Samenvatting

Summary Oncology Molecular Biology of Cancer chapter 1-6

9 keer verkocht

Vak
Oncologie (AB_1184)

Instelling
Vrije Universiteit Amsterdam (VU)

Boek
Molecular Biology of Cancer

This is a summary of Molecular Biology of Cancer chapter 1-6. This is the perfect summary to prepare yourself for the first exam in the Oncology course. It contains figures and detailed explanations. My exam grade was an 8!

[Meer zien]

Voorbeeld 2 van de 29 pagina's

Bekijk voorbeeld

Heel boek samengevat? Nee
Wat is er van het boek samengevat? 1-6
Geupload op 13 april 2021
Aantal pagina's 29
Geschreven in 2020/2021
Type Samenvatting

Volgen

isabella3 Lid sinds 4 jaar 76 documenten verkocht

€11,19

Ook beschikbaar in voordeelbundel v.a. €20,49

In winkelwagen

Opslaan

100% tevredenheidsgarantie
Direct beschikbaar na je betaling
Lees online óf als PDF
Geen vaste maandelijkse kosten

Ook beschikbaar in voordeelbundel (1)

Summary Oncology (G&L) Molecular Biology of Cancer

€ 22,28 € 20,49

1x verkocht

2 items

1. Samenvatting - Summary oncology molecular biology of cancer chapter 1-6
2. Samenvatting - Summary oncology molecular biology of cancer chapter 7-14
Meer zien

SUMMARY OF
PECORINO’S MOLECULAR BIOLOGY OF
CANCER
Chapter 1: Introduction

1.1 What is cancer?

Cancer:
- Group of disease characterized by unregulated cell growth and invasion and spread
of cells from site of origin or primary site to other sites in body.
o Carcinomas: occurring in epithelial cells
o Sarcomas: occurring from mesoderm cells (bone or muscle)
o Adenocarcinomas: occurring from glandular cells (breast)

Hallmarks of cancer:
- Growth signal autonomy:
o Can happen through acquired mutations
- Evasion of growth inhibitory signals:
o Acquired mutations or gene silencing influences this
- Reprogramming energy metabolism:
o Uncontrolled cell division needs more energy and therefore increases of fuel
and biosynthetic precursors by adjusting energy metabolism. Cancer cells
carry out glycolysis, even when oxygen is around.
- Avoiding immune destruction:
o Successful cancer cells may not stimulate immune responses or are able to
interfere with the response to avoid it.
- Evasion of cell death:
o Cancer cells evade apoptotic signals
- Unlimited replicative potential:
o Cancer cells have active telomerase
- Genome instability and mutation:
o By faulty DNA repair
- Tumor-promoting inflammation:
o All tumors contain inflammatory immune cells
o The inflammation can provide growth factors and enzymes to promote
angiogenesis and invasion. It can also produce ROS.
- Angiogenesis:
o Growth of new blood cells
o Usually by altering the balance between inhibitors and inducers.
- Invasion and metastasis:
o Alterations of genome may affect activity or level of involved enzymes to
promote invasion.

, Benign tumors can still be dangerous, because of their location, but are not cancer.

1.2 Evidence suggests that cancer is a disease of the genome at the
cellular level

Carcinogens:
- Can cause cancer by causing alterations to DNA sequence (mutations).
- Inheritable modifications of genome and chromatin structure can play a role in
carcinogenesis

Development of cancer is clonal: all cells in a primary tumor arise from a single cell. Only
one in 1014 cells needs to accumulate enough mutations and then a tumor can arise. This
also explains heterogeneity of tumors, as selection of the fittest plays a role in selecting
mutations. Mutations that do not get repaired continue to the daughter cell.

Processes affecting number of cells:
- Proliferation
- Apoptosis
- Differentiation

Carcinogenesis relies on:
- Oncogenes: a gene that’s mutated to form more or more active proteins and can
ensure tumor formation. A mutation in only one allele is enough. An oncogene can
also be a gene that produces a higher quantity of a certain receptor, so it’ll always be
on and does not require signals.
- Tumor suppressor genes: genes that make proteins who inhibit formation and
growth of tumors. Loss of growth inhibition happens when mutations result in loss of
function. Both of the alleles need to be nonfunctional.

Haploinsufficiency:
- Only one mutated allele can lead to cancer, because one allele only produces half of
what it normally does.

1.3 Influential factors in human carcinogenesis

Chimney sweeps resulted in chronic exposure to soot, which resulted in scrotal and nasal
cancer.

UVB radiation can alter DNA by forming pyrimidine dimers and then cause mutations.

Having children reduces the breast cancer risk for women. Also, age of woman at time of
giving birth and start of menstrual cycle affect cancer risk and so do hormonal contraception
and fertility treatments. Breast cancer risk can be reduced if women were more physically
active.

Kaposi’s sarcoma arises from HPV type 8 infection, usually only in people who have a bad
immune system because of HIV infection.

Dit zijn jouw voordelen als je samenvattingen koopt bij Stuvia:

Bewezen kwaliteit door reviews

Studenten hebben al meer dan 850.000 samenvattingen beoordeeld. Zo weet jij zeker dat je de beste keuze maakt!

In een paar klikken geregeld

Geen gedoe — betaal gewoon eenmalig met iDeal, creditcard of je Stuvia-tegoed en je bent klaar. Geen abonnement nodig.

Direct to-the-point

Studenten maken samenvattingen voor studenten. Dat betekent: actuele inhoud waar jij écht wat aan hebt. Geen overbodige details!

Veelgestelde vragen

Wat krijg ik als ik dit document koop?

Je krijgt een PDF, die direct beschikbaar is na je aankoop. Het gekochte document is altijd, overal en oneindig toegankelijk via je profiel.

Tevredenheidsgarantie: hoe werkt dat?

Onze tevredenheidsgarantie zorgt ervoor dat je altijd een studiedocument vindt dat goed bij je past. Je vult een formulier in en onze klantenservice regelt de rest.