Lecture 2 - cancer development

Question 1

describe malignant vs benign tumours.

Answer 1

being tumour cells grow only locally and cannot spread by invasion or metastasis. malignant cells invade neighbouring tissues, enter blood vessels and meta size to different sites.

Question 2

what are the differences between normal cell structure vs cancer cell structure

Answer 2

cancerous cells have a smaller cytoplasm, multiple nuclei, multiple nucleolus’s and coarse chromosomes.

cancer cells are irregularly shapes, large numbered, variation in cell size and shape, disorganised arrangement of cells, poorly defined tumour boundary.

Question 3

describe benign vs malignant tumours.

Answer 3

being have slow rate of growth, necrosis and ulceration is uncommon, and slight vascularity.

malignant tumours have rapid growth rate, moderate marked vascularity, necrosis and ulceration is common.

Question 4

what is a feature of both benign and malignant tumours and what is the contrast between them?

Answer 4

local invasion is a feature of both being and malignant tumours. however all benign tumours grow as cohesive, expansive masses. they do not have the capacity to infiltrate, invade or metasise to distant sites, as do malignant tumours. they remain localised at their site of origin and as they grow, usually develop a rim of compressed connective tissue, a fibrous capsule that separates them from the hot tissue

in contrast the growth of malignant tumours is accompanied by progressive infiltration, invasion and destruction of the surrounding tissue. poorly demarcated from the surrounding normal tissue and a well defined cleavage plane is lacking. most malignant tumours are obviously invasive

Question 5

what are metastases?

Answer 5

metastasis are tumours that develop secondary to and discontinuous with the primary tumour. metastasis marks the tumour as malignant as benign tumours don’t metastasise.

Question 6

what are exceptions of benign neoplasms that metastasis?

Answer 6

glial cells in the CNS and basal cell carcinomas of the skin. they are highly invasive forms of neoplasia but rarely metastasise.

Question 7

what enables malignant tumours to metastasise ?

Answer 7

they invade other organs and are infiltrated by blood vessels which enable them to metastasis

Question 8

what are the most common sites of metastasises forming?

Answer 8

brain, lymph nodes, respiratory, liver, skeletal. where cancers metastasise depends of the route of spread

Question 9

what are the steps in metastasis?

Answer 9

1) cells grow locally as a tumour
2) cells break away from tumour and enter the bloodstream or lymphatic system
3) cells travel via the blood or lymph vessels to other parts of the body
4) cells escape from the blood or lymph vessels into local tissues
5) cells grow and divide in a new location, producing secondary tumours elsewhere in the body

Question 10

what is angiogenesis?

Answer 10

angiogenesis is when capillaries grow into the cancer to provide oxygen and nutrients

Question 11

what are the 3 main types of cancer?

Answer 11

leukemias - cancer of the blood or bone marrow.
sarcomas - cancers of the connective tissue of supportive tissue (bone marrow, cartilage, fat, muscle, blood vessels) and soft tissue - rarer
carcinomas - cancers that arise from the pitfall cells - these include breast, liver, lung, stomach etc

Question 12

describe carcinomas

Answer 12

carcinomas develop from epithelial cells. a carcinoma is a cancer that begins in tissue that line inner or outer surface of the body and generally arises from cells originating in endothermic or ectothermic germ layer during embryogenesis. carcinomas may affect breast, lung, prostate and colon and are the most common types of cancers in an adult

Question 13

what are the 6 subgroups of carcinomas?

Answer 13

adrenocortical carcinoma which affects the adrenocorticoid, thyroid carcinomas which affects the thyroid glands, nasopharyngeal carcinoma which affects the nose and pharynx, malignant melanoma which describes skin cancer,

Question 14

what are mesenchymal cells?

Answer 14

they are multipoint stem cells that can differentiate into a variety of cell types.

Question 16

describe the phases of the cell cycle

Answer 16

G1 - is the gap 1. the cell increases in size, produce RNA and synthesises proteins.

S phase is the DNA synthesis phase. DNA replication takes place

G2 - the cell will continue to grow and produce new proteins required for cell division.

finally moves onto mitosis.

Question 17

what controls the cell cycle?

Answer 17

cyclins - the proteins which control the progression thorough the cell cycle. cyclins by activating cyclin-dependant kinase enzymes. each gets turned on when required to allow progression through the next phase

Question 18

describe the role of cdks

Answer 18

cdks signal the cell that it is ready to pass into the next stage of the cell cycle. cdks are dependant on cyclins another class of regulatory proteins. cyclins bind to cdks activating the cdks to phosphorylate other molecules.

Question 19

what are cdks controlled by?

Answer 19

controlled by inhibitors.

Question 20

what is cell cycle arrest ?

Answer 20

cell cycle checkpoints that can lead to cell cycle arrest. these are points where the cell check is the dn is healthy and proper for cycle to proceed. if not okay, cells arrest at these points. cell checks to see if it repairs. arrest is controlled by tumour suppresors such as p53 and pRB.

Question 21

what is the Rb protein?

Answer 21

the Rb protein is a tumour suppresor, which plays a pivotal role in the negative control of the cell cycle and in tumour progression. it has been shown that the Rb protein is responsible for a major G1 checkpoint, blocking S phase entry and cell growth.

Question 22

what happens when hormones bind to their receptors?

Answer 22

when hormones bind to their receptors special messages are delivered to the cell. if the cells are normal, they will grow in unorganised pattern. if they are abnormal or cancerous, they will grow in a disorganised way.

Question 23

what are possible carcinogenic mechanisms of estrogen?

Answer 23

1. estrogen bins tot receptor and sends grow signal to the cell.
2. estrogen also directly induces cell growth pathways such as MAP kinase 3. estrogen metabolism which makes nasty metabolites that directly cause DNA damage

Question 24

what are risk and protective factors for breast cancer ?

Answer 24

early menarche - internal hormones, late menopause, alcohol consumption?, post menopausal obesity, hormone replacement therapy.
protective factors are young age at first full term pregnancy, prolonged lactation and exercise

Question 25

how do we target the oestrogen receptor?

Answer 25

reduce/block the formation of oestrogen’s using aromatase inhibitors eg aromas or block estrogen interaction with estrogen with ER antagonists eg tamoxifen.

Question 26

what is the difference between aromatase inhibitors and tamoxifen mechanism of action?

Answer 26

aromatase inhibitors are ted to be used when tamoxifen fails. tamoxifen blocks the binding of estrogen to the estrogen receptor and stopping the signal transduction process that causes the cells to proliferate. whereas aromatase inhibitors prevents the production of oestrogen’s. aromatase coverts androgen to oestrogen’s so the aromatase inhibitors prevents the production of these estrogens

Question 27

what breast cancer cannot be targeted?

Answer 27

triple negative breast cancers cannot be targeted as they do not express the oestrogen receptor and and her-positive.

Question 28

what is Herceptin?

Answer 28

HER2 is overexpressed in some breast cancer cells, which can contribute to their growth and spread.Herceptin binds to the HER2 protein on the surface of cancer cells, blocking its activity and inhibiting the growth and division of these cells. By targeting HER2-positive breast cancer cells, Herceptin can slow down or even halt the progression of the disease.

Question 29

what are other mechanisms of action of Herceptin and side effects of it?

Answer 29

other mechanisms of action are antibody dependant cell mediated cytotoxicity and lysis of HER-2.

most common side effect are infusion reactions such as itching, nausea, and abdominal pain.

Question 30

what are treatment options for hormone receptor positive breast cancer?

Answer 30

hormone replacement options, surgery, chemotherapy, radiotherapy, targeted: tamoxifen and other anti-endocrine therapy.

Question 31

what are treatment options for HER2 and hormone receptor positive and HER2 positive?

Answer 31

HER2 positive options are surgery, chemotherapy, radiotherapy, targeted: Herceptin and other anti-HER2 therapy