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Oncology Notes (AB_1184)

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These are my notes for the oncology course in Biomedical sciences :)

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Voorbeeld van de inhoud

Oncology
MID TERM
LECTURE 1: Introduction to the Nature of Cancer


 Incidence of cancer: the absolute number of new patients diagnosed with cancer in a
year or any particular period of time

 Prevalence of cancer: All people have been diagnosed with cancer over a certain
period of time (5 years)  even if they are cured

 Mortality: number of patients that died due to cancer within a certain period mostly
1 year

 Survival: Percentage of people still living at a certain period after diagnosis (5 years)

 Mortality trends of 2000 and 2010  Lung cancer increase in women as women
have started smoking and decrease in me as men have been smoking for years and
have started reducing now




 Cancer  group of diseases  invasive and forming metastasis

 Malignant tumour can cause death  invades and disturbs organ fiction and take
nutrients from cells

 Carcinomas  from epithelia  most common (85%)  epithelia most exposed to
carcinogens (alters DNA)

 Adenocarcinoma  from glandular cells

, Sarcomas  from mesodermal tissues

 Lymphomas  from progenitors of WBC

 Oncogenesis




 Cancer is clonal and heterogenous  all tumour cells come from each other
(daughter cells) however during the process daughter cells can metastasise
differently so heterogenous

 Cancer is not inheritable  somatic mutations are not inherited  you can pass
germline mutations that increase your chance to develop cancer

 Cancer risk increases with age

 Hallmarks of cancer (Hanahan & Weinberg)  10 now 14

 Tumour consists of other cells that are not cancerous but part of tumour 
fibroblasts, immune cell etc.






 Oncogenes drive cancer and tumour suppressor genes stop them

, Characteristics of cancer cells:
 Have different morphology
 Do not need substrate to grow on
 Can grow in low serum media
 Don’t stop proliferation even when in contact with neighbouring cells

 Oncogenes can be checked for these characteristics  isolation of gene 
transfection of DNA into immortalized primary cells  check if transfected cells have
altered growth  if it grows on agar then oncogene

 Treatment of cancer  surgery, radiotherapy, chemotherapy  either cytostatic
(prevent cell division) or cytotoxic (kill cells)

 Chemotherapy side effects  therapeutic window is small (max tolerated dose –
min dose to get some effect)




 Chemotherapy window isn’t big enough  novel anticancer agents with selective
activity against cancer  targeted drugs being developed  mediocre efficacy only
small number of patients benefit

 Mediocre efficacy because some of these targets not present in cancer cells or 50%
present in patient  different patient need different treatments  personalized
medicine

 Personalized medicine  diagnostics  genetics, imaging, and immunochemistry

, LECTURE 2: DNA Structure and Stability

 Cancer from epigenetic alteration

 Stability genes  for repair  mutated  become inactivated

 Oncogenes  for growth  mutated  activation

 Tumour suppressor genes  mutation inactivation

 Changes in DNA  base pair sub, deletions, insertions, single or double strand
breaks

 Large DNA changes  chromosome rearrangements

 DNA aberration causes
 Exogenous  smoking, alcohol, sun (UV), radiation
 Endogenous  ROS (oxidative phosphorylation in mitochondria causes
release of ROS)




n

 Modified base example  oxoguanine  caused by ionizing radiation or normal
aging  DNA polymerase reads oxoguanine as thymine

 DNA repair mechanism

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Geüpload op
19 december 2022
Aantal pagina's
62
Geschreven in
2022/2023
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College aantekeningen
Docent(en)
Victor van beusechem
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