MCBoM- Tumours

Question 1

Malignant, bone

Answer 1

Osteosarcoma

Question 2

Benign, cartilage

Answer 2

Chondroma

Question 3

Malignant, cartilage

Answer 3

Chondrosarcoma

Question 4

Benign, fat

Answer 4

Lipoma

Question 5

Malignant, fat

Answer 5

Liposarcoma

Question 6

Benign, smooth muscle

Answer 6

Leiomyoma

Question 7

Malignant, smooth muscle

Answer 7

Leiomyosarcoma

Question 8

Benign, skeletal muscle

Answer 8

Rhabdomyoma

Question 9

Malignant, skeletal muscle

Answer 9

Rhabdomyosarcoma

Question 10

Benign, blood vessels

Answer 10

Hemangioma

Question 11

Malignant, blood vessels

Answer 11

Angiosarcoma

Question 12

Benign, melanocytic (skin pigment)

Answer 12

Naevus

Question 13

Malignant, melanocytic

Answer 13

Melanoma

Question 14

Benign, meningeal

Answer 14

Meningeioma

Question 15

Benign, nerve sheath

Answer 15

Neurofibroma

Question 16

Malignant, nerve sheath

Answer 16

Malignant peripheral nerve sheath tumour

Question 17

Benign, mixed structures

Answer 17

Mature teratoma

Question 18

Malignant, mixed structures

Answer 18

Immature teratoma

Question 19

Benign, bone

Answer 19

Osteoma

Question 20

Hamartoma

Answer 20

Developmental malformation, mass of disorganised but mature specialised tissue indigenous to site, eg birthmark

Question 21

Dysplasia

Answer 21

Disordered growth
Variable cell shape and size
Deeply stained nuclei
Increased number of cell divisions
High nuclear:cytoplasm ratio

Question 22

Grading

Answer 22

Degree of differentiation

1-3-anaplastix

Question 23

Staging

Answer 23

Extent of disease spread

TNM or I - IV

Question 24

Apoptosis mechanism

Answer 24

Mitochondria release cytochrome c to cytoplasm
Binds to APAF 1 (apoptosis protease factor) to form wheel of death
Activates to form apoptosome

Question 25

Proto oncogenes examples

Answer 25

C ras, c myc, N myc, EGF | Promote proliferation

Question 26

Tumour suppressor genes examples

Answer 26

Rb, p53, APC (adenomatous polyposis coli), TGF beta | Arrest growth at G1/S checkpoint

Question 27

Primary abnormalities

Answer 27

Gatekeepers | Genes whose mutation or altered expression relieves normal controls and promotes outgrowth of cancer cells

Question 28

Secondary abnormalities

Answer 28

Caretakers | Genes whose disruption caused genome instability, increasing the frequency of alteration in gatekeeper genes

Question 29

Gain of function mutation

Answer 29

Dominant effect, one defective allele needed | Proto oncogene to oncogene

Question 30

Loss of function mutation

Answer 30

Both alleles need to be inactivated to give phenotypic change Tumour suppressor gene to non functioning

Question 31

Growth factors

Answer 31

Epidermal and platelet derived GFs-> stimulates growth and leads to cascade for cyclin D and proliferation Transforming growth factor beta-> inhibitory, switches on CDK inhibitor protein so stops proliferation

Question 32

Colorectal tumour initiation

Answer 32

Mutation stops destruction complex from forming, so beta catenin is deregulated Beta catenin can then switch on genes that drive cell survival and proliferation

Question 33

E-cadherin

Answer 33

Cell surface transmembrane proteins expressed by cells Mediates cell-cell adhesion Acts as receptor and ligand, bind to each other and to catenins in cell which are bound to cytoskeleton Ca dependent Tumour suppressor, down regulated in tumour invasion

Question 34

Integrins

Answer 34

Cell surface transmembrane proteins Alpha and beta units Mediate cell-ECM adhesion Provides polarity for survival and migration

Question 35

Lymphatic spread

Answer 35

Mainly carcinomas (epithelial)

Question 36

Haematogenous spread

Answer 36

Mainly sarcomas (mesenchymal) through blood vessels

Question 37

Transcoelomic spread

Answer 37

Through body cavities | Mainly carcinoma

Question 38

HPV

Answer 38

DNA oncogenic virus Viral DNA integrated to host genome Clonal integration, same site on same chromosome Leads to overexpression of E6 and E7 proteins, prevents inhibition of CDK4 and facilitates degradation of p53 gene product

Question 39

Epstein-barr

Answer 39

DNA oncogenic virus BURKITTS LYMPHOMA B cell neoplasm Should be controlled by immune system, but in Africa chronic malaria favours spread, endemic Overexpression of c-myc oncogene B CELL LYMPHOMA In immunosuppressed individuals Tumours in lymphoid tissue or CNS HODGKINS DISEASE Distinctive neoplastic giant cells Express LMP1 which has transforming activity NASOPHARYNGEAL CARCINOMA Affects epithelial cells of oropharynx and B lymphocytes Episome genome, doesn't integrate

Question 40

Hepatitis B

Answer 40

DNA oncogenic virus Chronic persistent infection HBx protein binds to p53, disrupts growth control of liver cells leading to cirrhosis

Question 41

Human T cell leukaemia

Answer 41

RNA oncogenic retrovirus | Infection by transmission of infected T cells by fluid exchange