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TIN > WK 5- NEOPLASIA > Flashcards

WK 5- NEOPLASIA Flashcards

1
Q

What does neoplasia mean

A

new growth

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2
Q

What are the two components that a tumour consists of

A

Parenchyma

Stroma

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3
Q

What is a neoplasm

A

an abnormal mass of tissue that’s growth is uncoordinated and does not respond to normal growth controls and will persist in the same excessive manner after the cessation of the stimulus which evoked the change

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4
Q

What is the parenchyma

A

Are neoplastic cells and determines the biological behaviour of the tumour (cells of the tumour)

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5
Q

What is the stroma

A

Made up of non-neoplastic host derived connective tissue and blood vessels and provides support for the growth of the parenchyma

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6
Q

What are the characteristics of benign growths terms of; differentiation, growth rate, local invasion, metastasis

A

Differentiation: Well differentiated, structure is sometimes typical to origin tissue
Growth: Progressive but slow, may come to a stop or regress, mitotic figures are rare and normal
Invasion: Well demarcated masses that do not invade surrounding tissue, may be surrounded by a stromal capsule
Metastasis: Absent

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7
Q

What are the characteristics of malignant growths terms of; differentiation, growth rate, local invasion, metastasis

A

Differentiatino: Lack of differentiation, structure is atypical
Growth: Eractic, mitotic figures may be numerous and abnormal
Invasion: Locally invasive and will infiltrate surrounding tissue
Metastasis: Frequent- more likely with large undifferentiated primary tissues

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8
Q

What is anaplasia

A

lack of differentiation (don’t look like the cells they develop from)- key mark of metastasis

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9
Q

What does differentiation mean

A

extent to which parenchymal tumour cells resemble comparable cells both morphologically and functionally (look like the cells of the tissue it is growing in)

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10
Q

What is pleomorphism

A

cells of large irregular size with large hyperchromic nuclei and multinucleated cells, the cells will grow in a disorganised pattern with frequent and abnormal mitosis, increased nuclei to cytoplasmic ratio

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11
Q

What kind of cells display pleomorphism

A

Malignant cells

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12
Q

Do malignant cells display polarity

A

No, epithelial cells display polarity (all face the same uniform way)

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13
Q

What is metastasis

A

tumour moves through basement membrane and will travel through the blood to develop as secondary growths discontinuous with the primary tumour and often in possible remote zones

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14
Q

What are the 3 pathways by which malignant growth metastasise

A

Lymphatic, haematogenous and seeding of body cavities

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15
Q

What carcinoma most commonly spreads by lymphatic metastasis

A

Lung cancer

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16
Q

What is haematogenous spread and what cancers does it commonly occur in

A

Tumour will work into blood stream and spread to other organs via blood-> organs that recieve large amounts of blood are most commonly affected eg. liver and lung

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17
Q

What is seeding of body cavities

A

Tumour will seed the walls of cavities (pleural and peritoneal) or cerebral ventricles-> ovarian cancer can occur this way

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18
Q

What is carcinoma-in-situ

A

Dysplastic changes across the whole width of the epithelium- can be reversed and does not necessarily progress to cancer- known as the state between benign and malignant

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19
Q

What is dysplasia

A

the loss in uniformity/ orientation of individual cells and occurs mainly in the epithelia
-cells show some degree of pleomorphism with an increase in mitosis

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20
Q

What is the suffix of benign tumours of mesenchymal tissue

A

‘oma’

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21
Q

What is a benign tumour in fibrous tissue

A

fibroma

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22
Q

benign tumor arising in fatty tissue

A

lipoma

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23
Q

benign tumor arising in cartilage

A

chondroma

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24
Q

benign tumor arising in smooth muscle

A

leiomyoma

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25
Q

What is the prefix for smooth muscle

A

leiomyo

26
Q

What do you call a benign epithelial neoplasm looking like a gland/derived from a gland

A

Adenoma

27
Q

What do you call a benign epithelial neoplasm with finger like growths

A

Papilloma

28
Q

What suffix does a malignant tumor of mesenchymal tissue have

A

sarcoma

29
Q

What suffix does a malignant tumor of epithelial origin have

A

carcinoma

30
Q

What do you call a malignant tumour of fibrous tissue

A

fibrosarcoma

31
Q

What do you call a malignant tumour of squamous cell

A

squamous cell carcinoma

32
Q

What are the 5 exceptions to nomenclature in cancer naming

A 
Melanoma- should be melanocarcinoma
Lymphoma- lymphosarcoma
Leukemia
Seminoma
Teratoma
33
Q

What is a polypous growth pattern

A

a polyp attached to via a stalk

34
Q

What is a papillary growth pattern

A

rounded finger-like protuberances

35
Q

What is a nodular growth pattern

A

rounded lump or ‘node’

36
Q

What is a lobulated growth pattern

A

distinct such parts divided by a fissure

37
Q

What is a multicystic growth pattern

A

distinct independent growths

38
Q

What is a infiltrating growth pattern

A

spreading or invading through tissues

39
Q

What is a ulcerated growth pattern

A

exposing underlying tissue layers

40
Q

What is carcinogenesis

A

a clonal expansion of a single progenitor cell that has incurred genetic damage

41
Q

What are the 4 main classes of genes involved in carcinogenesis

A
  1. growth-promoting proto-oncogenes
  2. growth-inhibiting tumor suppressor genes
  3. genes that regulate apoptosis
  4. genes involved in DNA repair
42
Q

What are the 4 stages of the cell cycle

A

G1- growth 1
S- synthesis
G2- growth 2
M- mitosis

43
Q

What regulates the progression of the cell cycle

A

Cyclin binding to cyclin-dependent kinases (CDKs) and phosphorylating and activating other downstream kinases

44
Q

What is a proto-oncogene

A

normal cellular genes that promote autonomous cell growth when expressed

45
Q

What are some of the functions of proto-oncogenes

A

Regulating growth factors, growth factor receptors, signal transduction proteins, cell cycle and apoptotic proteins and nuclear transcription factors

46
Q

What is an oncogene- does it cause a loss or gain of function mutation

A

oncogenes are mutated/overexpressed proto-oncongene-> only requires mutation of one allele to have a ‘gain of function’ mutation
-oncogenes cause cells to become constitutively active

47
Q

What is the most frequently mutated proto-oncogene

A

RAS
-in healthy cells RAS becomes activated by a growth factor which results in cell cycle progression→ when RAS is mutated it causes the protein to be permanently activated resulting in constant activation of the pathway and entry into cell cycle

48
Q

What is the function of TP53

A

TP53-> in normal cells activation of transcription factor p53 will act as a sensor to detect any damage, if damage is detected it activates cell cycle arrest and induces apoptosis through→ inducing the expression of cell cycle inhibitors to prevent proliferation of a cell until damage is repaired

49
Q

What is a tumour suppressor gene

A

Common functions of tumour suppressor genes: DNA damage repair, protein degradation, cell cycle regulation, apoptosis, cell adhesion, cell signalling

50
Q

Is a mutation to a tumour suppressor gene a gain or loss of function mutation

A
  • Loss of function- normally prevent uncontrolled growth though when mutated allows transformed phenotype to develop and grow
  • usually both alleles need to be mutated
51
Q

What are 4 types of main DNA repair mechanisms

A

mismatch repair, base and nucleotide excision repair, repair of depurinated sites and repair of double-strand breaks

52
Q

What is the function of Rb gene (tumour suppressor gene)- what happens when it is mutated

A

normal retinoblastoma gene product (Rb protein) binds DNA and controls the cell cycle at the transition from the G1 to the S phase→
alteration in the RB1 gene located on the Q arm of chromosome 13 results in rare cancer retinoblastoma

53
Q

What is the multistep theory of cancer progression

A

tumour progression requires accumulation of multiple genetic alterations

(ie. knudsons two hit hypothesis in retinoblastoma)
- this can explain why old age is a significant risk factor for cancer

54
Q

What type of mutational events are commonly associated with proto-oncogenes

A

translocations between chromosomes, deletions on chromosomes and gene amplifications, epigenetics, microRNA (proto-oncogenes turning into oncogenes is by amplification)

55
Q

What are the top 3 causes of cancer

A
  1. chemicals
  2. ionizing radiation
  3. microbes
56
Q

How doe microbes cause cancer (HPV)

A

contain viral oncogenes in their genomes that are derived from cellular proto-oncogenes-> HPV produces E6/E7 oncoproteins→ bind to Rb and p53 and neutralise their function

57
Q

How does ionizing radiation cause cancer (X-ray and UV)

A
  • X-rays and radioactive radiation tend to induce DNA double-strand breaks
  • UV radiation results in the formation of pyrimidine dimers, by cross-linking of adjacent pyrimidine bases
58
Q

How do chemicals cause cancer

A

-alkylation or deamination of DNA bases, or through intercalation between base pairs and formation of DNA adducts (e.g. aromatic hydrocarbons); oxidative damage may also affect DNA integrity–> tobacco causes cancer through these mutations

59
Q

What happens if you delete an miRNA

A

miRNAs are small, non-coding, single-stranded RNAs that incorporated into silencing complexes and can mediate post-transcriptional gene silencing→ deletions of miRNA sequences can increase oncogene expression, while overactivity can inhibit tumor suppressor gene function

60
Q

What is retinoblastoma- what are the two forms it comes in

A

Rare cancer due to a mutated Rb gene- that affects the retina
Familial form; Rb gene has been mutated in one allele, causes high predisposition and only requires one more hit for formation of Rb
Sporadic form; 2 random mutations/hits are acquired

TIN (14 decks)

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