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Cell Biology > Cancer > Flashcards

Cancer Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Characteristics of Cancer

A

 An uncontrolled proliferation of cells
 And invasion and spread from site of primary
tumor to other sites in the body

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2
Q

Tumour

A

Tumours are a dense collection of cells that are created
when the orderly process of cell division goes out of
control and cells divide more rapidly

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3
Q

Benign

A

These are abnormal but they don’t metastasise

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4
Q

Malignant

A

A malignant tumour or a cancer metastasises

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5
Q

Metastasis

A
  • The main difficulty with cancer cells is that they can
    spread from their original location and populate other
    regions-this is metastasis
  • They usually travel in blood vessels or through the
    lymphatic system
  • Patients usually die as a consequence of metastasis
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6
Q

Carcinomas

A

originate from the cells that cover external and internal
body surfaces. Lung, breast, and colon are the most frequent

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7
Q

Sarcomas

A

are cancers arising from cells in the supporting tissues such
as bone, cartilage, fat, connective tissue and muscle

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8
Q

lymphomas

A

are cancers that arise in the lymph nodes and tissues of
the immune system.

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9
Q

Leukemias

A

are cancers of the immature blood cells that grow in the
bone marrow and are found in large numbers in the bloodstream.

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10
Q

Morphology of Cancer Cells

A
  1. Cancer cells can grow indefinitely in culture
  2. They can pile up on each other
    (no contact inhibition)
  3. They can have multiple nuclei
  4. There can be more than 46 chromosomes
  5. The chromosomes can be abnormal
    The overall morphology can be completely different
    to that of the parent
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11
Q

Grade of a cancer

A

determined using cancer cell morphology - how cells look like under the
microscope (grades I-IV). High grade is associated with lower survival.

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12
Q

Stage

A

measure of the tumour size and metastasis and is based on how
large is the tumor, has it invaded surrounding tissues, and spread to regional
lymph nodes or metastasized to other regions of the body
A patient’s chances for survival are better if cancer is at a lower stage.
Traditional Tumor Classifications- Tumor Staging

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13
Q

Carcinogen

A

a cancer –causing substance or agent

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14
Q

Causes of cancer

A

 Cancer ultimately results from the interaction between hereditary
and environmental factors
 Usually not a single factor but a multiple factors with accumulated
effects through life-time
 However, a single factor may be so important that in its absence
a significant number of specific cancers would not occur, for
example smoking
 a single type of cancer can be caused by different
agents
– skin cancer can be caused by UV, ionizing radiation,
polycyclic aromatic hydrocarbons
 many types of cancer are caused by a single agent
– ionising radiation can cause myeloid leukaemia,
osteosarcoma, thyroid cancer, skin cancer or breast
cancer
 complex interactions for a single cancer
– age, UV exposure and DNA repair capacity

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15
Q

Chemicals

A

– e.g. Oils/tars (scrotal cancer in chimney
sweeps; benzo[a]pyrene)
– Fibres (asbestos) and mesothelioma
– Natural products (aflatoxin and liver cancer)
– Heavy metals Chromium, Cadmium etc
– Benzene

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16
Q

Radiation

A

– X-rays, γ-rays, α&β particles
* Cosmic radiation (aircrew)
* Nuclear industry
* Medical (radiotherapy)
– Ultraviolet light
* Sunlight & tanning

17
Q

Viruses

A
  • Viral Infections
    – Human papillomavirus (HPV): cervical cancer
    – Hepatitis B: liver cancer
    – Kaposi’s sarcoma: associated with HIV/AIDS
18
Q

Heredity

A
  • Cancer is not considered an inherited disease
  • However, chances of some people developing cancer can be influenced by
    genetic factors
  • Genetic predisposition
  • BRCA1 & BRCA2 breast cancer genes
  • Ataxia telangiectasia: Hypersensitivity to ionizing radiation, leukaemia &
    lymphoma (mutation in ATM kinase)
  • Familial retinoblastoma (mutations in Rb tumor suppressor)
  • Li-Fraumeni Syndrome: p53 mutations; breast, brain, leukaemia, soft tissue
    sarcomas
19
Q

BRCA1 and BRCA2 genes

A
  • BRCA1 and BRCA2 are tumour suppressor
    genes
  • They are involved in repairing damage to DNA
  • If these genes do not function correctly then
    mutations in DNA occur that can lead to cancer
20
Q

Diet/lifestyle

A
  • Carcinogens in food? e.g. aflatoxin, other chemicals
  • Obesity and cancer: increased risk of breast (in
    older women), endometrial, kidney, colon and
    esophagus cancer
  • Some studies show that large quantities of red and
    preserved meat increases the risk of stomach and
    colorectal cancers, whereas a diet high in fruits and
    vegetables may decrease the risks of these
    cancers. And calorie restriction reduces cancer risk
    of cancer.
21
Q

Hormones

A
  • Androgens linked to prostate cancer
  • Estrogens linked to breast cancer
  • These hormones are considered initiators of cancer
    because they increase proliferative capacity of target
    tissues
22
Q

Cancer Development

A
  • One mutation in a pre-cancerous cell makes it
    more likely that other mutations will persist in
    the genome, e.g. deletion of DNA repair genes
  • Leads to an accumulation of mutations
  • These mutations confer a growth advantage to
    the cancer cells
  • Eventually give rise to Hanahan & Weinberg’s
    ‘Hallmarks of Cancer
23
Q

Oncogenes

A
  • Oncogenes are mutated versions of normal
    genes called proto-oncogenes
  • Products of oncogenes are proteins involved
    in cell growth and division. They function
    normally in the complex network of regulation
    of cell growth. Under abnormal
    circumstances, they may over-stimulate cell
    growth, proliferation or cell survival.
  • A single mutant allele may affect the
    phenotype of a cell therefore dominant
24
Q

Mechanisms of Proto-oncogene
Activation

A
  1. Mutations
    Point mutations/deletions/insertions
  2. Gene amplification
    For reasons not understood, a particular chromosome segment may
    form a very large number of copies. This happens rarely, and in
    most cases the cell does not survive. However, if the repeated
    element includes an oncogene, this may result in abnormal growth.
  3. Chromosomal re-arrangement
    Chromosome rearrangements, such as translocation, can place a
    cellular oncogene under control of the wrong promoter, or lead to
    formation of the gene fusions that code for chimeric proteins
25
Q

Tumour Suppressor Genes

A

Tumour suppressor (TS) genes encode
proteins whose normal function is to inhibit cell
proliferation. Cancer cells have lost function of
TS genes. Both alleles have to be inactivated to
change the phenotype of the cell ….therefore
recessive
 A tumour suppressor gene that normally
acts as a brake must be inactivated.
 Full inactivation requires two mutations—
both alleles must be turned off
 People with inherited predisposition to
cancer are born with one mutant allele,
and need only one more mutational event
for inactivation of the tumour suppressor
gene

26
Q

p53

A

Major functions
p53 protein acts as a transcription factor
p53 consensus binding site has been identified in
promoters of several target genes involved in slowing
down cell cycle and causing apoptosis (e.g., p21, Bax)
p53 acts as a G1 checkpoint control for DNA damage
e.g., following IR, UV irradiation, p53 activity is induced
resulting in cell cycle arrest to allow time for repair
p53 participates in the initiation of apoptosis

27
Q

E2F Transcription Factor is a Major
Controller of the Cell Cycle

A
  • Cell cycle progression, arrest and apoptosis
    (E2F-1), however other members of the family
    other effects (E2F1-8); function as heterodimers
    with DP1 and 2
  • Crucial in growth control, specifically G1 to S phase
  • Target genes
  • growth stimulation (DHFR, DNA pol α)
  • growth inhibition (ARF, APAF-1)
28
Q

DNA Repair Mechanisms

A
  • Nucleotide excision repair (NER)
    Removes larger areas of DNA damaged by
    chemicals or irradiation
  • Base excision repair (BER)
    Targets chemically altered bases
  • Mismatch repair (MMR)
    Corrects replication errors that have escaped
    editing by polymerases
29
Q

Apoptosis

A

Apoptosis is a highly regulated process of cell
death which controls cell numbers and
eliminates damaged cells and therefore plays an
important role in tumour suppression.

30
Q

Surgery

A
  • If the cancer can be completely removed -then
    curative
  • Problem – metastasis
  • Metastasis – cancer cells split from the primary
    tumour, travel around the body and form
    secondary cancers in remote sites
  • Most cancer deaths arise from secondary
    cancers
  • Can not always treat metastasis by surgery
31
Q

Radiotherapy

A
  • Use radiation to kill cancer cells.
  • Can be external radiation (a beam of x-
    rays) or internal (radioactive implant).
    Problems:
  • Metastasis
  • Damage to normal tissues.
32
Q

Chemoptherapy

A
  • Drugs come in contact with every cell in the
    body
  • Therefore metastasis can be treated
  • Most drugs are targeted at killing dividing
    cells
    Problems:
  • Normal tissue toxicity. Most healthy cells in an
    adult are non dividing – exception hair, bone
    marrow etc.
  • Resistance
  • In children most cells dividing

Inhibitors of DNA synthesis
I. Alkylating agents and platinum based drugs
(Chlorambucil, Cyclophosphamide, Cisplatin,
Carboplatin)
II. Antimetabolites (5-Fluorouracil)
* Inhibitors of microtubule formation (Vincristine,
Vinblastine, Paclitaxel)
* Hormones (glucocorticoids, tamoxifen,
antiandrogens)
* Organic drugs (Doxorubicin)

33
Q

Inhibitors of Oncogenic Activity

A

Kinase inhibitors
Anti-EGFR (Iressa and Tarceva are drugs that inhibit EGFR kinase
activity, Herceptin is a monoclonal antibody)
Anti Bcr-Abl [Philadelphia chromosome, (Gleevec is tyrosine-
kinase inhibitor)]

34
Q

Types of Immunotherapy

A
  • Monoclonal antibodies
  • Cancer vaccines
  • Non-specific immunotherapies and adjuvants
  • New approaches
35
Q

How to Find New Treatments

A
  • Identify a difference between a cancer cell
    and normal cells
  • Design and synthesise a drug to target this
    difference
  • Test the drug in model systems
  • Clinical trials in patients
36
Q

Clinical Trials

A
  • How much drug is ‘safe’?
  • How much drug is needed to get clinical
    effect?
  • How much drug can be given before
    toxicity (side effects) are seen?
  • Start with mice, continue with clinical
    trials.
  • Future approaches-personalised
    therapy

Cell Biology (10 decks)

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