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POM > Introduction to Tumour Biology > Flashcards

Introduction to Tumour Biology Flashcards

1
Q

Differentiation in the Embryo

A

Early cells identical
Cells become different from one another
-ectoderm, mesoderm, endoderm
Cells also differentiate within each layer

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2
Q

Post embryonic Differentiation

A

Occurs at the level of cells rather than whole tissues
Maturation of Differentiated cells from (basal) Proliferating cells
-mitotic activity gradually migrating to surface, differentiating as they move up producing keratin, forming flakey layer and terminating proliferation genes

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3
Q

Differentiation involves:

A

Inactivation fo Proliferation genes

-Activation of specific Function genes

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4
Q

De-differentiation involves:

A

Involves reversion to Primitive, embryonic, proliferative phenotype as occurs in neoplasia
-when things go wrong
-not the mature cells,
-is more the proliferating cells, instead of maturating, continue proliferating and forming abnormal tissues that are incompletely differentiated and have excess proliferative activity
-“neoplasia” = new growth
“tumour”= swelling

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5
Q

Disorders of Growth

A

Disorders in the regulation of cell proliferation or differentiation

  1. Embryo - malformation
  2. Post-natal
    - Abnormalities of Tissue function
    - Abnormalities of Tissue Mass
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6
Q

Malformations

A

Caused by abnormality in growth and development in utero

  • Haematoma= malformation of mature tissue
  • e.g. “haematoma” in brain - arterial venous malformation –> can lead to hemoorahge/rupture
  • Disorders in the regulation of cell proliferation or differentiation in the Embryo
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7
Q

Clinical Implications of disorders of Growth

A
  • Not all are “disorders” - some normal (physiological) (callus thickening of skin in epidermis on hands with manual labour/hyperplasia)
  • some have clinical consequences (ventricular hypertrophy –increased risk of myocardial infarct, decompensation and heart failure)
  • some are reversible (cell enviro- hormones, irritation) (if stimulus removed tissue will return to normal state)
  • others are irreversible (dysplasia, neoplasia- DNA change) (if cell divides changes are inherited by daughter cells)
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8
Q

Reduction in tissue mass

A

Agenesis/Aplasia: total absence
-e.g. one kidney doesnt develop
Hypoplasia: Congenital Reduction in size
-one kidney smaller than normal due to small number of callusies
Atrophy: Acquired reduction in size
-kidney w. poor blood supply due to atheromic plaque in renal artery –> shrinked/hypoplastic kidney (normal number of calluses)
-muscle in cast, less use, leads to atrophy

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9
Q

Change in Myocardium

A

all same magnification as nucleus size is the same
Atrophy: elderly or malnourished people. brown pigmenting
Hypertrophy: increased size of heart due to increase in size of heart muscle fibres. due to increased strain. e.g. due to increased systemic BP (hypertension)/ malfunctioning of valves in heart –> increased tendency to myocardial infarct –> dilation and failure
-Left Ventricular Hypertrophy
–> dilation
–> failure

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10
Q

Hypertrophy and Hyperplasia

A 
Not neoplasia
Hypertrophy=increased growth
-organ and cells
-e.g. only one kidney so enlarged
-no relationship to cancer
Hyperplasia= increased number of cells
-relationship to cancer
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11
Q

Hyperplasia

A

Some examples are Premalignant (statistical/hyperplasia of uterus endometrium, rate of carcinoma of endometrium, discover risk)
Causes:
-“Functional” (Physiological) (thickening of epidremis in hands)
-Endocrine Stimulation (ovarian tumour produce estrogen causing hyperplasia (premalignant))
-Chronic Stimulation (ulcers thickening on edge)
Effects:
-Increased function (endocrine) (thyroid)
-Risk of Malignancy (some types)

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12
Q

Prostatic hyperplasia/Hypertrophy

A

Hyperplasia + Atrophy
Small Transition state of Prostate enlargens considerably
-hypertrophic/hyperplastic prostate
-hyperplasia increase in cell number occurs only in that cell
–not assoc. w increased carcinoma rate
–common but cancer risk is no larger compared to those with normal prostate
-simultaneously outer zone undergoes atrophy (thin epithelium lining glands)

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13
Q

Hyperplasia- Thyroid

A

Grave’s Disease= abnormal antibody
=autoimmune disease
TSH receptor= self
Hyperplastic
-stimulation of TSH receptor by autoantibody
-would do same if had tumour of pituitary to produce TSH
-same in Adrenal gland ACh inappropriately secreted –> hyperplasia of adrenal cortex
-histology: proliferation, cells chew up colloid , making into thyroid hormone –> hyperthyroidism
- density increases + gland expands
-gland becomes a visible palpable mass in the neck
= doesn’t predispose to malignancy

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14
Q

Which Hypertrophy/Hyperplasias result in predisposition of Malignancy?

A

Breast Hyperplastic changes
-accompanied by cystic change
-Endometrial changes in Uterus
=increased chance of cancer of those organs

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15
Q

Metaplasia

A

Some examples PRe Malignant
Change from one mature tissue type to another
Bronchus: normally only squamous as far as larynx, then respiratory epithelium in trachea/bronchus (which contain cilia)
-Smokers= irritation changes epithelium to squamous epithelium of throat/larynx
=premalignant change
=has to undergo additional change to undergo dysplasia - manifestation of premalignant features

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16
Q

Cervical metaplasia

A

Squamous metaplasia is normal
Endocervix (canal)= columnar epithelium
Squamous metaplasia
Ectocervix (vaginal) squamous epithelium
-occurs in every girl
-maturing to menarche, uterus grows and cervix changes in shape
-exposes thin glandular layer, upon exposure to different vaginal environment (from canal) changes to squamous epithelium
-can all look like vaginal ectocervical squamous epithelium - non keratinising squamous epithelium
-occurring in response to a stimulus

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17
Q

Metaplasia

A

Some types Premalignant
Cause: due to change of environment or irritation
-noxious change cigarette smoke in trachea/bronchi
May be normal (cervix)
-reflux in oesophagus (becomes gastric epithelium) Barrets oesophagus= premalignant = consistently cheked for dysplasia or malignancy devel.
Most common in epithelial tissues
Usually change to that of adjacent tissue type (protection for dif. stimulus/enviro)
-CT metaplasia - fribrous –> cartilagneous/boney (usually due to irritation/abnormality)
Some types are premalignant
-cancer type is same/ that of metaplastic epithelium
-squamous cell carcinoma in lung (from smoking)
metaplasia –> dysplasia –> carcinoma

18
Q

Dysplasia

A

ALL examples premlaignant (By definition)- increased chance of becoming cancer (not inevitable)
Histological Abnormality
Partial Malignant Transformation (histologically and genetically)
-nuclei enlarged and irregular
-structure disorganised
-less severe than cancer. and NOT invasive
-remains confined by epithelium and bound by BM of epithelium
May be macroscopically Evident (colon adenoma)
Various grades -mild. -moderate -severe (carcinoma in situ= “in place” in normal posiion not invaded)
Remains same mass/ Flat= cervix (smears)
-becomes more vascular
Adenoma of Colon= benign tumour = dysplastic increased mass

19
Q

Dysplasia and Cacner

A

Dysplastic cells are clonal (in fact, neoplastic)
-every cell has orginiated form one cell (esp. when becomes higher grade. Monoclonal/single clonal)
Alternative terminology -INTRAEPITHELIAL Neoplasia (IEN))
So for cervix:
-CIN1 (cervical intraepithelial neoplasia 1)
-CIN2
-CIN3 (carcinoma in situ)
Opportunity to remove tissues, prevent invasive cancer

20
Q

Clinical importance of Dysplasia

A

Can follow it and interrupt it
-not all will devleop to cancer (immune system defeats)
Opportunity to remove tissues, prevent invasive cancer
-cervical surgery w/o damaging uterus or compromising pregnancy , to prevent invasive cancer occuring

21
Q

Dysplasia Solar Keratosis

A

Solar Keratosis

  • Precursor of squamous cell carcinoma of skin
  • light skinned people from sun burn
  • proliferation, increased keratin produced, irregularity of cells
22
Q

Reactive Atypia

A

NOT malignant
Looks atypical like dysplasia, but is “Reacting to inflammatory or ulcerative stimulus”
Similar to dysplastic progression, even though may not be any genetic abnormality
-bladder uretherial cells enlarged, irregular, some inflammatory cells
-increased genetic activity, makes them show morphological (not genetic) features of dysplasia
-try and distinguish between dysplasia and reactive atypia
-if worried, do 2nd biopsy after inflammation has settled
Injury –> cell Loss –> Regeneration
a) If chronic –> Suspicious Microscopic Nuclear Changes
b) Proliferation “ Promotor effect” –> Real increased risk of cancer
-Inflammation can lead to increased chance of cancer developing (Ulcerative colitis). promotor effect. increased inflammation and proliferation.
If mutation or genetic abnormality occurs, since cells are rapidly turning over, cell division can fix abnormality before repair happens, upon accumulation of these cells, tumour can develop

23
Q

Dysplastic Mass

A

Adenoma of Large Intestine

-dysplasia + benign neoplasm

24
Q

Not Pre-Malignany

A 
Adenoma of Parathyroid
Lypoma in skin
-still monoclonal proliferations and genetic abnormalities
-but limited ability to cause disease
-Benign Neoplasm
25
Q

Flat dysplasia

A

CIS or cervix - which is also metaplasia

metaplastic epithelium can undergo dysplasia to become premalignant

26
Q

Where are there genetic abnormalities?

A

Cancer
Dysplasia
Benign NEoplasm

27
Q

Where are there No genetic abnormlities

A

Metaplasia

Hyperplasia

28
Q

Carcinoma in situ vs Invasive Carcinoma

A

Carcinoma In situ is still “in place” so hasnt invaded
-abnormal irregularly arranged epithelial cells that are larger than normal
Invasive C = additionally genetic changes have occurred= given tumour additional ability to proliferate and invade normal tissues to stimulate and angiogenic response and act like a carcinoma
=spikes of growth invading downwards
=balls of tumours inside lymphatic channels (possibility of spread)

29
Q

Benign Neoplasma

A

Grow slowely
Does Not Metastasize
Cells are differentiated
-similar to the normal tissue from where they have come
Expansile Growth
Rarely Fatal
-sometimes can if in strategic spot, obstruction of bile duct, infection which causes death

30
Q

Malignant Neoplasm

A

Most types metastasize
-some do damage locally
-carcinomas matastasize
Matastasis= discontinuous growth of the tumour. Moves along peritoneal cavity, vein, lymphatic vessel, lodges and grows
Cells less differentiated Infiltrative growth (tongues/spikes of tumour), rapid
Fatal if untreated

31
Q

Neoplasms and space

A

Not all neoplasms take up increased space
-leukemia clone proliferates in bone marrow
-displaces normal heamopoetic cells in bone marrow
but doesnt form tumour as such

32
Q

Tumour vs Neoplasm

A

Tumour =Mass

Closely related

33
Q

Advances related to identifying through Miscroscopy

A

cutting and staining tissues to be able to see inside tumours
-info gained from post mortem biopsy

34
Q

Structure of Solid Malignant Tumours

A

Majority
Interaction between normal cells and tumour cells
=Together called Tumour Stroma
1. tumour invasion
2. angiogenesis (occupy new space and need BV)
-oxygen limited nutrient for tumour growth. diffusion distance of 0.1mm)
3. desmoplasia
-fibrosis/fibrous tissue increase
-CT firboblasts of where tumour is gowring to produce excessive collagenous tissue
4. immune response
-large numbers of different immune cells

35
Q

Lymphomas

A

Space occupying examples of leukemia

36
Q

Tumour stroma

A

Everything in the tumour apart from the tumour cells
-Fibroblasts, collagen fibres and matrix
-New blood vessels
-Inflammatory cells
-may occupy vast majority of tumour than what the tumour cells do
Volume of tumour: more of fibrous tissue/desmoplastic stroma vs tumour cells themselves
Carcinoma of breast
Seminoma of testis

37
Q

Tumour cell hypoxia

A

Surrounding Tumour vessel (tumour vasculator)
-encourage BV growth from host –> tumour
-disorganised growth (shunts form) and hyflows through some regions of tumour (help to identify tumour (high blood flow useful in diagnosis))
-Viable tumour cells
–> Hypoxic tumour cells
=cells on the boundary of necrotic tissues, are resistant to some treatment
=Resistant to Radiation therapy which requires Oxygen for its full effects = sensitises tumour cells 3x to damage of radiation
=Chemotherapeutic agents dont work as well as further out are dividing slowly
=drugs with limited diffusion cant get out
=Reservoir of resistant tumours (try target hypoxic cells)
–> Necrotic Tumour cells (100 microns)
for some tumours, if necrosis is present can mean prognosis is worse

38
Q

What is required for a definite diagnosis of a mass being malignant?

A

Histological confirmation

-key to diagnosis and classification

39
Q

Patholgical Diagnosis

A

Specimen from mass
–> Inflammatory (swelling). Hyperplastic. Non-neoplastic Cyst (secretory gland blocked, secretion continues and space with fluid. e.g. ovarian neoplasm). Neoplastic?
Neoplastic –> Benign or Malignant (histological, surgery, scrape/cytology, urine)
–> Benign –> Type?
–> Malignant –> Stage? Type? Grade?

40
Q

Microscopic Diagnosis of Malignancy

A
  1. Architecture (tissue structure)
    -disorganised
    -invasion of normal tissues
  2. Cytology (cell features)
    -increased nuclear staining (DNA)
    -increase in nuclear size
    -variation in nuclear shape
    -mitoses
    -decreased cell cohesion
    Cytopathology= cytology (cell features)
    Histopathology= Architecture + Cytology
    -neoplastic invasion

POM (33 decks)

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