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Neoplasia Flashcards

1
Q

What does neoplasm mean

A

‘new growth’

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2
Q

What is a tumour

A

Neoplasm
Abnormal mass of tissue
Growth is unco-ordinated and exceeds that of normal tissues
Persists after removal of the stimuli that initiated the change

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3
Q

In what tissue do neoplasms usually occur

A

Epithelial – lining/covering/glandular tissue ​

Connective tissue​

Other tissues

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4
Q

What are the types of tumours

A

Benign
Malignant

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5
Q

What are the differences between the growth of benign and malugnant tumours

A

BENIGN
-expansion
-may be encapsulated
-localised
-slow

MALIGNANT
-Invasion/Infiltration
-No capsule
-matastasis (outwith normal area)
-rapid variable

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6
Q

What are the clinical effects of benign tumours

A

Lump/pressure/obstruction depending on site and size
+/- hormone secretion
Treates by local excision

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7
Q

What are the possible clinical effects of a malignant tumour

A

-Local pressure, infiltration and destruction, distant metastasis
-+/- hormone secretion
-local excision and chemotherapy or radiation if metastasis presents

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8
Q

What are the epithelium origins of both benign and malignant epithelial tumours

A

BENIGN
squamous epithelium - papilloma
Glandular epithelium - adenoma

MALIGNANT
squamous epithelium - squamous cell carcinoma
Glandular epithelium - adenocarcinoma

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9
Q

How do we name tissues originating in the connective tissue

A

Smooth = Leiomyoma - Leiomyosarcoma

Fibrous = Fibroma - Fibrosarcoma​

Bone = Osteoma - Osteosarcoma​

Cartilage = Chondroma - Chondrosarcoma​

Fat = Lipoma - Liposarcoma​

Blood vessel = Angioma - Angiosarcoma

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10
Q

What causes papilloma

A

Variety of HPV (16, 18)

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11
Q

What coes carcinoma indicate

A

Epithelial tumour

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12
Q

Where do lymphoma and leukaemia originate

A

Lymphoid and haemopoietic

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13
Q

What tumours are found in melanocytes

A

naevus (mole)
melanoma

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14
Q

What tumours could be found within germ cells

A

Benign teratoma
Malignant teratoma

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15
Q

What is a carcinogen

A

Any substance or agent with the potential to cause cancer

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16
Q

What are some chemical carcinogens

A

Smoking polycyclic hydrocarbons including tars
Diet, drugs, alcohol
Asbestos

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17
Q

What are the two stages of chemical carcinogenesis

A
  1. Initiation – permanent DNA damage (mutations)​
  2. Promotion – agent promotes proliferation
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18
Q

What is the latent period

A

Time from promotion to clinical tumour

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19
Q

What is involved in the initiation step of carcinogenesis

A

When a carcinogen induces a genetic change resulting in a neoplastic potential

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20
Q

What is promotion and progression of carcinogenesis

A

Promotion: Another factor stimulates the initiated cell for division. (clonal proliferation). Does not act on non-initiated cells.​

Progression; Additional mutations resulting in malignancy

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21
Q

What are examples of physical carcinogenesis

A

Ionising radiation​

damages DNA, causing mutations​

radioactive metals and gases ​

radium - bone and bone marrow tumours

Ultraviolet light

Damages DNA
skin cancer

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22
Q

What makes a tissue sensitive to radiation

A

The speed at which cells are renewed (more rapid, more sensitive)

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23
Q

List the tissues from most to least sensitive to radiation

A

embryonic tissues​

haematopoietic organs (spleen, bone marrow)

gonads ​

epidermis​

intestinal mucous membranes (variable) ​

connective tissue​

muscle tissue and nerve tissue

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24
Q

What are the classifications of viruses

A

DNA viruses ​
-more common​
-viral DNA inserted into host DNA​

RNA viruses​
-reverse transcribed and then inserted​

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25
What viruses causes tumours
Epstein-Barr virus - Burkitt’s lymphoma nasopharyngeal carcinoma Hepatitis B/C - hepatocellular carcinoma Human papillomavirus - cervical and oropharyngeal carcinoma
26
What is the epidemiology of cancer
20% of deaths​ 2nd most frequent cause of death​ 30% of population will develop cancer​ highest in elderly​ **type​** 90% carcinoma​ 10% lymphoma or sarcoma (more in young)
27
What is the most common form of cancer
Carcinoma
28
What is the aetiology of oral cancer
**multifactorial** tobacco - smoking or smokeless tobacco​ betel quid (chewing habits)​ alcohol​ diet and nutrition​ oral hygiene​ viruses HPV EBV HHV-8​ Immunodeficiency​ Socioeconomic factors​ GORD
29
What is leukoplakia
White patch that cannot be rubbed off or attributed to any other cause (oral cancer)
30
Why is it important to identify dysplasia and get it checked
Tissue that shows dysplasia: HAS THE POTENTIAL TO BECOME MALIGNANT​ Abnormality confined to epithelium; underlying tissue not affected. Not all become malignant-may regress.​ Dysplasia (histopathology) is the gold standard for assessing this (at present)​
31
What epithelial tissues does dysplasia affect
Squamous eg. oral, cervix - the basis of cervical screening ​ Glandular eg Barrett’s oesophagus, colonic polyps​ Transitional eg bladder
32
What are the accelerator genes in carcinogenesis
Oncogenes
33
Which genes act as the brakes
Tumour suppressor genes
34
What is an epigenetic mutation
No change to the DNA itself Groups attach to the DNA and influence expression of the genes ex silence or increase activity
35
What do oncogenes do
Regulate cell division
36
What are the proteins that oncogenes code for called
Oncoproteins
37
What do oncogenes do to accelarate uncontrolled division
tight regulation may be lost mutation​ -increases activity of product​ excess normal product​ -duplication of the gene ​ -viral product​ enhanced transcription ​ -translocation​ -chromosome rearrangement
38
What do tumour suppressor genes do
Act to inhibit cell division and suppress growth
39
How does TP53 act in response to damages DNA
stops the cell cycle to allow DNA repair​ apoptosis (if repair not possible)​
40
What gene is often inactivated in cancer
TP53 - mutation/deletion
41
What is the two hit hypothesis
Oncogene - 1 cell deleted Tumour suppressor - both must be deleted Before the cell begins to become malignant
42
At what point does cell division stop and DNA checked
Restriction points
43
How many cases of head and neck cancer show deletion or mutation of the TP53 gene
50%
44
What are some inherited cancer syndromes
Retinoblastoma Some colon cancers
45
What causes familial cancer
family clusters​ gene(s) and pattern of inheritance not clear -Breast, ovary, colon
46
What are the modes of spread of cancer
local spread​ lymphatic spread​ blood spread (haematogenous)​ transcoelomic spread​ Intraepithelial spread ( Paget’s disease of the breast)
47
What is metastasis
spread of the malignant cells to distant organs forming secondary tumours​
48
What are the patterns of spread of sarcomas and carcinomas
carcinomas​ -lymphatic​ -blood (often later)​ sarcomas​ -blood (lymphatic spread rare)​ predictable patterns of spread​ -lung to local nodes, liver, bone and brain​ -tongue to neck nodes, later lung and spine​
49
What are the 6 hallmarks of cancer
Evading apoptosis Insensitivity to anti-growth signals Self-sufficiency in growth signals Sustained angiogenesis Tissue invasion & metastasis Limitless replicative potential
50
What does the grading of a tumour mean
Biological nature of the tumour (hitsopathology)
51
What is the stage of a tumour
Extent of spread
52
How can we determine the grade of a tumour
Histological assessment of :​ Invasion into underlying tissue​ Cellular atypia : abnormal mitotic activity, nuclear pleomorphism, differentiation, necrosis​ Various methods​ -numerical grades (1,2,3 etc)​ -low, intermediate, high​ -degree of differentiation (squamous cell carcinoma
53
What is staging
The extent or severity of a person’s cancer
54
How can staging be determined
Physical exams, imaging procedures, laboratory tests, pathology and surgical reports - determine staging​
55
What staging system is used for oral cancer
TNM Tumour size Lymph node involvement Presence of metastases
56
What is the immune response to tumours
Immune surveillance. ​ Can suppress or enhance carcinogenesis Elimination - equilibrium - escape
57
How can the immune system recognise tumour cells
Products of mutated genes​ Overexpressed proteins (tyrosinase)​ Viral proteins (HPV,EBV)​ Oncofetal antigens (carcinoembryonic antigen)
58
What is the elimination response
Cell mediated immune response​ -Cytotoxic T-lymphocytes (CD8+)​ -Natural killer cells. First line of defence against tumour cells.​ -Macrophages. Mechanisms similar to anti-microbial killing.
59
How can tumour cells evade the immune response
Cells may acquire molecular changes such as:​ -Alter tumour antigen expression regularly, Lack of T-cell recognition​ -Activation of immunoregulatory pathways leading to T-cell unresponsiveness and apoptosis.​ -Immunosuppressive factors eg. cytokines (TGF-β). Inhibit T-cell response​
60
What is immunotherapy
Use the patient’s own immune response to control and destroy malignant cells
61
What are the methods of immunotherapy
-Active immunisation.(HPV, Hep B)​ -Reversal of immunosuppression​ -Adopted cell transfer (ACT) Tumour- infiltrating lymphocytes (TILs)​ CAR T-cell therapy- haematological malignancies​ -Strengthening natural immune responses-research still needed.​
62
What is the equilibrium stage
Cancer cells evade detection and lie dormount in the body for a period of time until escape of the immune system due to activation
63
What are the 3 Es
Elimination Equilibrium Escape

Immunology + Pathology (11 decks)

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