ONCOGENESIS PART 1 Flashcards

1
Q

MOST DISRUPTED CHECKPOINT IN CANCER

A

G1/S CHECKPOINT

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2
Q

WHAT ARE THE 3 GROUPS OF CDK

A

G1 : CDK 2, 4, 5, 6
S : CDK 2
G2 / M : CDK 3 (CDC 2)

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3
Q

WHAT ARE THE 3 GROUPS OF CYCLIN

A

G1 : CYCLIN D, E
S: CYCLIN A
G2 / M : CYCLIN B/A

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4
Q

NORMAL GENES THAT ARE ACTIVATED WHEN THERE IS A NEED FOR PROLIFERATION AND GROWTH

A

PROTO-ONCOGENES

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5
Q

PROTO-ONCOGENES IS REGULATED BY __________

A

TUMOR SUPPRESSOR GENE

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6
Q

CELL UNDERGOES DNA MUTATIONS AND TARGET PROTO-ONCOGENE TO BE MUTATED

A

ONCOGENES

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7
Q

A TYPE OF MUTATION WHEREIN PROTO-ONCOGENE BECOMES ONCOGENES

A

DOMINANT MUTATION

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8
Q

A TYPE OF MUTATION WHEREIN TUMOR SUPPRESSOR GENE OR DNA REPAIR GENE BECOME DANGED AND LOSE FUNCTION

A

RECESSIVE MUTATION

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9
Q

CHARACTERISTIC OF CANCER

A
  1. COLONALITY
  2. AUTONOMY
  3. ANAPLASIA
  4. INVASION AND METASTASIS
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10
Q

TUMORS ARISES AS CLONES FROM A SINGLE CELL

A

CANCER IS A GENETIC DISEASE

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11
Q

REGULATES CELL CYCLE

A

PROTEIN KINASE

CYCLIN (CDK)

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12
Q

DETERMINES WHETHER THE CELL PROCEEDS TO THE NEXT PHASE OF CYCLE

A

CHECKPOINT

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13
Q

2 IMPORTANT CHECKPOINTS

A

G1/ S CHECKPOINT

G2/ M CHECKPOINT

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14
Q

ACTIVITY OF G2/M CHECKPOINT

A
  1. CHROMOSOME CONDENSATION
  2. NUCLEAR MEMBRANE BREAKDOWN
  3. SPINDLE FORMATION
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15
Q

ACTIVITY OF G1/S CHECKPOINT

A
  1. ACTIVATES SEVERAL GENES THAT NEEDS S PHASE PROGRESSION

2. PROMOTES DIFFERENTIATION OF CELL VIA TRANSCRIPTION FACTOR

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16
Q

WHAT WILL HAPPEN IF PRB IS INHIBITED (HYPOPHOSPHORYLATED STATE)

A
  • THERE IS NO REPLICATION OF CELL
  • PRB WILL BIND TO E2F NO TRANSCRIPTION WILL OCCUR
  • CELL ARREST
17
Q

WHAT WILL HAPPEN IF PRB IS STIMULATED (HYPERPHOSPHORYLATED STATE)

A
  • THERE WILL BE CELL PROGRESSION

- PRB CANNOT BIND TO E2F CAUSING IT TO ACTIVATE TRANSCRIPTION

18
Q

REGULATES THE CHECKPOINT OF G1/S CHECKPOINT

A

RB GENE (TUMOR SUPRESSOR GENE)

19
Q

CYCLINS AND CDK ARE REGULATED BY ____

A

CDKI OR CDK INHIBITOR

20
Q

A CDKI THAT INHIBITS CELL CYCLE PROGRESSION AND PERMITS DNA REPAIR`

A

P21

21
Q

A CDKI THAT REGULATES SEVERE DAMAGE CELL TO UNDERGO APOPTOSIS BY INCREASING BAX

ALSO KNOWN AS GUARDIAN GENOME

A

P53

22
Q

TRUE OR FALSE

P43 HALTS THE DAMAGED CELL IN PROCESSING BY ACTIVATING P21

A

TRUE

23
Q

FORMATION OF NEW BLOOD VESSEL

A

ANGIOGENESIS

24
Q

IMPORTANCE OF ANGIOGENESIS TO TUMOR CELL

A

TUMOR CELL NEEDS NUTRIENTS AND THROUGH THE FORMATION OF NEW BLOOD VESSEL. TUMORS SECRETE A LOT OF VEGF AND IT HELPS GROW BLOOD VESSELS AND THEREFORE HELPS GROW AND SPREAD THE TUMOR.

25
Q

ENCODES P21 IN CELL CYCLE AND PROMOTES CELL ARREST

A

RAS GENE

26
Q

RAS PROTO-ONCOGENE BECOME RAS ONCOGENE BY A MUTATION REPLACEMENT OF ___ TO ___ AT CODON ___

A

MUTATION REPLACEMENT OF GLYCINE TO VALINE AT CODON 12

27
Q

CLASSIFICATION OF TUMOR SUPPRESSOR GENE

A

CELL ADHESION - APC AND DCC

REGULATORS OF CELL CYCLE - TP53 AND RB1

28
Q

SUBTYPE OF KNUDSON’S TWO HIT HYPOTHESIS

A
  1. TS MUTATION IS INHERITED - SMALL ISOLATED CHANGES IN THE GENE
  2. GROSS CHROMOSOMAL LOSS - COMPLETE LOSS OF THE CHROMOSOME
29
Q

WHAT IS THE TRANSLOCATION OF CHRONO MYELONGENIC LEUKEMIA

A

BCR-ABL FUSION OF CHROMOSOME 9 TO 22

30
Q

WHAT IS INVOLVE IN BURKITTS LYMPHOMA

A

c- myc IS TRANSLOCATED FROM CHROMOSOME 8 TO CHROMOSE 14

31
Q

KEEPS CELL FROM DIVIDING TO FAST AND PROVIDE INSTRUCTION IN MAKING PRB GENE

A

RB1 GENE

32
Q

TP 53

A

PRODUCT OF P53, IT WILL STOP DAMAGED CELL AND ACTIVATE P21 TO REPAIR IT HOWEVER IF THE CELL IS SEVERLY DAMAGED IT WILL STIMULATE INCREASE PRODUCTION OF BAX THAT WILL TRIGGER CELL APOPTOSIS OR CELL DEATH

33
Q

WHAT WILL HAPPEN IF THERES A MUTATION IN P53

A

THERE WILL BE NO DETECTION OF DAMAGED CELL WHICH MAY LEAD TO INAPPROPRIATE CELL SURVIVAL AND FORMATION OF CANCER