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2420A Pathology (Definitions) > Module 5 - Neoplasia > Flashcards

Module 5 - Neoplasia Flashcards

1
Q

What are the 5 cellular adaptations to stress?

A

1) Atrophy
2) Hypertrophy
3) Hyperplasia
4) Metaplasia
5) Dysplasia

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2
Q

Describe atrophy

  • Definition
  • Causes
  • What happens if it persists for too long? Example.
A

Atrophy:
- Decreased in size and function of a cell.

Causes:

  • Decreased workload.
  • Decreased blood supply.
  • Loss of innervation.
  • Interruption of trophic signal. - Aging.

If atrophy persists the cells may die
- E.g. Atrophy of thyroid following pituitary resection;
atrophy of muscles if nerve supply is cut off Atrophy of brain in aging.

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3
Q

Describe hypertrophy:

  • Definition
  • Causes / Examples
A

Hypertrophy: Increase in the size of a cell accompanied by an augmented functional capacity.

Causes:

  • Increased functional demand (E.g. Myocardial hypertrophy in hypertension - Muscle hypertrophy in athletes)
  • Physiologic (hormonal) hypertrophy (E.g. sex organs at puberty)
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4
Q

Describe hyperplasia:

  • Definition
  • Causes / Examples
A

Hyperplasia: Increase in the number of cells in an organ or tissue.

Causes:

  • Increased functional demand (E.g. increased number of RBCs in high altitude)
  • Hormonal stimulation (E.g. endometrium in early phase of menstrual cycle; prostate enlargement in elderly men (BPH))
  • Persistent cell injury (E.g. skin in calluses)
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5
Q

Describe metaplasia:

  • Definition
  • Example
  • Protective mechanism?
A

Metaplasia: Conversion or change of one differentiated cell type to another

E.g. conversion of bronchial ciliated columnar epithelium to squamous epithelium in smokers.

Although it is a protective mechanism, there may be loss of function.

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6
Q

Describe dysplasia:

  • Definition
  • Features
  • Significance
  • If persistent, leads to?
A

Dysplasia: Alteration in size, shape and organization of the cellular components of a tissue.

Features:

  • variation of shape and size of cells (cellularpleomorphism).
  • variation in nuclear shape and size (nuclear pleomorphism)
  • enlargement, irregularity and hyperchromatism of the nuclei.
  • disordered arrangement of the cell

Significance:
- Dysplasia is a pre-malignant (i.e., no invasion is present) lesion

If persistent, leads to:

  • dysplasia in bronchial epithelium.
  • dysplasia in cervical epithelium
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7
Q

How many new cases of cancer were there in 2019?

How many deaths from cancer were there in 2019?

A

220, 400

82, 100

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8
Q

How many Canadians will develop cancer in their life time?

How many will die from cancer?

A

1/2

1/4

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9
Q

What is the leading death in Canada? What percentage is it responsible for?

What is the second leading cause of death?

A

Cancer - 30%

Cardiovascular disease

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10
Q

What accounts for half of all new cancer cases diagnosed?

A
  • Lungs and bronchus (lung)
  • Breast
  • Colorectal and prostate cancer
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11
Q

What is the leading cause of cancer deaths?

What has improved?

A

Lung cancer
- Causes more cancer deaths among Canadians than the other three major cancer types combined

With investments in cancer control including prevention, early detection and treatment, the 5 year cancer survival rate has increased from about 55% in the 1990s to 63% in 2019.

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12
Q

How many men and women were diagnosed with cancer in 2019?

How many men and women will die of cancer?

A

113,000 men and 107,400 women

43,00 men and 39,000 women

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13
Q

What % of women and men will develop some for of cancer?

How many will die of cancer?

A

43% of women and 45% men

1/4 will die of cancer

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14
Q

What are half of all cancer deaths due to?

A
  • Lung
  • Breast
  • Prostate
  • Colorectal
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15
Q

What does neoplasia stand for?

A

Neoplasia = New growth = Tumour

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16
Q

What does oncology stand for?

A

Oncos = tumour; study of tumour

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17
Q

What does cancer mean?

A

Malignant neoplasm

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18
Q

What is a malignant tumour?

A

A tumour that invades and spreads to distant site

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19
Q

What is a benign tumour?

A

Tumor that does not invade or spread

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20
Q

Define neoplasm:

  • What are they composed of?

- How are they named?

A

Neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of normal tissue & persists in the same excessive manner after the cessation of the stimulus which evoked the change.

  • The neoplasms are composed of proliferating neoplastic cells and supporting stroma.
  • The neoplasms are named according to the type of tumor cells (indicating the tissue of origin) and nature of the tumor whether benign of malignant.
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21
Q

Define benign tumour:

  • Adenoma
  • Papilloma
  • Polyp
  • Exceptions
A

Benign Tumors: In general these tumors have suffix “oma” following tissue type. Majority are named by tissue type, some are named by architectural patterns

  • Adenoma: Benign tumor that forms gland or originating from glands.
  • Papilloma: Benign tumors with finger-like projections.
  • Polyp: Elevated mucosal lesions (descriptive term).

Exceptions: melanoma/lymphoma.

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22
Q

Define malignant tumour:

- Examples

A

A similar system as benign neoplasms is used. Malignant tumors composed of mesenchymal cells are called sarcoma (sar = fleshy). Malignant tumors composed of epithelial cells are called carcinoma

  • Adenocarcinoma is a malignant epithelial tumor with cells forming glandular growth pattern
  • Squamous cell carcinoma is a malignant epithelial tumor composed of squamous cells.
  • Fibrosarcoma is a malignant tumor composed of fibrous tissue
23
Q

Define:

  • Mixed tumour
  • Teratoma

Other terms:

  • Choristoma
  • Hamartoma
  • Cyst
A

Tumors may show divergent differentiation
- These are call mixed tumors; They can either be benign or malignant.

Teratoma: Consists of 2 or more germ layers arising from mesenchymal cells. Ovary & testis. Could either be benign or malignant.

Choristoma: Ectopic rest

Hamartoma: Disorganized normal tissue in normal location

Cyst: Fluid filled space

24
Q

What are the 5 characteristics of Benign and Malignant Neoplasms?

A

1) Differentiation & Anaplasia
2) Rate of Growth
3) Invasion
4) Metastasis

25
Q

What are the 5 characteristics of Benign and Malignant Neoplasms?

A

1) Differentiation & Anaplasia
2) Rate of Growth
3) Invasion
4) Metastasis

26
Q

Characteristics of Benign and Malignant Neoplasms:

Differentiation & Anaplasia

  • What is it?
  • Features
  • Functional Differentiation
A
  • Differentiation =Extent to which tumor cells resembles normal counterpart (morphologically & functionally).
  • well, moderately or poorly differentiated
  • benign tumors are well differentiated.
  • Lack of differentiation = Anaplasia [The term anaplasia is used with respect to an invasive (see below) neoplasm].

Features of Anaplastic (undifferentiated) cells:

  • Variable cell size & shape (cellular pleomorphism).
  • Variable nuclear size & shape (nuclear pleomorphism).
  • Hyperchromatic nuclei.
  • Increased mitosis and atypical mitosis.
  • Loss of polarity
  • Tumour giant cell.

Functional differentiation

  • correlate roughly with structural differentiation.
  • Poorly differentiated tumours are less functionally active e.g., Keratin production by squamous cell carcinoma; well differentiated endocrine tumours produce more hormones
27
Q

Characteristics of Benign and Malignant Neoplasms:

Rate of Growth

  • Benign vs. Malignant
  • Exception
  • Rate of growth
A
  • benign tumors are slow growing
  • malignant tumors are fast growing,

Exception:

  • Growth of leiomyoma during pregnancy
  • Rate of growth correlates with blood supply
  • Rate of growth inversely correlates with differentiation
  • Poorly differentiated tumors grow faster
28
Q

Characteristics of Benign and Malignant Neoplasms:

Invasion

  • Reliable feature of what
  • Do benign tumours invade? How do they grow?

How do most carcinomas begin?

What do malignant tumours do? How?

A

Next to metastasis, invasion is a reliable feature of malignancy.

  • Benign tumors are circumscribed and do not invade. They grow by expansion and show a rim of compressed stromal and connective tissue (capsule).
  • However the absence of a capsule is not always equivalent to malignancy (e.g. benign tumors such as hemangioma or dermatofibroma do not have capsules).
  • Most carcinomas begin as localized growth originating from a single cell (monoclonal origin) and are confined to the epithelium of their origin
  • As long as the basement membrane is intact, they are termed carcinoma in situ (severe dysplasia)

Malignant tumors invade and destroy the tissue. They secrete proteases to facilitate invasion.

29
Q

Characteristics of Benign and Malignant Neoplasms:

Metastasis

  • Definition
  • What is it a sign of?

Pathways

a) Seeding
b) Lymphatic Spread
c) Hematogenous Spread

A

Metastasis is defined as a tumor implant discontinuous from the primary tumor.
- Metastasis is an unequivocal sign of malignancy

Pathways of metastasis:

  • seeding via body cavities
  • lymphatic
  • hematogenous

a) Seeding via body cavities:
- peritoneal cavity - most common
- pericardial/pleural/subarachnoid cavities.
- E.g. ovarian carcinoma

b) Lymphatic Spread
- most common initial dissemination.
- follows natural drainage.

c) Hematogenous Spread
- favoured by sarcoma, but carcinomas also use it.
- liver and lung are frequent sites.

30
Q

Compare the following for benign and malignant tumours:

  • Differentiation/Anaplasia
  • Rate of Growth
  • Local Invasion
  • Metastasis
A
  1. Benign:

a) Differentiation/Anaplasia
- Well-differentiated; structure may be typical of tissue of origin

b) Rate of Growth
- Usually progressive & slow

c) Local Invasion
- Usually cohesive & expansile, well- demarcated masses that do not invade or infiltrate the surrounding normal tissues.

d) Metastasis
- Absent

  1. Malignant:

a) Differentiation/Anaplasia
- Some lack of differentiation with anaplasia

b) Rate of Growth
- Erratic and may be slow to rapid, mitotic figures may be numerous and abnormal

c) Local Invasion
- Locally invasive, infiltrating the surrounding normal tissues

d) Metastasis
- Frequently present

31
Q

What is the biology of tumour growth (4 steps)?

A

Natural history of malignant tumor consists of four phases

  1. Transformation → A normal cell changed to a malignant cell (carcinogenesis)
  2. Growth of transformed cell
  3. Local invasion
  4. Distant metastases
32
Q

Biology of Tumour Growth:

The Transformed Cells

  • What are they subject to?
  • What do they show?
A

Most human tumors are derived from a single transformed cell (monoclonal in origin).

The tumor cells may not be subject to normal growth and differentiation control - They show

  • self sufficiency in growth signal
  • insensitivity to growth-inhibitory signal
  • resistance to apoptosis
  • defective DNA repair
  • unrestricted proliferation
  • angiogenesis, invasion and metastasis
33
Q

Biology of Tumour Growth:

Tumor Growth
- Definition

Minimum size for clinically detectable tumour?

A

Time required for a tumor to double in volume or mass depends on:

  • growth fraction = # of cycling cells / # of total cells
  • cell loss factor
  • in tumors there is excess cell production over loss producing a rapid growth.
  • cells are lost due to apoptosis, ischemia and host defense mechanisms.
  • tumor cells go through cell cycle phases similar to normal cells
  • doubling time of tumor cells are similar to or sometimes more than normal counterpart
  • earlier majority of the cells are in the proliferative pool.
  • tumors with high growth fractions are susceptible to chemotherapy.

Minimum size for clinically detectable tumor is 1cm3 (1gm) which is equivalent to 108 to 109 cells. This translates to 30 doubling from a single cell not including the cell loss. Ten population doublings from this stage will lead to a tumor size of 1kg (lethal).

34
Q

Biology of Tumour Growth:

Tumor Angiogenesis

  • What is a major factor for tumour growth?
  • Factors
A

-Blood supply a major factor modifying tumor growth.

Angiogenic factors:

  • Produced by tumor cells
  • Produced by inflammatory cells infiltrating tumor. o
  • Chemotactic & mitogenic for endothelial cells.
  • Induce production of proteolytic enzyme.
  • E.g.: Fibroblast growth factors (FGFs), vascular endothelial growth factor (VEGF)
35
Q

Biology of Tumour Growth:

Tumor Progression & Heterogeneity
- What develops over time?

A
  • Over period of time tumors develop various subpopulation of cells.
  • The sub population may vary in antigenicity, invasiveness, metastatic potential, growth factor requirement, etc. The sub population “beat the odds” and survive.
36
Q

Biology of Tumour Growth:

Mechanism of Local & Distant Spread

  • What does it acquire as it grows?
  • Two phases?
A

As the tumor grows, certain subclones acquire more metastatic potential than others.

Two phases of metastasis are of importance, which are:

1) invasion of extracellular matrix.
2) vascular dissemination & homing of tumor cells.

37
Q

Biology of Tumour Growth:

Invasion of Extracellular Matrix

A

Cancer cells are less adherent to each other due to lack of cell adhesion molecules

  • They degrade basement membrane by secretion of proteolytic enzymes that dissolve matrix proteins, e.g., collagenase, cathepsin B (Benign tumors secrete little or no such enzymes.)
  • They attach to the basement membrane through laminin receptors and integrins
  • Tumor cells trigger production of cytokines, such as autocrine motility factors and cleavage products of matrix component
38
Q

Biology of Tumour Growth:

Vascular Dissemination & Homing (metastatic site) of Tumor Cells

A

Single or many tumor cells form emboli by aggregating with platelets & WBC. They form adhesion with endothelium and finally exit through basement membrane
- Site of metastasis may be predicted by vascular or lymphatic drainage

Metastasis may be related to:

  • presence or absence of endothelial adhesive molecules in some sites.
  • chemoattractant.
  • unfavourable environment (e.g.: skeletal muscle).
39
Q

What are the clinical features of a tumour?

A

1) Effect of Tumour on Host
- Local effects
- Hormonal effects
- Cancer Cachexia
- Paraneoplastic syndrome

2) Grading and Staging of Cancer
- Grading
- Staging

3) Lab Diagnosis of Cancer
- Tissues
- Sampling Methods
- Tissue processing
- FNAB
- Cytologic smear
- Cytology of Body Fluids
- Additional Techniques
- Biochemical tumour markers

40
Q

Clinical Features of Tumours

  1. Effect of Tumour on Host:
    a) Local Effects
    b) Hormonal Effects
    c) Cancer Cachexia
    d) Paraneoplastic Syndrome
  • Examples
A

a) Local effects:
Effects may be varied depending on location and infringement. Local effects are seen in both benign & malignant neoplasm.
- benign submucosal leiomyoma - bleeding.
- neoplasms (benign or malignant in gut) → obstruction.
- pituitary adenoma → expansile growths destruction of remaining gland.
- gastrointestinal tumors/urogenital tumors → bleeding
- ovarian tumors → torsion.

*Tumor may undergo infraction, rupture, ulceration and secondary infection.

b) Hormonal effects:
- β cell adenoma in pancreas → insulin → hypoglycemia, may be lethal.
- adrenal cortex adenoma → steroid → secondary effects.
- carcinoid tumor - hormones → carcinoid syndrome

c) Cancer Cachexia
- Definition: Progressive loss of fat & lean body mass with weakness, anorexia & anemia. Several factors may be responsible.
- reduced food intake - abnormalities of taste & central control.
- reduced synthesis & storage of fat, increased mobilization of fatty acids fromadipocytes.
- probable candidate tumor necrosis factor α (TNF ).

d) Paraneoplastic Syndrome:
- Definition: symptom complex in cancer bearing patients that cannot readily be explained, either by local or distant spread of the tumor or by the elaboration of the hormones indigenous to the tissue of origin.

Importance:

  • may be earliest manifestation of an occult neoplasm.
  • may cause significant even lethal clinical problem.
  • may mimic metastatic disease.
  • May produce:
  • endocrine symptoms
  • neurological symptoms
  • blood cell abnormalities
  • renal symptoms

For example Bronchogenic Carcinoma may cause:

  • Cushing’s Syndrome
  • Syndrome of inappropriate antidiuretic hormone secretion.
  • Hypercalcemia
  • Myesthesia
  • Acanthosis Nigricans
  • Hypertrophic osteoarthropathy
  • Venous thrombosis
41
Q

Clinical Features of Tumours

  1. Grading and Staging of Cancer
    a) Grading
    b) Staging
A

a) Grading is an estimate of aggressiveness of the neoplasm and based on the level of differentiation
- Variable criteria are used in various neoplasms.
- Commonly based on differentiation, mitosis, and
necrosis
- Commonly described as well, moderately or poorly differentiated tumors.

b) Staging is of greater clinical importance than grading
- Staging is based on tumor size, lymph node spread, and metastasis to other organs
- There is clinical and pathological staging
- Clinical staging is based on evidence acquired prior to the decision as to definitive treatment
- Pathological staging includes information obtained at surgery and from examination of tissues by the pathologists
- Staging is based on size of the primary lesion, extent of spread to regional lymph nodes, and the presence or absence of blood-borne metastases
- There are two major systems. The TNM (T-tumor, N-nodes, M- metastases) system was developed by the Union Internationale Centre Cancer (UICC)
- The system used by the American Joint Committee (AJC) on Cancer Staging divides tumors into stages O to IV
using factors similar to the TNM system

42
Q

Clinical Features of Tumours

  1. Lab Diagnosis of Cancer
    a) Tissues
    b) Sampling methods
    c) Tissue Processing
    d) Fine Needle Aspiration Biopsy
    e) Cytologic Smear
    f) Cytology of Body Fluids
    g) Additional Techniques
    h) Biochemical Tumour Markers
A

Clinical information is of great importance.

Without clinical information an incorrect diagnosis is easily reached

a) Tissues
- fresh
- formalin fixed
- other fixatives - gluteraldehyde
- fine needle aspirations
- cytology smear.

b) Sampling methods
- biopsy.
- excision.
- fine needle aspiration biopsy
- smear.
- body fluid.

c) Tissue Processing
- formalin fixative.
- dehydration in graded alcohol.
- xylene.
- paraffin embedding.
- sections cut & stained with hematoxylin & eosin

d) Fine Needle Aspiration Biopsy
- useful for palpable lesions.
- office procedure - thyroid, breast, salivary glands.
- deeper tissues (liver) - imaging guided.
- smear, cell blocks

e) Cytologic Smear
- cervical cancer detection.
- can be adapted for other lesion.

f) Cytology of Body Fluids
- pleural & peritoneal fluid.
- CSF.
- sputum
- urine.

g) Additional Techniques
- immunocytochemistry.
- electron microscopy.
- flow cytometric analysis; marker, DNA ploidy
- molecular diagnosis
- cytogenetics.

h) Biochemical Tumour Markers
- PSA (prostate specific antigens); prostatic adenocarcinoma
- They are not diagnostic as they may be elevated in inflammatory conditions
- Used in screening.

43
Q

What are the two aspects of carcinogens?

A

1) Predisposing factors

2) Carcinogenesis

44
Q

Carcinogenesis

1) Predisposing Factors
a. Geographic Factors
b. Environmental Influence
c. Age
d. Hereditary
e. Acquired preneoplastic conditions

A

a. Geographic Factors
- age adjusted death rate for breast cancer: US - 27, England - 36, & Japan -7.
- stomach cancer - 7 times higher in Japan than US
- hepatocellular carcinoma  infrequent in US, some African populations #1 lethal cancer

b. Environmental Influence
- smoking
- sunlight

c. Age
- in general increases with age
- Peak 55-75 yrs

Exceptions:

  • sarcomas younger age group (osteosarcoma)
  • childhood cancers: occurs exclusively in children; neuroblastomas, Wilms tumor (kidney), retinoblastoma

d. Hereditary: There is definite hereditary predisposition
i) Inherited Cancer Syndromes (autosomal dominant)
- MEN (Multiple Endocrine Neoplasia)
ii) Familial Cancers:
- shows clustering but hereditary predisposition in individual cases is notclear. e.g. breast/colon/ovary.
iii) Hereditary Preneoplastic Conditions
- DNA repair defect (autosomal recessive). e.g. xeroderma pigmentosa

e. Acquired Preneoplastic Conditions
- Barrett’s esophagus (intestinal metaplasia) -> adenocarcinoma

45
Q

Carcinogenesis

  1. Carcinogenesis
    - What is it?
    - Agents?

a) Chemical Carcinogens
b) Radiation Carcinogenesis
c) Viral Oncogenesis
d) Bacterial Infection

A

Cancer is a genetic disease. The genetic damage can be caused by chemicals, biological or physical agents.

Carcinogenic agents causing genetic damage may be:

  • chemicals.
  • physical agents such as radiation.
  • oncogenic virus.
  • bacteria.

a) Chemical Carcinogens
- Diverse natural & synthetic products are of importance. - They may be direct acting or indirect acting (following conversion in the body) from pre-carcinogens to carcinogens in the body.
- They are highly reactive molecules which reacts with RNA or DNA or proteins. Several chemical carcinogens may act together or along with other virus or radiation

b) Radiation Carcinogenesis:
- Radiant energy, whether in the form of ultraviolet (UV) rays of sunlight or as ionizing electromagnetic and particulate radiation can transform virtually all cell types
- Acts by DNA damage via direct ionization of cellular macromolecules or indirectly by generating free radicals and damage to critical molecules.
E.g:
- UV rays – squamous cell carcinoma
- Ionizing radiation – leukemia

c) Viral Oncogenesis:
- A large number of viruses have proved to be oncogenic in animals
- Only few have been linked with human cancer.
- Oncogenic viruses fall into two classes:
i) DNA Oncogenic Viruses:
- HPV (Human papilloma virus)
- More than 50 subtypes have been identified. Types 16, 18, 31 are associated with
cervical cancer.
- EBV (Epstein-Barr virus): Nasopharyngeal Ca; Burkitt’s lymphoma
- HBV (hepatitis B virus): Hepatocellular Ca
ii) RNA Oncogenic Viruses: Human T-cell leukemia virus (HTLV-1) - human T cell leukemia/lymphoma.

d) Bacterial Infection:
- H. pylori infection is associated with B cell lymphoma in the Mucosa Association Lymphatic Tissues (MALToma).

46
Q

What are the 8 mechanisms of carcinogens?

A
  1. Genetic Change in Tumors
  2. Oncogenes and Cancer
  3. Tumor Suppressor Genes
  4. Apoptosis Regulating Genes
  5. Mutator (Caretaker) Genes
  6. Telomeres
  7. Epigenetic
  8. Molecular Basis of MultiStep Carcinogenesis
47
Q

Mechanisms of Carcinogens

  1. Genetic Change in Tumors
    - Karyotypic Changes
    - Point Mutations
A

The genetic changes in tumors may be subtle (point mutations) or large, to be detected as chromosomal changes

Karyotypic Changes:

  • balanced translocation → CML-t (9,22)
  • deletion → retinoblastoma → del 13q14
  • gene amplification: neuroblastoma → N-MYC.

Point Mutations:

  • RAS in colon carcinoma:
  • Carcinogenesis affects several classes of genes such as:
  • oncogenes.
  • tumor suppressor genes
  • apoptosis regulating gene
  • mutator (caretaker) genes *Carcinogenesis is a multi-step process.
48
Q

Mechanisms of Carcinogens

  1. Oncogenes and Cancer
    - Activation
    - Protein Products
A

Proto-oncogenes are normal genes that play key roles in controlling cell proliferation and differentiation.
Oncogenes are deregulated or altered proto-oncogenes that lead to development of cancer.

Activation of Oncogenes:

  • The activation of oncogene can be secondary to change in gene structure or due to a change in regulation of gene expressions. The changes are secondary to the following mechanisms.
    a) Point Mutation: RAS mutation is the most common mutation in human cancer.
    b) Translocation: e.g. t(9,22) in chronic myeloid leukemia.
    c) Gene Amplification
  • NMYC in neuroblastoma.

Protein Products of Oncogenes:

  • Oncogenes encode for protein products called oncoproteins - They are devoid of regulatory elements
  • Oncogenes may lead to the development of tumor by acting at different levels of signal transduction
49
Q

Mechanisms of Carcinogens

  1. Tumor Suppressor Genes
A

These genes acts as an inhibitor of cell proliferation.
- When mutated the inhibition is lost.

Examples:

P53 → lung, colon, breast, ovary & other cancers

BRCA1, BRCA2 → Breast carcinoma

RB → retinoblastoma

50
Q

Mechanisms of Carcinogens

  1. Apoptosis Regulating Genes
A

Genes that prevent or induce apoptosis may also be important in carcinogenesis.
- E.g. BCL2 in lymphoma.

51
Q

Mechanisms of Carcinogens

  1. Mutator (Caretaker) Genes
A

These are DNA repair genes. They are not oncogenic by themselves

  • However, when mutated, they allow mutation in other genes in normal cell division.
  • E.g. MSH2, MLH2 in hereditary non-polyposis colon cancer
52
Q

Mechanisms of Carcinogens

  1. Telomeres
A

Present at the end of the chromosome, are progressively shortened with age. Cancer cells make the enzyme telomerase which maintain their ability to replicate

53
Q

Mechanisms of Carcinogens

  1. Telomeres
A

DNA methylation, histone acetylation and de-acetylation microRNA alteration play important roles in carcinogenesis

54
Q

Mechanisms of Carcinogens

  1. Telomeres
A

Carcinogenesis is a multistep process. Multiple oncogene as well as one or multiple tumor suppressor genes works together to produce cancer

2420A Pathology (Definitions) (12 decks)

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