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CNUR 803 > Chapter 10 Biology of Cancer > Flashcards

Chapter 10 Biology of Cancer Flashcards

1
Q

What is Cancer disesases

A

A group of diseases each driven by unique genetic and epigenetic alterations

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2
Q

What is a turmor

A

Abnormal growth resulting from uncontrolled proliferation

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3
Q

Benign vs Malignant Cancer

A

Benign : Grows slowly, well-defined capsule, not incase, well differentiated does not metastasize
Malignant tumour
Grow rapidly, not encapsulated, invade, poorly differentiated, high mitotic index, metastasize

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4
Q

How are benign tumours named?

A

Benign tissues are named from where they arrive and they include the suffix -oma

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5
Q

How are malignant tumours name?

A

They are named from where they arise

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6
Q

Carcionoma origns

A

Epithelial tissueA

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7
Q

Adenocarcinoma orignins

A

Ductal or glandular tissue

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8
Q

Sarcoma origins

A

Mesnchymal tissue

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9
Q

Lymphoma origins

A

Lymphatic tissue

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10
Q

Leukemia

A

Blood forming cells

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11
Q

What is anaplasia

A

The loss of cellular differentiation

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12
Q

What is a pleomorphic cell

A

It is a cell with marked variability in size and shape

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13
Q

Carcinoma in situ

A

Carcinoma that has not yet moved

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14
Q

Cancer hallmarks include

A

Resisting cell death
sustained proliferative signalling
evading growth supressor, genomic instability
metastasis

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15
Q

Enabling traits of Cancer

A

angiogenesis and reprogramming energy metabolism

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16
Q

Stages of Cancers

A

Genetic mutations an microenvironental factors that transforms cells to cancers cells
Cancer cells expand mutates and diversify getting new function that promotes growth
3. Cancer spreads

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17
Q

Characteristics of Cancer

A

Cancer arise from multiple genetic mutations tumours and made up of both cancerous and non cancerous cells

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18
Q

Genetic changes in cancer

A

Can be small or large scale, epigenetic play a role, driver mutation propel cancer groeth

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19
Q

How does cancer cell evolve

A

Cancer cells undergo a process of clonal expansion gaining a survival advantage

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20
Q

ow does cancer cells interact with the invorment

A

They interact with surrounding stromal cells immune caells and other components creating a supportive environment that prevents cancer treament

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21
Q

Protogenesis

A

Normal genes that direct protein synthesis and cellular growth

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22
Q

What causes proliferative signals

A

Growth factos

23
Q

Oncongenes

A

Mutant genes that stimulate growth

24
Q

Tumor suppresor genes,

A

When cancer cells secreates the other growth factorsO

25
Q

Oncogene activation

A

Point mutation in RAS gene converts from regulated to unregulated growth

26
Q

Tumour suppression genes are

A

Anti oncogeners gene

27
Q

Because inactivation of tumour suppressor genes requires at least 2 mutations (finish sentence)

A

A single germ cell mutation results in the transmission of cancer caseing gene from one generation to the next

28
Q

What do caretake genes do

A

They encode for proteins that are involved in repairing DNA Damage

29
Q

Genomic instability can lead to

A

Silencing or modulation of gene function

30
Q

What is cancer cell life span

A

Immortal

31
Q

What are telomeres

A

Protective caps on each chromosome that eventually tell cells to stop divinding

32
Q

Over time does telomeres grow larger or small in normal physiologt

A

Smaller

33
Q

What is vgef

A

Secreted by chancers to promote growth of cancer

34
Q

What is waburg effect

A

Uses glycoside during normal breathing conditions allows products of glycoside to be used for rapid cell growth and activated by oncogenes

35
Q

Apoptosis regulation is important in

A

cancer survival by regaining ability to complete apoptosis that promotes the ability to fight cancers

36
Q

Relationship between cancer and inflammation

A

Inflammation increases chances of cancer

37
Q

Parenoplastic syndroms

A

Triggered by cancer but not caused by direct local effects of tumour, can be the earlierest indicator of cancer, symptoms are non specific

38
Q

Cachexia

A

Includes anorexia, early safety, weight loss, anemia, taste alteraitnos, altered protein lipid are carbohydrate metabolism

39
Q

Stages of Metatstasis

A

Stage 1 No metastasis
Stage 2 Local invasion
Stage 3 Spread to regional structures
Stage 4 Distant metastasis

40
Q

Describe what the TNM syssten stand for

A

T - Primary tumor size and extent
N for node involvement
M for extent of distant metastasis

41
Q

T - Tumor size variations

A

T1 - 0-2 CM
T2 2-5 CM
T3- >5 CM
T4 - Tumor has broken through skin or attached to chest wall

42
Q

N - Variations of lymph node status

A

N0- Surgeon can’t feel any nodes
N1 Surgeon can feel swollen nodes
N2 Nodes feel swollen and lumpy
N3 Seollen nodes located near collarbone

43
Q

M- Metastasis Variation

A

M0- Tested nodes are cancer-free
M-1 Tested nodes show cancer cells or micro metastasis

44
Q

Why is a neoplasm

A

A new growth

45
Q

Mutations in (proto-oncogenes, oncogenes) that converts them to (oncogenes, prontooncogenes) drive the develpoment of cancer by causing uncontrolled cell growth

A

Proto oncogenes
Oncogenes

46
Q

Progression form a benign polyp to a malignant tumor requires how many mutations 1,2, or multiple

A

multiples

47
Q

The normal (oncogene, protonconges) was becomes the (oncogenes, protooncogens) was when a mutation makes the RAS protein active all the time

A

Proto oncogenes
oncogenes

48
Q

Malignant tumors in the colon most commonly metasize to the

A

Liver

49
Q

In the presence of oxygen normal cells metabolsze glucose by

A

Oxidative phosphylorization

50
Q

Cancer cells metabolizes glucose byq

A

Glycolysis

51
Q

For a cell to become cancerous (simultaneous, stepwise mutations must occur in its (genes, enzymes)

A

Stepwise, genes

52
Q

(Acute, chronic) inflammation predisposes to development of cancer

A

Chronic

53
Q

The TNM system is used to (grade, stage) cancer

A

Stage

CNUR 803 (12 decks)

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