cancer Flashcards

1
Q

define neoplasia

A

new growth

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2
Q

define neoplasm

A

uncontrolled proliferation and growth of cells
/ tumour

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3
Q

what is benign cancer

A

tumour cells growing locally and not speed by invasion or metastasis

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4
Q

whats malignant cancer

A

tumour cells invade neighbouring tissues, can enter blood vessels and metastasise to different sites

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5
Q

what are the characterisistcs of benign tumours

A
  • fibrous capsule
  • cells divide slowly and closely resemble normal cells
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6
Q

what are characteristics of malignant tumours

A
  • less well differentiated
  • invade surrounding tissue
  • can get into blood/lymph/spaces and establish secondary growth
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7
Q

1 in 2 ppl in uk get diagnosed with cancer in their lifetime

A
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8
Q

breast, prostate, bowel and lung cancer account for 50% of all cancer deaths

A
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9
Q

what are the 2 components of cancer classification

A
  1. where they start in the body (e.g breast or lung)
  2. type of cell or tissue they start in (e.g carcinoma, leukaemia etc)
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10
Q

what are the 5 types of cancer origination

A
  • carcinoma ( skin or tissue of internal organs)
  • sarcoma ( bones, cartilage, fat, muscle, connective tissue)
  • leukaemia ( bone marrow and causes large no of abnormal blood cells to be produced and enter blood)
  • lymphoma and multiple myeloma ( start ion lymphatic system and myeloma starts in plasma cells in bone marrow)
  • central nervous system (begin in tissue of brain and spinal cord)
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11
Q

how does cancer begin

A

genetic mutations/ change in DNA sequence in genes that control cell proliferation etc

can also be influenced by epigenetic changes that affect gene expression on/off

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12
Q

cancer is a multistep process where alterations at genome level cause cells to proliferate out of control, invade and erode normal tissue

A
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13
Q

what is the biggest risk factor for developing cancer

A

advancing age
half of all cancers are in ppl over the age of 70

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14
Q

67% cancers are linked to some type of environmental factor

A
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15
Q

in a general manner, how do cells respond to damaging agentq

A
  1. cell sensors to sense damage
  2. sends signals to arrest cell cycle
  3. appropriate repair process activated
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16
Q

why is having cell cycle checkpoints important + what are they

A

it aims to repair any DNA damage and prevent the transmission of damaged/mutated DNA to daughter cells

g1, s, g2 allow repair of lesions before they are converted into permanent mutations

17
Q

what are proton-oncogenes

A

Proto-oncogenes are genes that normally help cells grow and divide to make new cells, or to help cells stay alive.

18
Q

explain the process of protons-oncogenes and normal cell poliferation

A
  • proton-oncogenes encode components of the ells normal growth-control pathway (which are growth factors, receptors, transcription factors and signalling enzymes)
  • growth factors bind to receptors on the cell surface, which activate signalling enzymes inside the cell
  • the activates transcription factors in the nucleus
  • activated transcription factors ‘turn on’ the gene required for cell growth and proliferation
19
Q

how do tumour suppressor genes stop cell poliferation

A
  • tumour supressor genes are normal genes that instruct cells to produce proteins that restrain cell growth and division / slow down cell growth and division
  • the loss of tumour suppressor gene function will allow a cell to grow and divide in an uncontrollable fashion
20
Q

what is the main purpose of apoptosis

A

eliminate cells that contain potentially dangerous mutations
if apoptosis function is not working properly, cell can grow and divide uncontrollably and form tumour

21
Q

how does programmed cell death/apoptosis have a role in homeostatis

A
  • eliminate unwanted cells and tissues, sculpts developing structures, controls cell no and removes abnormal cells
22
Q

what are the 5 steps in the transformation process of cancer

A

normal
hyperplasia
mild dysplasia
carcinoma
cancer

23
Q

what is the Warburg effect (form of cancer reprogramming cellular metabolism)

A

cancer cells with a metabolic switch to aerobic glycolysis with increased glucose uptake producing only 2 ATP molecules per molecule glucose

an increase in the rate of glucose uptake and preferential production of lactate, even in the presence of oxygen

24
Q

in contrast to Warburg effect, how do normal cell metabolism work

A

relies primarily on mitochondrial oxidative phosphorylation with the production of 35 ATP molecules per molecule of glucose

25
Q

what is tumour angiogenesis

A

growth of new blood vessels that tumours need to grow

26
Q

what causes tumour angiogenesis

A

release of chemicals by the tumor and by host cells near tumour

27
Q

explain how hypoxia affects properties of tumour

A
  • tumour hypoxia (insufficient oxygen)
  • hypoxia turns on intracellular factors called HIF (hypoxia-induced factor) in tumour
  • changes in expression of genes responsible for angiogenesis (formation of new blood vessels) allow tumour to expand and provides route for metastasis
28
Q

explain the process of metastasis

A
  • tumour cells detach from primary tumour
  • break through basement membrane and extracellular matrix surrounding tissues and INTRAVASATE into systemic circulation
  • it then survives circulation
  • evades immune atttacks
  • adhere to capillaries and extravate
  • then they are able to colonise distant organs
    (tumour cells corrupt the surrounding environment to allow for metastasis)
29
Q

what is the most common organ to be metastasised and why

A

liver, because the liver is responsible for filtering most of the blood to other organs

30
Q

what are the top 4 areas for metastasis

A

brain, bone, lungs, liver

31
Q

what are the tumour staging and grading systems

A

staging: TNM system ( tumour size, nodes, metastasis)
- stage 0 - 5

grading: degree of anaplasia and rate of growth
- stage 1-5

32
Q

chemo and radiation are NOT tumour specific

A
33
Q

immunotherapy stimulates the patients immune system

A
34
Q

targeted therapies interfere with specific tumour properties

A