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FunMed Random > :))) > Flashcards

:))) Flashcards

1
Q

explain c-MYC proto-oncogene

A
  • proto-oncogene: c-MYK (~50% of cancers)

- promotion of transcription of cyclin genes (promotes cell cycle progression)

  • c-MYK is correlated with agressive tumour pattern and poor clinical outcome

( - causes increased growth, metabolism, cell adhesion, differentiation and metastasis)

  • seen in: Burkitt lymphoma, breast cancer
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2
Q

what are progenitor cells?

A

Progenitors are typically the descendants of stem cells, only they are more constrained in their differentiation potential or capacity for self-renewal, and are often more limited in both senses.

The most important difference between stem cells and progenitor cells is that stem cells can replicate indefinitely, whereas progenitor cells can divide only a limited number of times

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3
Q

anti-mitotic drugs?

A
  • vinca alkaloids and taxanes are two main groups.
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4
Q

which genes normally regulate apoptosis?

A

Bax: pro-apoptotic protein

Bcl2: anti-apopotic protein

a balance is required for normal apoptosis

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5
Q

how are cancer cells self sufficient in growth signals?

A
  • normal cells need mitogenic growth signals before they can move into proliferative state
  • many oncogenes can mimick normal growth signals and generate own growth signals (autocrine signalling)
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6
Q

which cells would u find in loose CT?

A

fibroblasts, mast cells and other leukocytes

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7
Q

what is difference between gram +ve and gram -ve cell walls

what colours do they stain?

A

depends on level of peptidoglycan: (and therfore the staining)

  • *- thick peptidoglycan: gram postive - purple stain**
    a) just one membrane
    b) lipotechoic acids sticking out
  • *- thinner peptidoglycan: gram negative** - negative stain
    a) have inner and outer membranes
    b) lipopolysaccarides sticking out
    c) holes in outermembrane
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8
Q

what test do u use to see if can lyse blood?

A

lancefield antigen testing

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9
Q

Enterobacteriaceae are what type of bacteria?

A

gram negative bacteria

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10
Q

disease caused by Streptococcus pyogenes (Group A)?

A
  • *Streptococcus pyogenes (Group A)**
  • sore throat
  • fever
  • rash (strawberry tongue) - scarlet fever
  • tonislitis
  • infection of upper dermis: if on face: erysipelas ; arm: cellulitis. deeper that skin: can develop into sepsis, flesh eating strep
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11
Q

how do homologous chromsomes line up in prophase I in meiosis?

what process happens here?

A

via chiasmata

crossing over !!

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12
Q

how are gram postive cocci subclassed? how do u test?

A

gram postive cocci - to differentiate between cocci do catalase test

  • *- streptococci: catalase negative
  • straphylocci: straphylocci positiive**

subclassify straphylocci further: coagulase stain:

  • *- straphylocci coagulase +ve
  • straphylocci coagulase -ve**

subclassify Streptococci further:: if can lyse blood or not

  • *- beta-haemolytic: lyse blood - complete haemolysis
  • alpha-haemolytic:: partially lyse blood
  • non-haemolytic: dont**
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13
Q

which caspases are the initiator and which are executioner caspases/

A
  • *initiator:** caspases 2, 8 & 9
  • *executioner:** caspses 3,6 & 9
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14
Q

what are the two pathways initated by growth factor binding to cell, that eventually lead to activation of gene expression and transcription factors occur.

A

MAPK pathway and PI3 Kinase Pathway

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15
Q

which out of ligament and tendons connects bone to bone?

A

ligament - bone to bone

tendon: muscle to bone

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16
Q

what happens if overexpress growth factors?

A

get hyperplasia (Hyperplasia, or hypergenesis, is an enlargement of an organ or tissue caused by an increase in the amount of organic tissue that results from cell proliferation)

  • can be precancerious or not lead to cancer
  • genes are often amplified
  • autocrine loops and unregulated growth
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17
Q

what is p53? why important?

A

P53 - guardian of the genome!

  • blocks progression of cell cycle by of synthesis p21 (a CDKI) which inhibits CDK2 ( which inhibits activation of cyclin E and A)
  • is an important tumour suppressor gene
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18
Q

explain what BRCA1 and BRCA2 normally do and what their mutations cause

A

BRAC1:

  • normally: triggers the activation of the CDK inhibitor: p21WAF-1 and p53, so can control cell cycle
  • also involved in DNA repair
  • mutations lead to genomic instability
  • *BRAC2**:
  • normally facilitates HR
  • BRAC2 deficient cells: cant recruit RAD51 (protein that binds to ssDNA and needed in dsDNA repair
  • mutations: cant repair ss and dsb DNA breaks
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19
Q

why do cancer cells want to not be differentiated?

A

once differentiated, no longer divide/ divide less

onco-genes reduce differentation

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20
Q

name 3 gate keeper genes

A
  1. Bax
  2. p53
  3. Rb
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21
Q
  1. how is limitless replicative potential achieved by cancer cells?
A

maintain telomere length

22
Q

structure of ion gated channels?

A

alpha helix:

  • hydrophobic a.a. stick out of alpha helix and interact with hydrophobic lipid membrane.
  • hydrophilic a.a. are tucked into the alpha helix
23
Q

what is Aspergilliosis?

A

Aspergillosis is an infection caused by a type of mold (fungus). The illnesses resulting from aspergillosis infection usually affect the respiratory system, but their signs and severity vary greatly.

24
Q

what are the main groups of genes that implicate cancer?

A

1. oncogenes

2. tumour supressor genes:

a) gatekeepers (regulate cell cycle)
b) care takers (DNA repair)

25
Q

where is embroynic mucous CT found? function?

A
  • umbilical cord
  • protects umbilical cord vessels
26
Q

what type of mutation? how is kras perm. switched on?

A

GTP is bound to ras in unhydroloysed form - ras is permenantly switched on. continois proliferation and growth.

point mutation

RAS proteins were some of the first proteins identified that possessed the ability to regulate cell growth.

27
Q

collagen macrostructure?

what makes collagen?

A

This consists of three polypeptide chains (each called an alpha chain and not necessarily all identical), bound together to form a helical protein structure 300 nm long and 1.5 nm in diameter

fibroblasts

28
Q

process of gram staining?

A

Gram stain: Crystal violet –> Iodine –> Ethanol –> Safranin

29
Q

what are the three types of connective tissue fibres?

A
  1. collagen fibres
  2. reticular fibres / tissue
  3. elastic tissue
30
Q

which cells are CT derived from?

what are the two type of embryonic CT?

A

derived from mesoderm.

  1. embryonic connective tissue:
    - mesenchyme
    - mucous connective tissue
31
Q

what are examples of hyperplasia and cancer?

A

hyperplasia leads to increased growth: can be:

benign - VEGF (vascular endothelial growth factor) - (up regulate the synthesis of blood vessels.): leads t benign prostatic hyperplasia (enlarged prostate). benign growth

malignant - platelet derived growth factor (PGDR) - leads to glioblastoma

32
Q

what do u use to stain:

( a) Mycobacteria:

b) fungi:
c) spirochaetes:

A

( a) Mycobacteria: Zielh-Nielson stain

b) fungi: Cotton blue stain
c) spirochaetes: darkfield microscopy )

33
Q

what is the name of structure where centromere and mitotic spindle fuse in metaphase?

A

kinetochore

34
Q

what are the five categories of proto-oncogenes?

A

1. growth factors

2. growth factor receptors

3. signal-transduction proteins

4. transcription factors

5. anti-apoptotic proteins

mutations change structure in these proto-oncogenes -> oncogenes

35
Q

explain ion-channel linked receptor: nicotinic actylcholine receptor

structure?

what bind to?

how work?

A
  • five subunits across the membrane
  • two binding sites for acetylcholine
  • binding opens channel and allows sodium to enter cell -> skeletal muscle contraction
36
Q

which cell-surface receptors are homologous in structure, which are heterogenous?

A

heterogenous: enyzme linked receptor
homologous: G-protein linked receptor, ion channel linked receptor

37
Q

what does type 3 collagen make?

A

embroynic tissue, uterus, blood vessels

38
Q

how does muscarininc acetylcholine receptor work?

A
  • acteylcholine binds to acteylcholine receptor
  • trimeric G-protein activated
  • alpha subunit of trimeric G-protein binds to activated ion channel
39
Q

can c-MYC induce cancer on its own? what else needed?

A

NO

need secondary mutations to occur in:

  • proliferative arrest
  • apoptosis
  • sencescence

MYC OVEREXPRESSION ALONE DOES NOT INDUCE TUMOURIGENESIS

40
Q

what is p53 activated by?
what is normal function and how does it work?

A
  • p53 activated by DNA damage, hypoxia or cell injury
  • causes cells with mutations to undergo cycle arrest, allows DNA repair or entry to apopotic pathway
  • p53 activation activates p21 -> inhibits cyclin complexes (prevents cell leaving G1 / entering S-phase
41
Q

which proteins regulate cell divison?

A

1. Cyclins (cylin A,B, D) - allow cell cycle to continue

2. cyclin dependent kinases (CDK) add P groups to cyclin -> activates the cyclins

3. cyclin dependent kinases inhibitors (CDKIs)

depending on if CDK or CDKI is more prominant - regulates cell cycle

42
Q

why cant Mycobacter be used by gram stain?

why cant see spirochates?

A
  • *mycobacteria**
  • waxy cell wall - lipid rich: resistance to drying, antiobiotics and disinfectants, acids and alkalis, survives in macrophages

spirochaetes:
too thin cell wall to see with gram stain

43
Q

when is each cyclin actived?

A
  • G1 checkpoint passed: activates cyclin D (regulates early G1 phase) and cyclin E (regulates early G1 phase and triggers S phase)
  • S checkpoint passed: activates cyclin A (cyclin A acitvates DNA replication in S phase and movement into G2 phase)
  • G2 / M checkpoint passed: activates cyclin B (takes cells into mitosis)
44
Q

which type of collgaen makes cartilage?

A

type 2

45
Q

what is cAMP activated / generated AND degraded by?

what does cAMP stimulate?

A
  • activated / generated from ATP by the enzyme adenylyl cyclase
  • cAMP degraded / inactivated by enzyme phosphdiesterase
  • *stimulates**:
  • protein kinase A (PKA) PKA aka cAMP-dependent protein kinase
46
Q

what does cohesin do in dna replication (anaphase)?

A

Cohesin mediates cohesion between replicated sister chromatids and is therefore essential for chromosome segregation in dividing cells.

47
Q

which pathways does Ras pathway swtich on?

A

ERK and AKT pathways

48
Q

mesenchyme embroyonic CT - where found? loose or dense tissue? what does it give rise to?

A
  • loose tissue
  • found in embryo and umblical cord
  • embryonic mesenchyme gives rise to muscle, vasuclar and uro-genetial systems and serous membranes
49
Q

internal factors that can cause necrosis?

A

immune system

oxidative stress

50
Q

location of loose CT?

function?

A

location: Dermis, lamina propria of the digestive and respiratory tracts, mucous membranes of reproductive and urinary tracts, glandular stroma, mesentery

function: involved in immune response

51
Q

example of a uncontrolled GF & receptor causing cancer?

A

HER2 or ErbB2

  • tyrosine kinase receptor known as HER2 or ErbB2
  • uncontrolled growth, survival of cells containing mutations, invasion of tumour cells, migration tumour cells

FunMed Random (19 decks)

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