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G e n e t i c s N e w s. Helen Fillmore talks today on therapies for neurodegenerative diseases. 12:30. Here. Problem Set 10 on line. On Our Plate Genetics of Cancer. Clonal Nature of Cancer G6PD experiment Somatic vs. Germline Mutation RB: A Tumor Suppressor Gene Signal Transduction

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Presentation Transcript
slide1

GeneticsNews

  • Helen Fillmore talks today on therapies for neurodegenerative diseases. 12:30. Here.
  • Problem Set 10 on line
on our plate genetics of cancer
On Our PlateGenetics of Cancer
  • Clonal Nature of Cancer
  • G6PD experiment
  • Somatic vs. Germline Mutation
  • RB: A Tumor Suppressor Gene
  • Signal Transduction
  • Oncogenes & Tumor Suppressors
  • Progression of Cancer
demonstration of clonality
Demonstration of Clonality

What does the gel represent? (e.g. DNA fragments?)

Protein from Leukocytes

Protein from Skin cells

Protein with G6PD activity

What do “L” and “S” represent?

demonstration of clonality1
Demonstration of Clonality

Why two genotypes?Which was she born with?

XAXB is the germline genotype

SQ2 and 3: What is the mother’s genotype?

XBXB and XAXB

demonstration of clonality2
Demonstration of Clonality

1

1

3

2

3

1

1

Lactate dehydrogenase???

Glc-6-P dehydrogenase

4

8

SQ4: Why three bands in skin cells?

cancer infection or clonal
Cancer: Infection or Clonal?

What is meant by “A” and “B”?

Why do some cells have “A” and others have “B”?

Why do cells in panel C have a mixture of cell types?

Why do cells in panel B have the same cell type?

Fig. 2. Two models to explain cancer. ... Half of the cells have an active X chromosome carrying the A allele and half have an active X chromosome carrying the B allele.

control over cell division
Control over Cell Division

Mitosis

Gap2

Gap1

DNA synthesis

control over cell division1
Control over Cell Division

Hormones

Build up of signal(cyclin-CDK complex)

What happens if the cell is Rb-?

phosphate

the menace of familial retinoblastoma
The Menace of Familial Retinoblastoma

Rb dominant

Mutation rare(say 1 in 109)

What is the result of a single Rb- mutation?

What about here?

study question 9
Study Question 9

Cell #1: Suddenly loses eye pigment enzyme

Cell #2: Suddenly loses Rb

Normal retinal cells don’t divide

Derepressed cells divide once a day

Ratio of Cell #1:Cell #2 after 30 days?

Cell #1

Cell #2

Day 0

Day 1

Day 2

Day 3

Day 4

study question 8
Study Question 8
  • Loss of RB in retinal cells causes retinoblastoma
  • Sporadic cases show tumors only in one eye
  • Inherited cases show tumors occur often in both eyes
  • WHY?
control over cell division2
Control over Cell Division

Hormones

Build up of signal(cyclin-CDK complex)

signal transduction activation of receptor1
Signal Transduction:Activation of Receptor

No hormone

Mutant signaltransducing protein(e.g. Ras)

signal transduction activation of genes1
Signal Transduction:Activation of Genes

No hormone

Mutant signaltransducing protein(e.g. Ras)

control over cell division3
Control over Cell Division

Hormones

Suicide?(Apoptosis)

Build up of signal(cyclin-CDK complex)

p53

Mismatch Repair

control over cell division4
Control over Cell Division

Hormones

Build up of signal(cyclin-CDK complex)

oncogene vs tumor suppressor
Oncogene vs Tumor Suppressor
  • OncogenesWhen mutated, stimulates cell division
  • RAS - Stimulates protein kinase
  • MYC - Transcriptional factor
  • Tumor suppressorsWhen mutated, releases division to cell block
  • RB - Inhibits transcription factor
  • P53 - Many functions (e.g. transcription factor)
study question 12
Study Question 12
  • Protein monitors DNA for DNA damage
  • If DNA damaged, protein blocks cell division
  • Is protein tumor suppressor or from an oncogene?
study question 15
Study Question 15

Lots of p53 mutations in dead people. WHY?

A. p53 is prone to mutation?

B. p53 is not prone to mutation, but leads to death?

C. p53 related to feedback?

causes of particular cancers
Causes of Particular Cancers

Study Question 13

Why does the chromosome 8/14 translocation lead specifically to lymphomas?

What is myc? What’s its threat?

What is Pimm? Where is it on?