
68
What must each daughter cell receive?
A full chromosome complement
69
How is the normal cell cycle controlled?
By active and inactive enzyme switches in checkpoints
70
What are normal cell cycle checkpoints?
System of active and inactive enzymes
71
Where do normal cell cycle checkpoints occur?
On several points in the cycle
72
How is an active enzyme complex formed?
When CDK is activated by cyclins
73
Are CDK and cyclin always present?
No, only CDK is always present. Cyclins are only present when needed
74
What is the function of an enzyme switch?
Activates/inactivates and phosphorylates target proteins
75
What is CKI?
CDK inhibitor that prevents molecules from binding to the active enzyme complex
76
What is cancer?
Abnormal cell cycle function due to uncontrolled cell proliferation via cell cycle dysregulation
77
What is carcinogenesis?
Failure of cell cycle control as the balance between proliferation and apoptosis is disrupted
78
What occurs as a result of carcinogenesis?
Formation of DNA adducts and a mass of cells with genetic abnormalities. Cell cycle regulators are mutated
79
What are the causes of carcinogenesis?
Radiation (UV, X-ray and Gamma), Viruses (Hep. B, HPV and EBV) and a series of mutations
80
What is the process of viral carcinogenesis?
Virus genome inserts near a host proto-oncogne which causes port-oncogene over expression. Retroviruses then insert on the oncogenes and causes cell division.
81
What does HPV cause?
Cervical cancer
82
What does Hepatitis B cause?
Liver cancer
83
What does EBV cause?
Lymphomas
84
What is the process of chemical carcinogenesis?
Adduct formation at particular chromosome sites that activates oncogenes and suppresses anti-oncogenes
85
What are the 4 cell-regulatory genes?
Cyclin D, CDK4, p16 and Rb
86
What happens to cell-cycle regulator genes?
They are mutated
87
What pathways of the normal cell cycle does carcinogenesis disrupt?
Cyclin pRb and p53 pathway
88
What is the function of p53?
It maintains the integrity of the genome and expresses p21 to repair DNA
89
What occurs in the cyclin pRb pathway?
pRb acts as a cell cycle brake which controls growth and proliferation
90
What happens when the cyclin pRb pathway is mutated?
The pRb brakes are released which causes uncontrolled proliferation
91
What occurs in the p53 pathway?
Cell cycle is stopped when the cell sustains damage so it can be repaired
92
What does p53 trigger when cells are badly damaged?
Apoptosis
93
What happens when p53 is mutated?
Cells do not enter G1 arrest which prevents DNA repair
94
How is the cell cycle prevented from stopping?
Mutations, which causes cancer
95
What are DNA adducts?
They are covalently bound products that activate oncogenes and causes the loss of anti-oncogenes
96
What are tumour suppressor genes?
Recessive anti-oncogenes that are normal regulatory and genes.
97
What is an example of a tumour suppressor gene?
pRb (anti-oncogene)
98
What are the functions of tumour suppresser genes?
Regulates DNA and mitosis (negatively)
99
What happens when pRb is released from the cell cycle?
Cell cycle brakes are released
100
What is the function of pRb?
It prevents cells from entering the cell cycle by inactivating E2F
101
What is the difference between somatic and inherited mutations?
In somatic, both hits occur in a single cell whereas for inherited there is one defective inherited copy of pRb so both cells are affected
102
What is oncogenesis?
Formation of cancer cells, same as carcinogenesis. It is autosomal recessive and takes longer to develop
103
What chemical activates oncogenes?
Benzopyrene
104
What is an oncogene?
A cell that can transform a cell into a cancer cell. They are derived from photo-oncogenes
105
How are oncogenes activated?
Dysregulation of proto-oncogene expression and translocations
106
What do oncogenes form when expressed?
Oncoprotein
107
What is a proto-oncogene?
Normal cells that promote cell growth and mitosis
108
How do photo-oncogenes promote cel growth?
They code for growth promoting proteins
109
What is the connection between oncogenes and proto-oncogenes?
Oncogenes are produced when the DNA sequence of photo-oncogens is changed
110
What are the products of oncoproteins?
Growth factors and cell cycle regulators
111
What colour signals are used to detect abnormalities in cell cycle regulators?
Yellow
112
What type of process in tumour formation?
Multi-step
113
What is the process of tumour formation?
Normal cells are exposed to carcinogenic factors that causes DNA damage and mutations. This inactivates tumour suppressor genes and activates growth-promoting oncogenes which causes cell cycle dysregulation and the formation of tumours
114
What is formed at the end of the process of tumour formation?
A malignant neoplasm
115
What are the major aetiological agents?
Predisposition, viruses, radiation and chemicals
116
What type of inheritance is a cancer predisposition?
Autosomal dominant
117
What are exmaples of inherited predispositions?
Familial retinoblastoma that has an early age of onset
