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Cellular and Molecular pathology > 6. Introduction to cancer > Flashcards

6. Introduction to cancer Flashcards

1. What is cancer? 2. What causes cancer? 3. How are normal and tumour cells different? 4. What are the challenges for cancer therapy?

1
Q

how does 1 cell become millions of billions?

A

through a very complex and closely regulated process

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2
Q

Human cellular complexity

A
  1. can code 30,000-50,000 proteins despite way fewer genes
  2. about 200 different models of cell type specialisation
  3. typical replication time for a mammalian cell is 24 hours which is very short considering the processes that need to happen
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3
Q

what cells are most cancers derived from?

A

epithelial cells

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4
Q

why is knowing the cell of origin of the cancer important?

A

to give the right treatment and prognosis

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5
Q

what are the sub-divisions of epithelial cancers?

A
  1. Ectoderm: bilayer epithelium or multi-layer epithelium
  2. Ectoderm: single-layer epithelium or multi-layer epithelium
  3. Mesoderm: single-layer epithelium
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6
Q

examples of epithelial cancers

A

breast
Thyroid
lung
pancreas
colon
kidney
skin
bladder

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7
Q

what are the sub-divisions of non-epithelial cancers?

A
  1. Mesoderm: mesenchymal
  2. Mesoderm: hematopoietic
  3. Neuroectoderm
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8
Q

examples of non-epithelial cancers

A

blood cancers and nervous system cancers

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9
Q

what are mixed multilineage cancers?

A
  1. generally germ cells
  2. more likely to be childhood cancers
  3. not derived from classical epithelial cells
  4. usually a block in the normal differentiation processes
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10
Q

define neoplasia

A

a pathologic process in which a permanent alteration in a cell’s growth controlling mechanism that permits its continuous proliferation

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11
Q

define neoplasm

A

a mass of tissue that is actively and progressively growing because of permanent defect in its cells’ growth-controlling mechanisms

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12
Q

define benign

A

“good” a group of neoplasms that do not threaten life

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13
Q

define malignant

A

“bad” a group of neoplasms that invariably kill if not treated

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14
Q

define cancer

A

any malignant neoplasm

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15
Q

define tumour

A

any neoplasm

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16
Q

characteristics of a benign tumour

A
  1. slow growing
  2. Encapsulated
  3. noninvasive
  4. well-differentiated
  5. nonmetastatic
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17
Q

Characteristics of a malignant tumour

A
  1. rapidly multiplying
  2. invasive
  3. infiltrative
  4. anaplasic and undifferentiated
  5. metastatic
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18
Q

what is anaplasia?

A

a condition of cells with poor cellular differentiation, losing morphological characteristics of mature cells and their orientation with respect to each other

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19
Q

how does cancer arise?

A
  1. a long and slow process
  2. huge numbers of mutations are needed to become a cancer
  3. it is hard to identify driving mutations required for cancer
  4. adult cancers tend to have slow development of the pre-malignant stage
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20
Q

What is PIN?

A

prostate intraepithelial neoplasia

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21
Q

what is CIN?

A

Cervical intraepithelial neoplasia

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22
Q

what does DCIS stand for?

A

ducal carcinoma in situ

23
Q

what is hard to pick out among the many mutations?

A

which mutations are the key driving mutations for the cancer

24
Q

what are many childhood cancers?

A

dysfunction of embryo development that gives rise to malignant growth

25
Q

how can early mesenchymal cells lead to cancers?

A
  1. mesenchymal cells differentiate into more and more specialised epithelial like structures
  2. lots of signalling between the cells
  3. lots of transcription and growth factors
  4. some of this signalling goes wrong and the differentiation doesn’t occur properly leading to cancer
26
Q

what is the neural crest?

A
  1. produces lots of cells for different areas in the body and different structures
  2. lots of Wnt signalling and lots of epigenetic factors
27
Q

what is important in the prognosis of neuroblastoma?

A

the grade of differentiation
undifferentiated histology leads to worse outcomes

28
Q

what is differentiation therapy for neuroblastoma?

A

high-dose, pulse retinoic acid induces differentiation in neuroblastoma which can improve treatment outcomes and prognosis

29
Q

what does differentiation therapy prove?

A

why it is important to understand the cellular origins

30
Q

what is cancer a disease of?

A

the genome

31
Q

what factors can cause cancer?

A

hereditary through acquired genetic changes
Environmental factors like chemicals, radiation and viruses

32
Q

how is the genome integrity affected in cancer?

A
  1. chromosomal structure: translocations and duplications
  2. qualitative alterations of the cellular proteome: mutations
  3. Quantitative variations of proteome: altered gene expression due to disruption/variation of regulatory elements or molecules
33
Q

how can mouldy peanuts cause cancer?

A

grow a fungus that contains aflatoxin which is a carcinogen as it is associated with p53 mutations

34
Q

what do cancer karyotypes look like?

A
  1. contains translocations
  2. contains alterations
  3. aneuploidy
35
Q

what are telomeres?

A
  1. A mitotic clock that is important for regulating chromosome integrity
  2. 6-12kb with 50-100bp lost per cell cycle
  3. recruit specific capping proteins to the ends of the chromosome
  4. protects the coding sequence from erosion
36
Q

what is the function of telomeres?

A
  1. involved in regulating ageing
  2. once the telomeres are short enough it forces the cell to enter senescence
37
Q

what happens to telomeres in cancer cells?

A

they overexpress telomerase to replace the telomere and keep dividing

38
Q

where is telomerase usually expressed?

A

stem cells and haematopoietic cells

39
Q

what are the consequences of unrepaired DNA damage?

A

The breakage fusion bridge cycle
1. a dsDNA breaks cause the loss of a chunk of the chromosome including the telomere
2. the unprotected chromosome ends form fused chromosomes
3. the fused chromosomes pull apart anyway causing more breaks and mutations
4. results in large scale chromosomal defects

40
Q

what are the 2 main categories of genes involved in oncogenesis?

A

oncogenes
tumour suppressor genes

41
Q

what are oncogenes?

A

a gene where a mutation leads to overactivity or gain of function that leads to cell proliferation

42
Q

what are tumour suppressor genes?

A

a gene where a mutation leads to under activity or loss of function that leads to cell proliferation
- needs to occur in both alleles to eliminate the tumour suppressor function

43
Q

what are some chromosomal alterations that give rise to fusion proteins?

A
  1. BCR-ABL in chronic myelogenous leukaemia = increased protein kinase activity
  2. PAX3-FOXO1 in alveolar rhabdomyosarcoma = chimeric transcription factor
  3. PML-RARa in AML= differentiation block, chimeric transcription factor
44
Q

what are some chromosomal alterations that give rise to altered gene expression?

A
  1. C-MYC in Burkitt’s lymphoma = moves Ig genes leading to over expression of MYC
  2. HOX11-TCRa/ß in T-cell acute lymphoblastic leukaemia = reconfiguration of control elements
  3. MYCN in neuroblastoma = gene amplification
45
Q

what can MYCN amplification in neuroblastomas indicated?

A

decreased survival chances
same as HER2 in breast cancer

46
Q

what else can change the way genes are expressed?

A

epigenetics

47
Q

what can prevent the cell cycle if damage is detected?

A

p53 and RB1

48
Q

what are p53 and RB1?

A

tumour suppressor genes whose function prevents cancer formation

49
Q

how is the cell cycle regulated in normal cells?

A
  1. TSGs regulate cell cycle signalling and can act as a firebreak
  2. TSGs keep everything at a regulated speed and push the cells into S phase
50
Q

how is the cell cycle regulated in cancer cells?

A
  1. excess mitogen signalling causing over activity of cyclins and CDKs
  2. enhanced DNA repair
  3. push the cell through the cell cycle faster leading to replication stress
  4. if the check points are overwhelmed then mutations can pass onto daughter cells and accumulate
51
Q

what are the 2 biggest problems for cancer therapies?

A
  1. EMT and metastases
  2. cancer stem cells
52
Q

why does metastasis cause a problem?

A

makes targetted treatment a lot harder

53
Q

why do cancer stem cells cause a problem?

A
  1. they are the main reason cancers come back
  2. they replicate a lot slower so are not targeted by normal treatments that target rapid replication

Cellular and Molecular pathology (25 decks)

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