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Pathology book > Chapter 7: Neoplasia > Flashcards

Chapter 7: Neoplasia Flashcards

1
Q

What does neoplasia mean?

A

New growth

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2
Q

How are benign tumors named?

A

They end in -oma - Adenoma = from glands, Papilloma = forms pillary stuctures and arise from epithelium.

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3
Q

How are malignant cancers named? ?

A 
Sarcoma = mesenchymal
Carcinoma = of epithelial origin
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4
Q

What does pleomorphic mean?

A

present in several forms.

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5
Q

What does anaplasia mean?

A

Lack of differentiation - cells do not look like the mesenchymal cells from which they came to be. In general malignant cell lines show more anaplasia. (Literally to form back - a more primal state)

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6
Q

Histological changes in cancers:

A

1) Lack of differentiation = Anaplasia
2) pleomorphism = variation in shape and size
3) High nuclear/cytoplasm ratio = enlarged nucleus
4) Mitosis
5) Loss of polarity
6) Angiogenesis - and necrosis from lack of oxygen

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7
Q

What is metaplasia?

A

Replacement of one type of cell with another

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8
Q

What is dysplasia?

A

Means disorganized growth.

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9
Q

What is a carcinoma in situ?

A

When dysplastic changes have occured in the full layer of epithelium but the integrity of the basement membrane remains intact.

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10
Q

Why does encapsulation of tumors occur?

A

Activation of fibroblasts as a result of hypoxic damage following the expansion of the tumor and pressure on the sorrounding tissues.

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11
Q

By with patways can cancers spread?

A

1) Direct seeding on body surfaces or cavities
2) Lymphatic spread - mostly carcinomas
3) hematogenous spread - mostly sarcomas

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12
Q

What is a sentinel lymph node?

A

The first lymph node which receives lymp from the tumor tissue.

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13
Q

Which genes are the principle targets of cancer causing mutations?

A

1) Proto-oncogenes
2) tumor-surpressor genes
3) DNA-repair genes
4) apoptosis regulating genes

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14
Q

The hallmarks of cancer:

A

1) Self-sufficiency of growth signals
2) insensitivity to growth signal inhibition
3) Altered cellular metabolism
4) Evasion of apoptosis
5) Immortality
6) Sustained angiogenesis
7) Ability to invade and metastasize
8) Ability to invade the host immune response

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15
Q

The hallmarks of cancer:

A

1) Self-sufficiency of growth signals
2) insensitivity to growth signal inhibition
3) Altered cellular metabolism
4) Evasion of apoptosis
5) Immortality
6) Sustained angiogenesis
7) Ability to invade and metastasize
8) Ability to invade the host immune response

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16
Q

How does a typical growth factor work?

A

1) binds receptor on surface
2) activates receptor - adaptor proteins
3) cytoplasmic effector proteins and second messengers confers signal
4) transcription factor activated
5) transcription of factors that positively affects cell cycle

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17
Q

ERBB1?

A

EGFR (epidermal growth factor receptor)

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18
Q

ERBB2?

A

HER2

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19
Q

Which pathway is BRAT (BRAF as protein) a part of?

A

The MAPK pathway - it is a serin/threonine kinase at the top of the pathway.

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20
Q

To eksempler på konstitutiv aktivering af Non-tyrosin kinaser:

A

Burkitt lymphoma and Chronic myelogenous

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21
Q

What is MYC?

A

A proto-oncogenic transcription factor involved in tumor development. Downstream of RAS/MAPK signaling

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22
Q

Where are the two major cell cycle checkpoints?

A

1) the G1 to S

2) the G2 to M

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23
Q

Which are the 3 major types of proteins mentioned in the book as oncogenes?

A

1) Proteins involved in Growth factor signaling, non-RTK and downstream signaling molecules
2) Master transcription factors like MYC
3) Mitosis affecting proteins like CDK4/D-cyclin complexes.

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24
Q

Which gene lays the basis of Knudson´s two hit theory?

A

RB - a tumor surpressor - a key negative regulator of the G1-S checkpoint.

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25
Q

What are the four genes controlling cell cycle of which one is almost always mutated in cancer?

A

1) P16/INK4a
2) RB
3) Cyclin D
4) CDK4

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26
Q

What is Li-Fraumeni syndrome?

A

An existing mutation in a TP53 allel.

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27
Q

What is the function of the protein MDM2?

A

It stimulates p53 degredation.

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28
Q

Which three types of proteins is p53 believed to be a transcription factor for?

A

1) Apoptotic proteins
2) Cell-cycle arrest proteins
3) catabolic or anti anabolic proteins

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29
Q

How is p53 activated?

A

1) DNA damage and hypoxia through ATM and ATR which phosphorylates p53 liberating it from MDM2 and inhibits p53 degredation
2) Oncogenic stress - activation of oncogenic proteins - p14/ARF replaces p53 binding to MDM2

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30
Q

p53 can induce?

A

1) Cell cycle arrest
2) Senescence
3) Apoptosis

31
Q

What is APC?

A

Adenomatous Polyposis coli - colon cancer - a tumor surpressor which works by down regulating growth promoting pathways and affecting Wnt signaling (important for polarity and differentiation). APC induces degredation of Beta-catenin. Beta-catenin normally binds TCF (transcription factor).

32
Q

Why is E-cadherin important?

A

Important cell-cell contact through beta-catenin and mutations in either can lead to cancerous behaviour.

33
Q

P14/ARF and P16/INK4a

A 
p16 = Cyclin dependent kinase inhibitor - blocks phosphorylation of RB
p14 = p53 activator - inhibits MDM2 binding
34
Q

TGF-beta

A

Tumor surpressor effect - binds TGF-beta receptor I or II thourgh SMAD affects CDK inhibitors and more

35
Q

What is PTEN?

A

Phospatese and TENsin homologue is a membrane bound phosphatase which inhibits PI3K/AKT pathway.

36
Q

NF1 and NF2

A

Gives rise to neurofibromatosis 1 and 2. NF1 = neurofibromin 1, GTPase which regulates RAS. NF2 = neurofibromin 2, a cytoskeletal protein involved in contact inhibition.

37
Q

WT1:

A

Encodes transcription factor which is involved in urogenitala system - associated with Wilms Tumor.

38
Q

PTCH1:

A

Negative regulator of hedgehog signaling. TM receptor which internalises when there is soluble hedgehog factors and thereby does not inhibit anymor. hedgehog stimulates pro-growth proteins like D-cyclin.

39
Q

STK11:

A

Important for cellular metabolism - gives rise to benign polyps in colon.

40
Q

VHL1:

A

Encodes ubiquitin ligase responsible for degredation of hypoxia induced factors. Loss of function gives cancer.

41
Q

How does PI3K/AKT influence the metabolism?

A

Upregulates glucose uptake. Upregulates activity of metabolic enzymes so that intermediates for biosynthesis are created.

42
Q

RTK infuence on metabolism?

A

Influences M2 isoform of pyruvate kinase which makes biosynthetic precursors pile up. (phosphorylates it so pyruvate cant go further in becoming energy). M1 is not dependent on growth factors.

43
Q

What is the warburg effect?

A

Warburg effect is the fact that even with ample oxygen supply a lot of cancer cells do a lot of anaerobic glycolysis - a lot of the glycotic intermediates are needed for biosynthesis. This means that a lot of glucose is needed making glucose uptake a possible marker for cancer cells.

44
Q

What is anoikis?

A

Loss of adhesion to the basement membrane.

45
Q

Three aspects of immortality:

A

1) Evasion of senesence - not really known but thought to be p53 upregulation - so p53 inhibition = minus senesence.
2) Evasion of mitotic crisis - Also known as shortening of telomeres. At some point the ends will be registrered as DSB - and the cells will die. Cancers have telomerase activity and can evade this problem.
3) The capacity for self renewal - there must be a population of cancer stem cells.

46
Q

Name some of the factors which can help induce angiogenic potential of cancer cells.

A

1) Hypoxia induces HIF1alpha which is responsible for VEGF and bFGF (basic fibroblast growth factor).
2) Some tumor surpressors (like p53) inhibits pro-angiogenic transcription - some oncogenes lead to more angiogenesis.
3) VEGF influenced by RAS-MAP.

47
Q

Which two phases does the book divide metastasis into?

A

1) Invasion of the ECM

2) Vascular dissemination, homing of tumor cells and colonization.

48
Q

The ECM part of metastasis can be divided into:

A

1) Loosening up of Tumor cell - tuomr cell interactions
2) degredation of ECM
3) Binding to novel ECM components
4) Migration and invasion of tumor cells

49
Q

How are tumor cell interactions weakened?

A

Different proteins are involved - the book specifically mentions E-cadherins (which are also connected to Beta-catenin)

50
Q

Important functions of ECM breakdown products:

A

1) ECM embedded pools of VEGF promoting angiogenesis
2) breakdown products work as chemokines
3) other growth factors bound by matrix molecules.

51
Q

What might be the basis of the seed and soil theory

A

1) Different tumors from different tissues have receptors which are tissue specific and the targets of these receptors are only in selct tissues.
2) Different sets of chemokines might attract different subsets of cancer cells.
3) Some places might just be unfavorable like muscles.

52
Q

What are SNAIL and TWIST?

A

Transcription factors that help induce EMT - eg by down regulating the E-cadherin expression.

53
Q

Name two classes of enzymes which are responsible for ECM degredation:

A

1) MMPs and

2) Cathepsins

54
Q

Name which sort of proteins that are usually tumor antigens:

A

1) Products of mutated genes
2) overexpressed or abberantly expressed cellular proteins
3) Tumor antigens produced by oncogenic viruses
4) oncofetal antigens - found in tumors and fetuses. Eg carcinoembryonic antigen (CEA)
5) Altered cell surface glycolipids and glycoproteins
6) Cell type-specific differentiation antigens - specific to the cells of origin

55
Q

Name the cells mainly responsible for cancer resistance in vivo (anti tumor effects in vivo are mostly cell-mediated):

A

1) Cytotoxic T-lymphocytes (recognize CD8)
2) Natural killer cells (kills weird looking cells with lack of signal or signal that tells to kill
3) Macrophages

56
Q

Overall mechanisms of cancer immune evasion:

A

1) selective outgrowth of antigen negative subpopulations of the tumor cells
2) Loss of MHC-1 expression (may also lead to destruction)
3) Activation of immunoregulatory pathways - Example CTLA-4 instead of CD28 (costimulatory) in communication with t-cells.
4) secretion of immunosupressive factors by cancer cells. Eg TGF-beta.
5) Induction of T-regs

57
Q

HNPCC

A

Hereditary nonpolyposis colon cancer syndrome. Due to defect mismatch repair. MSH2 and MLH most normal genes with mutations. They usually have microsattelite instability.

58
Q

Name three pathways which are often affected in genomic instability:

A

1) DNA mismatch repair
2) Nucleotide excision repair
3) Homologous recombination

59
Q

Function of BRCA 1 and 2:

A

Both are involved in DNA double strand break repair. Almost always familial cancers when mutated.

60
Q

What is chromothrypsis?

A

Chromosome shattering

61
Q

Name the different kinds of chromosomal changes:

A

1) Translocations
2) deletions
3) amplification (duplication)
4) chromothrypsis

62
Q

Name some of the most common epigenetic changes in cancer:

A

1) Silencing of tumer surpressors by hypermethylation locally
2) global methylations changes
3) changes in histones

63
Q

What are promotors? (the chemical substance)

A

Substances which induce cell proliferation but arent mutagenic.

64
Q

Name the most common types of carcinogens:

A

1) chemical carcinogens
2) radiation
3) Microbial (RNA + DNA viruses, heliobacter)

65
Q

What does uvB induce?

A

Pyrimidine dimers

66
Q

HTLV-1:

A

Human t-cell lymphoma virus type 1. RNA retro. Invades CD4+ t cells. has protein Tax which is pro growth stimulator.

67
Q

HPV:

A

DNA retrovirus. E6 bind to Rb, E7 to TP53.

68
Q

EBV:

A

Herpesvirus - Burkitt lymphoma. Normally only people with abornal T-cell mediated immunity. Infects B-cells.

69
Q

cachexia:

A

Loss of fat, muscle and a raise in metabolic rate.

70
Q

Why does cancers induce local hypercalcemia?

A

1) osteolysis.
2) calcemic humoral substances (secretes substances which might influence body calcium levels)eg PTHRP (looks a bit like PTH) which has effect in calcium transport.

71
Q

What is the grading bassed on?

A

The degree of differentiation of the ccells in the cancer.

72
Q

What is the staging based on?

A

size of the original tumor, spread in lymph nodes, presence of blood borne metastasis.

TNM = Tumor, Nodes, Metastasis

73
Q

Name some of the uses of immunohistochemistry in cancer treatment:

A

1) Categorization of undifferentiated malignant tumors
2) Determination of site of origin of metastatic tumor
3) detection of molecules with possible therapeutic significance.

Pathology book (8 decks)

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