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
what is tumour angiogenesis
growth of new blood vessels that tumours need to grow
26
what causes tumour angiogenesis
release of chemicals by the tumor and by host cells near tumour
27
explain how hypoxia affects properties of tumour
- 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
explain the process of metastasis
- 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
what is the most common organ to be metastasised and why
liver, because the liver is responsible for filtering most of the blood to other organs
30
what are the top 4 areas for metastasis
brain, bone, lungs, liver
31
what are the tumour staging and grading systems
staging: TNM system ( tumour size, nodes, metastasis) - stage 0 - 5 grading: degree of anaplasia and rate of growth - stage 1-5
32
chemo and radiation are NOT tumour specific
33
immunotherapy stimulates the patients immune system
34
targeted therapies interfere with specific tumour properties