Cancer cells and meiosis

Question 1

size of organ depends on total cell mass dependent o

Answer 1

total number of cells and their size

Question 2

processes regulated

Answer 2

cell growth, cell division, cell survival

by intracellular programmes and extracellular signal molecules

Question 3

3 external factors to reach cell from outside - affects progression of cell cycle

Answer 3

mitogen
growing factors
survival factors

Question 4

mitogen function

Answer 4

stimulate cell division by triggering waves of G1/S-Cdk activity - relieves intracellular negative control

Question 5

growing factor

Answer 5

stimulate cell growth by promoting protein synthesis and other macromolecules and inhibiting their degradation

Question 6

survival factors

Answer 6

promote cell survival - suppressing the form of programmed cell death(apoptosis)

Question 7

social control of cell

Answer 7

tells how cells act

from outside - extracellular signals

Question 8

cancer cells

Answer 8

cells that no longer respond to social signals

Question 9

cancer progression

Answer 9

evolutionary process driven by gene mutation(providing cell with competitive advantage)

Question 10

mechanism of mutated cells

Answer 10

suppresses mechanism of apoptosis

Question 11

evolution of cancer

Answer 11

initial clone of cancerous cells - additional mutation increase causing generation of diverse sub clones forming cancer cells

Question 12

Hall marks of cancer cells

Answer 12

organising principles of rationalising complexities of neoplastic disease

Question 13

hall marks includes

Answer 13

sustaining proliferative signalling, evading growth suppressors etc

Question 14

hallmarks genome instability

Answer 14

generates genetic diversity that expedites acquisition, inflammation which fosters multiple hallmark functions

Question 15

features of cancer cells of mutation

Answer 15

• display altered control growth
• contain and accumulate somatic mutation
• single mutation - not enough to change normal cells into cancerous cell
  have abnormal to survive stress and DNA damage
• create own microenvironment(niche) - evolve

Question 16

feature of cancer cells of control and spread

Answer 16

• can bypass normal proliferation control - independence of mitogens
• colonise other tissues
• develop gradually from increasingly aberrant cells
• altered sugar metabolism
• genetically unstable

Question 17

2 genes where mutation stimulates tumour progression

Answer 17

oncogene and tumour suppressor gene

Question 18

oncogene

Answer 18

act in dominant manner

gain of function

Question 19

oncogene function

Answer 19

promote cancer - protooncogene - overactive/overproduced

- regulate cell growth, division, survival or differentiation

Question 20

tumour suppressor gene function

Answer 20

normally restrain cell proliferation or tumour - loss of gene increases causing cancer formation

Question 21

example of oncogene

Answer 21

activation via mitogen stimulation

Question 22

process of activation via mitogen stimulation

Answer 22

• mitogens bind to cell surface receptor = initiate intracellular signalling pathway
• activation of small GTPas.Ra which activates MAP kinase cascade, increasing expression of numerous intermediate early genes including gene encoding transcription regulatory protein Myc

Question 23

Myc in example of oncogene

Answer 23

increase expression of delayed response gene expression which increases G1-Cdk activity which triggers phosphorylation of Rb family of protein

Question 24

inactivation of Rb proteins

Answer 24

freeing gene regulatory protein E2F

activating G1/S gene transcription including genes for G1/S-cyclin and S-cyclin

Question 25

activating G1/S gene transcription

Answer 25

enhances Rb protein phosphorylation = positive feedback loop

Question 26

E2F protein stimulate transcription of their genes after Rb protein phosphorylation

Answer 26

positive feedback loop formed as well

Question 27

tumour suppressor gene

Answer 27

actin submissive manner

loos of function

Question 28

defects that contribute to cancer

Answer 28

signalling pathways
cell cycle control
apoptosis regulation

Question 29

example of tumour suppressor

Answer 29

p53 - cellular stress sensor

Question 30

p53 function

Answer 30

responds to hyper-proliferation signals, DNA damage, hypoxia, telomere shortening and various stresses

Question 31

mutation of p53

Answer 31

enables cancer cells to survive and proliferate despite stress and DNA damage
even with DNA damage the cell cycle will continue = cancer as cell cycle cannot be arrested

Question 32

cell cycle is mis regulated in multiple cancers

Answer 32

change in genes which encodes cell cycle regulator - identified in human cancer cells

Question 33

most cancers have unstable genomes

Answer 33

genetic (genomic) instability
chromosomal instability (CIN)

Question 34

genetic (genomic) instability

Answer 34

abnormal increases in rate at which genes and chromosomes are mutated, rearranged or lost

Question 35

chromosomal instability (CIN)

Answer 35

abnormally high incidence of defects in chromosome number of chromosome structure

Question 36

meiosis

Answer 36

nuclear division leading to generation of haploid cells
in gametes
many control systems and molecular mechanisms are shared with mitotic division

Question 37

meiosis I

Answer 37

time taken longer than meiosis II especially prophase

homologous chromosome recognise each other and associate

Question 38

meiosis I structure

Answer 38

2 closely aligned duplicate homologs - bivalent

Question 39

meiosis I - synaptonemal complex (SC)

Answer 39

protein complex usually joining to homologs

Question 40

prophase I stages

Answer 40

leptotene, zygotene, pachytene, diplotene

Question 41

leptonene

Answer 41

homologous chromosomes condense partially, pair and genetic recombination begin

Question 42

sygotene

Answer 42

SC start to assemble; synapsis and recombination are taking place

Question 43

pachytene

Answer 43

SC complete and recombination finishes are very tightly linked

Question 44

diplotene

Answer 44

disassembly of SC, condensation and shortening of chromosomes

Question 45

after chiasmata are visible

Answer 45

homologies can segragate

Question 46

SC

Answer 46

each homolog is organised around protein axial core and SC form when these homolog axes are linked by rod shaped transverse filaments

Question 47

axial cores of each homolog

Answer 47

interacts with cohesin complexes that hold the sister chromatids together

Question 48

location of SC

Answer 48

between sister chromatid especially during crossover

uses cohesin

Question 49

homolog synapsis and desynapsis during different stage of prophase

Answer 49

2 sister chromatids coalesce and chromatid loops extend out from common axial core

Question 50

assembly of synaptonemal complex begins

Answer 50

in early zygotene and complete in pachytene

complex disassembles in diplotene

Question 51

SC under electron microscope

Answer 51

from meiotic cell at pachytene in lily flower

Question 52

cross over

Answer 52

chiasmata

Question 53

chiasmata

Answer 53

crossover seen as thin connection between homologs

Question 54

chiasmata in late stage bivalent

Answer 54

single crossover occurs between non sister chromatids

when SC disassembles and separate a little at end of prophase I

Question 55

difference in meiosis I to mitosis

Answer 55

• both sister kinetochores remain attached to same spindle pole
• chiasmata keep homologs together which allows bi-orientation
• centromeric cohesin on sister chromatid remains bound through anaphase