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MBBS > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

name the four characteristics of neoplasia

A

abnormal mass of tissue,

growth exceeds that of normal tissue, uncoordinated with normal tissue

persists in the same excessive manner after cessation of the stimuli which evoked the change.

irreversible.

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2
Q

Cancer formation?

A

Mutations of genes in cell cycle checkpoints: cause UNCONTROLLED cell proliferation

cells pile on top of each other to form tumor

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3
Q

Name 5 neoplastic phenotypes

A

1.Loss of response to normal growth control mechanisms

2.Continued proliferation even without a recognizable stimulus

3.Loss of differentiation

4.Aberrant differentiation function

5.Expression of ‘embryonal’ characteristics

3, 4, 5 (especially for malignant neoplasm)

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4
Q

Compare benign and malignant neoplasms in terms of: ability of invasion and ability of metastasis

A

Benign: cannot invade nor metastasize

Malignant: can both invade and metastasize

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5
Q

Compare and contrast a benign and malignant neoplasm in terms of growth:

1) mode of growth and ability to invade beyond basement membrane

2) growth rate

A

1) Mode of growth
Benign: expansive, limited by basement membrane

Malignant: Infiltrative and expansive, invades beyond basement membrane

2) Growth rate
Benign: slow and may cease
Malignant: Fast, commonly outgrows blood supply (causing irregular necrosis)

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6
Q

Compare benign and malignant neoplasms in terms of morphology:

1) Gross appearance,
2) Degree of differentiation,
3) nuclear to cytoplasm ratio,
4) size and shape of cells
5) nuclear staining (chromaticity)
6) mitosis

A

1) Gross appearance:
Benign: circumscribed, encapsulated
Malignant: poorly defined margins

2) Degree of differentiation
Benign: Well differentiated, resembles tissue of origin
Malignant: varying degree of differentiation

3) Nuclear: cytoplasm ratio:
Benign: low nuclear to cytoplasm ratio
Malignant: High nuclear-to-cytoplasm ratio

4) size, shape of cells:
Benign: Cell regularly shaped
Malignant: Cellular pleomorphism (different variations in nuclear and cellular size, shape)

5) Nuclear staining:
Benign: normochromatic nuclei
Malignant: hyperchromatic nuclei (dark, irregularly shaped)

6) Mitosis
Benign: absent/scanty mitosis
Malignant: Increased/abnormal mitosis (tripolar/multipolar spindles)

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7
Q

Compare benign and malignant neoplasms in terms of:

architecture disturbance
polarity retention

A

Benign: Mild architectural disturbance, maintained polarity
Malignant: Severe architectural disturbance, loss of polarity

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8
Q

Compare benign and malignant neoplasms in terms of:

clinical effects
fatality

A

Clinical effects:
Benign: mechanical or hormonal
Malignant: mechanical or hormonal, destructive and systemic

fatality:
benign: rarely fatal
Malignant: usually fatal

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9
Q

What can metastasis of malignant neoplasm to lungs lead to

A

Cannonball lesion

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10
Q

How can malignant neoplasms invade beyond basement membrane

A

type IV collagen cleavage by type IV collagenase

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11
Q

Define differentiation of neoplasm

A

degree of morphological and functional similarity to origin tissue

neoplastic cells still retain epigenetic memory during growth

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12
Q

What architectural structures do benign neoplasms form

A

Papillary foldings (papillary lesions) or invaginating glands (to increae surface area)

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13
Q

Nomenclature of tumors check Kihiro notes

A
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14
Q

Most common type of malignant tumor?

A

Carcinoma

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15
Q

Tendencies of adenocarcinoma spread and malignant neoplasia of connective tissue?

A

Adenocarcinoma: lymphatic system
Malignant neoplasia of connective tissue: blood

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16
Q

Know that:
1) most benign tumors remain benign and never become malignant
2) malignant tumors often arise de novo without recognizable benign phase

3) other benign tumors can undergo progressive malignant transformations and become malignant

A
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17
Q

Define dysplasia:

A

Cells undergo changes similar to malignant ones (increasingly reluctant to differentiate + gain cytological features of malignant cells) BUT no evidence of invasion AND NO ACTUAL tumor mass formation

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18
Q

Grading system of dysplasia?

A

Mild, moderate, severe

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19
Q

Define carcinoma in situ

A

Dysplasia spanning entire thickness of surface epithelial membrane

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20
Q

Know that:
dysplasia increases risk of malignant tumor but can be REVERSIBLE in early stages

A
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21
Q

Borderline lesion definition

A

has ability to invade but NOT the ability to metastasize

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22
Q

difference between neoplasia and hyperplasia/ hypertrophy

A

neoplasia: uncoordinated, irreversible
hypertrophy/ hyperplasia: coordinated, reversible

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23
Q

examples of hypertrophy and hyperplasia

A

hypertrophy: hypertrophy of skeletal muscle in response to exercise
hyperplasia: uterine smooth muscle in response to pregnancy

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24
Q

Name 3 genetic drivers of cancer

A

Proto-oncogenes (when they become activated to oncogenes), tumor suppressor genes (when they become inactivated), DNA repair genes

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25
Q

Between proto-oncogenes and tumor suppressor genes which needs only 1 allele to be inactivated for the gene to be cancer-causing

A

proto-oncogene

tumor suppressor genes require BOTH alleles to be inactivated for cancer

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26
Q

Know that: when TS genes are INACTIVATED they cause cancers

when oncogenes are ACTIVATED they overstimulate cell proliferation and cause cancer

A
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27
Q

Proto-oncogene function

tumor suppressor gene function

DNA repair gene function

A

Proto-oncogene: Stimulate normal cell proliferation and differentiation

TS gene: control (like a brake) normal cell proliferation and differentiation

DNA repair gene: repair damaged DNA

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28
Q

1 example of a proto-oncogene and its action?

Action of mutant KRAS without growth factor?

what fraction of cancers in humans are caused by RAS genes

A

RAS gene

includes KRAS, HRAS, NRAS

when growth factor binds onto receptor KRAS binds to GTP and promotes cell division

mutant KRAS remains active and promotes cell division even without growth factor

1/3

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29
Q

Name genetic changes that can lead to conversion of proto-oncogene to oncogene:

A

1) promoter insertion
2) Mutation in coding sequences - hyperactive proteins produced in normal amounts
3) Gene amplification: overproduction of normal proteins
4) Chromosomal rearrangements:
nearby regulatory gene sequence: normal protein overproduced
Fusion to actively transcribed gene: hyperactive fusion protein

30
Q

Name some examples of tumor suppressor genes

A

p53, p21, Rb, BRCA1/2

31
Q

Name the type of mutation that inactivates tumor suppressor genes

and examples of the category of mutation

A

Homozygous mutations

deletion, truncating mutations, point mutations, promoter methylation

32
Q

Cancer related epigenetic modifications on tumor suppressor genes?

A

1) histone modification - alters chromatin structure, transcription factors cannot access gene

2) DNA methylation - silences the gene

33
Q

Know that: when DNA is damaged p53 protein is phosphorylated, stabilized and activated

then active p53 protein binds to regulatory region of p21 gene, p21 protein transcribed

p21 protein (CDK inhibitor protein) binds to G1/S-Cdk and S-Cdk to inactivate the cyclin-Cdk complex to prevent faulty DNA replication

acts as a checkpoint in cell cycle

A
34
Q

Impact of mutation in DNA repair genes?

A

Cell tends to acquire mutation in other genes and becomes cancerous

35
Q

Know that for the concepts of clonality and heterogeneity in malignant neoplasia:

1) Random DNA mutations may confer a growth advantage to certain cells, the cells with mutation outcompete other cells and become the DOMINANT clone

2) Further DNA mutations create more growth advantages, cells accumulating enough mutations to become malignant dominate the whole population

3) In malignant tumours, the malignant cells are usually clonal in origin but have developed heterogeneity (e.g. invasiveness, metastatic ability, response to treatment) to increase the fitness of the tumour

A
36
Q

Steps in process of tumor development?

A

1) MULTIPLE mutations in somatic stem cell genome
eg: Activation of oncogenes
- Mutations of cell cycle genes / apoptotic genes / DNA repair genes
- Inactivation of tumour suppressor genes

2) expression of altered gene products and loss of regulatory gene products

3) Clonal expansion of cells with selective growth advantages

4) Additional genetic alterations → tumour formation under selection pressure

5) Additional genetic alterations → increased genome instability → formation of malignant neoplasm

37
Q

Define: driver mutations and passenger mutations

A

Driver: gene mutations that DIRECTLY contribute to cancer development/progression

passenger gene: incidental mutations, do not confer growth advantages to mutated cells

38
Q

Multi-step tumor development model?

A

stepwise molecular changes and morphological changes during malignant transformation

Mutations accumulate (in all 3 of: oncogenes, TSGs and mutator genes) that lead to tumorigenesis

39
Q

Know that: multistep tumor model is considered to be OVERSIMPLIFIED

We also need to account for heterogeneity in tumors - explained by the clonal evolution and CSC models (BOTH MODELS ARE NOT MUTUALLY EXCLUSIVE)

A
40
Q

Causes of heterogeneity in tumor cells:

A

Genetic mutations, epigenetic changes

Microenvironmental changes, eg: nutrient, oxygen levels, immune responses, ECM, signals for survival, proliferation, epithelial-mesenchymal transition (EMT involved in metastasis)

41
Q

Clonal evolutional model?

A

From the cancer founder cell gives multiple subclones (linear or branched evolution both possible BUT branched evolution is much more likely - branched evolution explains heterogeneity)

Tumor cell subclones compete for survival

microenvironment exerts selective pressure on cancer cells

42
Q

Hierarchical model: tumors arise from cancer stem cells (CSCs) - the origin of CSCs?

KNOW THAT: CSCs drive tumor growth, recurrence, and treatment resistance (SPECIFICALLY CSCs)

for clonal evolutional model can be any cell that generates a tumor

A

Mutated adult stem cells, progenitor cells, or differentiated cells (through epigenetic rejuvenation)

43
Q

Know that:

1) CSCs have ability to self-renew and give rise to different cell types in tumor (thus heterogeneity)

2) can undergo symmetric division (produce 2 CSCs) or asymmetric division (1 progenitor cell, 1 CSC)

3) progenitor cells can further differentiate into mature cells OR become new type of CSC

4) subclones need to compete for survival advantages

5) CSCs reside in their own niche to sustain their stemness

6) Can resist conventional therapies by hiding in quiescent state or slow-cycling states

A
44
Q

Compare CSC model and the clonal model in terms of:

1) frequency of cells with tumorigenic potential:
CSC: rare/moderate
Clonal: high

2) ability to seed tumors in different locations
CSC: only CSCs can seed tumors
Clonal: ALL tumor cells

3) phenotype of cancer cells:
CSC: MUST be heterogenic
Clonal: homogeneous or heterogeneous

4) tumor organization:
CSC: MUST be hierarchical (stem cells > progenitor > terminally differentiated cells)
Clonal: not necessarily hierarchical

A
45
Q

hallmarks of cancer, their effects and their relevance to therapy:

Know that when a tumor becomes malignant ALL hallmarks are usually expressed

Hallmarks include:

A

Deregulating cell energetics,

sustaining proliferative signalling,

evading growth suppressors,

avoiding immune destruction,

enabling replicative immortality,

Tumor-promoting inflammation,

Activating invasion and metastasis,

inducing angiogenesis,

genome instability and mutation,

resisting cell death

46
Q

Know some drugs that target each hallmark:

Deregulating cell energetics - treated by aerobic glycolysis inhibitors

Sustained proliferative signaling - treated by EGFR inhibitors

Growth suppressor evasion - treated by CDK inhibitors

avoidance of immune destruction - treated by immune-activating anti-CTLA4 mAb

enabling of replicative immortality - treated by telomerase inhibitors

tumor-promoting inflammation - treated by selective anti-inflammatory drugs

activation of invasion and metastasis - treated by HGF/c-Met inhibitors

Induce angiogenesis - treated by VEGF signalling inhibitors

Genome instability/mutation - treated by PARP inhibitors

Cell death resistant - treated by Proapoptotic BH3 mimetics

A
47
Q

Know factors of carcinogenesis and methods of carcinogenesis:

List out some causes/factors of carcinogenesis:

A

Age,

gender

environmental factors (chemical carcinogens, radiation, viruses),

Hereditary neoplasia (genetic risk)

Ethnic associations

Other factors eg hormones, chronic irritation/trauma, immunological defects

48
Q

On age as a factor in carcinogenesis: name the most common types of tumors in children and adults

A

Adults: carcinoma

children: leukemia/lymphoma (more common), CNS tumors

49
Q

Name the most common types of cancers by gender

A

Male: colorectum, lung, prostate, liver stomach

female: breast, colorectum, lung, corpus uteri, thyroid

50
Q

Know some examples of chemical carcinogens:
Alkylating agents, aromatic hydrocarbons/amines, asbestos, chloroethene, arsenical compounds, soot

Know that they need prolonged exposure for carcinogenesis and have long latent period

Susceptibility highly variable between individuals

Can be directly carcinogenic or indirect (eg need metabolic activation)

QUESTION: define initiating agents and promoting agents

A

Initiating: cause irreversible damage to DNA in isolated cells to form adducts, electrophilic

Promoting: do not cause DNA alteration but promote cell proliferation in initiated cells

51
Q

Radiation: know that it damages DNA by linear energy transfer (UV weaker, gamma stronger)

can lead to leukemia, osteogenic sarcoma in atomic bomb survivors and radiotherapy patients

A
52
Q

Virus causing cancer: what is the mechanism

A

Viral oncoproteins bind to + modify functions of growth-modulating cellular proteins

Further mutations on top of viral oncoprotein binding needed to cause cancer

53
Q

Know that: for viruses causing cancer viral DNA is found in cancerous cells, BUT the site of viral integration is variable and mutant cells show CLONAL expansion

A
54
Q

Name some examples of cancer-causing viruses and the viruses they cause

A

HPV: cervical/oropharyngeal/anal cancer (know that vaccine is available)

Epstein Barr virus: nasopharyngeal carcinoma/Burkitt lymphoma

Hepatitis B virus: hepatocellular carcinoma

55
Q

Hepatitis B virus mechanism that increases cancer risk?

A

Hep B virus increases risk of hepatocellular carcinoma because:

1) HBV induces chronic injury, increases cellular proliferation

2) viral HBx protein may activate host proto-oncogenes and protein kinase C > cause cancer

BUT KNOW THAT VACCINE AND ANTIVIRAL TREATMENT IS AVAILABLE

56
Q

Causes of hereditary neoplasia?

A

inheritance of defective TSGs

patients have early cancer onset and can develop multiple cancers, higher chance of 2nd-hit inactivation of TSGs during lifetime

may also have familial cancer clustering

57
Q

Know some forms of hereditary neoplasia:

1) Familial adenomatous polyposis (FAP)

2) Lynch syndrome

3) BRCA1 and BRCA2 associated hereditary breast and ovarian cancer

4) Xeroderma pigmentosum

A
58
Q

FAP: Inheritance pattern?

Know that: there is germline inactivation of APC gene in chromosome 5 - so there is increased risk of 2nd inactivation as there is inheritance of 1 inactivated APC gene

Hundreds of adenomas form starting from 2nd to 3rd decades of life (bc of 2nd inactivation)

if untreated leads to colon carcinoma by 4th decade of life

A

Autosomal dominant

59
Q

Lynch syndrome: inheritance pattern?

Know that:

Microsatellites in patients (small DNA repeat sequence in coding regions of important growth proteins, eg TGFβRII) are error-prone in replication > frameshift mutation > cannot synthesize intact protein

Patients carry defective MLH1 gene (DNA mismatch repair gene) - in heterozygous carriers 2nd inactivation makes patients unable to repair DNA replication errors

Predisposed to colon, endometrium, urinary tract cancer from young age

A

Autosomal dominant

60
Q

How to diagnose Lynch syndrome:

A

1) Measure satellite length (displacement/unequal lengths of cancer and normal bands implies microsatellite instability)

2) DNA sequencing (c.1452-1455delAATG in MSH2)

61
Q

BRCA1 and 2: the type of cancer? Inheritance pattern?

A

Breast and ovarian cancer, autosomal dominant

62
Q

Xeroderma pigmentosum: inheritance pattern?

Causes inability to repair UV-damaged skin when both alleles inactivated

high risk of cancer in sun-exposed skin

A

Autosomal recessive

63
Q

Know that: Southern Chinese people associated with nasopharyngeal carcinoma, Japanese with stomach cancer

High estrogen levels associated with endometrial, breast carcinoma
High androgen levels associated with prostatic carcinoma

A
64
Q

Know intrinsic and extrinsic factors affecting tumor growth:

Intrinsic: cell proliferation rate/death/maturation and stop of division

Extrinsic: host immune response, adequacy of blood supply, availability of hormonal and growth factors

A
65
Q

Routes of tumor spread:

A

1) Local invasion

2) metastasis: by lymphatic, by blood (haematogenous), transcoelomic, pagetoid spread

3) perineural spread

66
Q

Lymphatic spread: The route?

A

Tumor spread from primary organs to regional lymph nodes then to central lymph nodes

Know that when the tumor reaches central lymph nodes it is harder to treat

67
Q

Haematogenous spread: the route?

A

1) subclone invades beyond basement membrane and passes thru ECM

2) metastatic cells undergo intravasation and reach destination

3) metastatic cells adhere to basement membrane of destination tissues, undergo extravasation to form micrometastasis (deposit)

4) angiogenesis leads to full blown metastasis (Tumor growth)

68
Q

Know some haematogenous spread examples:

systemic venous system to lungs: osteosarcoma

Portal venous system to liver: adenocarcinoma of colon

also know that very few cells escaping from a 1st tumor can form a stable metastasis

A
69
Q

Transcoelomic spread through where or where?

A

pleural or peritoneal cavity

70
Q

Pagetoid spread:

Know that it is a kind of intra-epithelial spread

Individual glandular cells may grow into a layer of stratified squamous epithelium

eg in adenocarcinoma of breast

A
71
Q

Know about the staging system: derived from route of spread for each cancer type

elements:

1) T: extent of local invasion
2) N: extent of lymph node metastasis
3) extent of distant metastasis

informs: 1) extent of surgical resection, 2) need for additional local/systemic therapies and 3) chance of recurrence and prognosis

A

MBBS (19 decks)

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