Cancer Flashcards
(44 cards)
G1
G1 phase: cell grows larger, organelles duplicated
S phase
DNA and centrosome (microtubule- organizing structure) copied in nucleus
G2 phase
growth, proteins and organelles are made, preparation for mitosis
M phase
cell divides copied DNA and cytoplasm to make two new cells
Late g2
DNA is copied, so chromosomes in nucleus are two connected copies: sister chromatids
Two centrioles
prophase
Chromosomes begin to condense
Mitotic spindle forms (made of microtubules)
Nucleolus (where ribosomes are made) disappears
prometaphase
Mitotic spindle begins to organize chromosomes
Nuclear envelope breaks down
spindle anatomy
Microtubules bind to chromosomes at the kinetochore
Centromere is where the sister chromatids join together
Aster: structure of microtubules bound to chromosomes
metaphase
All chromosomes aligned at the metaphase plate
Two kinetochores of each chromosome should be attached to microtubules from opposite spindle poles
Spindle checkpoint: cell checks that sister chromatids will separate evenly
anaphase
Sister chromatids split - this is driven by motor proteins that “walk” along the microtubule tracks
telophase
Mitotic spindle is broken down
Two new nuclei form, nuclear membranes reappear
Chromosomes decondense
cytokinesis
Starts in anaphase/telophase
Separation of the cytoplasm
An actin ring forms a cleavage furrow
how cyclins work
Cyclin dependent kinases (CDK) - when bound to cyclin its active (phosphorylates targets) Kinase: adds a phosphate group CDK default function is to be inactive
G1 regulation
cycD, cycE
Phosphorylates Rb protein→ can’t inhibit DNA replication
s regulation
cycA
Activates DNA replication
G2 regulation
Cyc B
Activates mitosis/cell division
oncogenes
Cancer is a disease of uncontrolled cell division: cyclins expressed at high levels or overactive growth factor receptor
Proto-oncogene (normal cell growth) → oncogene (overactive, cancer-promoting) gene
how gene can mutate
AA mutation, amplification (cell gains extra copies of a gene), error in DNA repair where a proto-oncogene is attached to a different gene. This then makes an unregulated, new protein
oncogenes result from the activation (turning on) of proto-oncogenes
tumor suppressor genes
Genes that normally block cell cycle progression: tumor suppressors
Tumor protein p53 is involved in cellular response to DNA damage
Primarily acts at G1 checkpoint where it blocks progression in response to damaged DNA
tumor suppressor genes cause cancer when they are inactivated (turned off)
normal p53 protein
detects and binds damaged DNA. halts cell at g1 checkpoint, repairs it or apoptosis
what causes cancerous cell 4
Mutation that turns proto-oncogenes into oncogenes
- Change in AA sequence, Amplification, DNA repair error
Mutation causes a change in Ras and Raf structure
- Ras is a G protein - Switches between active and inactive forms
Ras protein is stuck in “active” form, unable to switch to “inactive” form
- Prompts cell division even in absence of growth factor
- missing or bad p53 (no stopping the mutations)
benign vs malignant
- Benign Tumor - Mass of cells that divide excessively but don’t have potential to invade other tissues
Is not considered cancerous yet - Malignant Tumor - Mass of cells that divide excessively and can invade other tissues (Metastasis)
- Offspring from original mutated cell may have enough mutations to become cancerous
causes of cancer 6
- smoking and tobaccco (radioactive)
- diet and physical activity (18% of cancer is due to fatness)
- UV rays, or xray and gamma ray
- radon
- viruses (15-20%) since they can insert genes OR alter cell behaviour
- HIV/AIDS are more likely to get kaposi sarcoma, non-hodgkin lymphoma, cervical cancer
inherited cancer
- 5-10%
- breast and ovarian
- lynch, colorectal, li fraumeni syndrome (see card)