Neoplasia Flashcards

1
Q

Neoplasm definition and distinguishing features:

A

Abnormal growth of cells which persists after initialising stimulus removed

Distinguishing features:
- Differentiation
- Rate of growth (malignant fast growing, benign slow growing)
- Local invasion
- Metastasis

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

Benign vs malignant

A

Malignant: A neoplasm with potentially lethal, abnormal characteristics which has the ability to invade metastasise

Benign: A neoplasm which does not have the above ability

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

What is differentiation, and what is meant by well/poor/undifferentiated differentiation?

A

The extent to which neoplastic tissues resemble their normal tissue of origin

Well differentiated:
- Closley resembles tissue of origin
- E.g Benign tumours

Poorly differentiated:
- Little resemblance of tissue of origin
- Variation in nuclear shape/size
- E.g Malignant tumours

Undifferentiated: Cannot be identified without molecular techniques

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

Benign and malignant suffixes for epithelial tumours:

A

Benign - OMA:
- Adenoma (glandular tissue)
- Papilloma (cell type)
- Identified by cell type and glandular tissue (e.g. squamous cell papilloma / colonic adenoma)

Malignant - Carcinomas:
- Adenocarcinoma (glandular tissue/degree of differentiation)
- Carcinoma (cell type)

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

Benign and malignant suffixes for mesenchymal tumours:

A

Benign - OMA (examples):
- Bones - osteoma
- Fat tissue - lipoma

Malignant - Sarcoma:
- All types have this suffix
- E.g fat tissue = liposarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hamartomas and choristomas

A

Hamartoma: Non-neoplastic disordered overgrowth of normal tissue, NORMAL to the site of occurrence

Choristoma: Benign normal tissue seen in ABNORMAL location

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Teratomas

A

Originate in germ cells

Teratoma cells contain all three germ cell layers:
- Endoderm
- Mesoderm
- Ectoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Melanoma vs melanocytic naevus:

A

Melanoma: Malignancy of melanocytes

Melanocytic naevus: Benign proliferation of melanocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Haematological malignancies based on cell of origin

A

Lymphoma:
- Malignancy of B or T cells, usually in lymph nodes

Myeloma:
- Malignancy of plasma cells

Leukaemia:
- Malignancy of WBC beginning in bone marrow

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

Metastasis definition:

A

The spread of tumour to a site discontinuous from the source organ / tissue

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

Dysplasia and carncinoma in-situ

A

Dysplasia:
- Neoplastic change confined within basement membrane
- Cytomorphological features of malignancy

Carcinoma in-situ:
- Severe dysplasia
- Cytomorphological features of malignancy but without invasion (basement membrane not penetrated)
- NOT malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hallmarks of cancer

A
  • Avoids immune destruction
  • Evades growth suppressors
  • Enabling replicative immortality
  • Resisting cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is clonality?

A

Proliferation of genetically unstable cells producing tumour cell variants

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

How do cells become immortal?

A

Autocrine growth stimulation:
- Abnormal expression of oncogenes
- Inactivation do tumour suppressor genes

Reduced apoptosis:
- Abnormal expression of gene that inhibits apoptosis

Telomerase:
- Prevents shortening of telomeres

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

What are tumour suppressor genes and their role?

A

Genes that inhibit neoplasticism growth:
- E.g TP53 (encodes for p53)

p53:
- Both caretaker (DNA repair) and gatekeeper (stops damaged cells dividing) function
- Missense and nonsense mutations can cause it to lose function

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

Oncogenes

A

Genes which drive the neoplastic behaviour of cells

Can be viral or can be genes that exist in normal cells

Five groups of oncogene / oncoprotein
•Growth factors
•Receptors for growth factors
•DNA binding transcription factors
•Signalling mediator with tyrosine kinase activity
•Signalling mediator with nucleotide binding activity

17
Q

Different types of carcinogens:

A

Chemical:
- Smoking
- Rubber/dye industry
- Cured meats
- PVC manufacture

Oncogenes virus:
- Human papilloma virus
- Epstein-Barr virus

18
Q

How do carcinogens (HPV and EBV) act on cells?

A

HPV:
- E6 acts on TP53
- E7 viral oncoprotein acts on RB (tumour suppressor)
- Neoplasticism cells with integrated viral gene keeps replicating

EBV:
- Drives B cells to proliferate
- Inactivates p16/CDKN2A and TGFBR2 leading to malignant transformation

19
Q

Predisposing factors:

A

Radiation:
- UV causes skin cancer, melanoma
- Ionising radiation (x-ray, gamma)

Bacteria (release toxins that activate oncoproteins) /Fungi

Hormones (excess oestrogen/growth hormones)

Lifestyle:
- Age
- Diet (obesity/processed meats)
- Alcohol

Inherited:
- BRCA1/2 genes (breast, ovarian)
- MEN gene (endocrine)

20
Q

What makes tumours behave badly (become invasive)?

A

Decreased cellular adhesion

Secretion of proteolytic enzymes:
- Damages surrounding tissue

Abnormal/increased cellular mobility

21
Q

How do tumours metastasise and what routes can they takes?

A

Steps:
1. Detachment
2. Invasion of surrounding tissue
3. Intravasation into vessels
4. Evasion of defences
5. Adherence to endothelium elsewhere
6. Extravasation of cells from vessel into surrounding tissue

Routes:
- Haematogenous (blood)
- Lymphatic
- Transcoelomic (across body cavity)