FINAL - CH 11 Flashcards by Taylor Nunes

Origin of Cancer

Begins from the growth of a single abnormal cell

A mutation occurs, allowing a cell to undergo inappropriate cell division

Division produces more abnormal cells, resulting in a tumor formation

Certain cell(s) in the tumor can undergo further mutation to produce metastatic cells that are able to dissociate from the original tumor and colonize at new organ sites (metastasis)

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Theories for metastasis

“Seed and soil”

Routes of blood supply theory

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Steps to metastases

Tumor grows to infiltrate surrounding tissues

Breaks through basement membrane

Breaks down the connective tissue proteins

Attach to the endothelium and enter lymph/blood

Evade immune cells in lymph/blood

Lodge in capillaries

Attach and travel through endothelium

Proliferate and produce tumor

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angiogenesis

local blood vessel formation

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Characteristics of Cancer Cells

Divide continually 
May contain heritable mutations if germline
lose their specialized identity
Lack contact inhibition
Induce angiogenesis 
Increased mutation rate
Invasive
Metastasize

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Carcinogens

are substances that cause cancer by mutating DNA (mutagens)

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Genes that control growth of cancer

Proto-oncogenes (accelerators)
Tumor supressor (brakes)

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Oncogenes

Mutated proto-oncogene

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Different proto-oncogenes

HIST
HRAS
CDK4

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HIST

Fibroblast growth factor

stomach cancer

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HRAS

GTPase

Colon, lung, pancreatic cancer

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CDK4

Cyclin dependent kinase

Malignant melanoma

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Her-2/neu

Product of an oncogene

Excessive levels in approximately 25% of breast cancer patients

Too many receptors for epidermal growth factor - tyrosine kinase receptors

Result: Too many signals to divide

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How are monoclonal antibodies made?

Inject animal with antigen

Get the B cells out

Fuse with myeloma from host

Make monoclonal antibody

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How are oncogenes created?

Viruses integrated next to a proto-oncogene can cause transcription when the virus is transcribed - whoch activates a proto-oncogene to be active when it shouldn’t

A proto-oncogene in a new location may cause cancer (translocation in burkitt lymphoma, cytogenic rearrangement in leukemias)

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Examples of tumor suppressor genes invloved in cancer

BRCA1
XPA
NF1

BRCA1

DNA repair protein complex

Familial breast/ovarian cancer

XPA

Nucleotide excision repair

Xeroderma pigmentosum

NF1

Down regulates ras protein

Neurofibromatosis 1

Two Hit Hypothesis

Two mutations are required

For somatic: 2 mutations needed in somatic cell

For germline: One mutation is already present, second mutation required for cancer, which is high in AD cases, creates a dominant “susceptibility”

If cell cycle does not allow time for ________, damaged DNA remains in __________ cells

DNA repair

all future daughter

Loss of control of _______ may contribute to loss of control of ______

telomere length

Cell cycle

In colon cancer: Loss of the ______ and other alterations are involved in the progression to malignant carcinoma and metastasis

TP53 gene

Function of TP53

Determines if a cell has repaired DNA damage

If can’t repair damage, p53 induces apoptosis

_____ human cancers involve abnormal p53

>50%

Environmental factors contributing to cancer

``` Organic chemicals radon gas in homes foods UV exposure from the sun Cosmic radiation exposure in airplanes X-rays, CAT scans, chemotherapy, drugs ```

Retinoblastoma

Phenotype: Cancer of the retina Etiology: Autosomal dominant mutation in Rb 1 gene, which is a tumor suppressor gene

Chronic myelogenous leukemia

Phenotype: Cancer in bone marrow Etiology: Mutation in ABL gene, protein kinase oncogene

Li-fraumeni

Phenotype: causes many different types of cancer in family members at early age Etiology: Mutation in p53 tumor supressor, transcription factor

Breast cancer

Phenotype: Breast/ovarian cancer Etiology: Mutation in BRCA1 tumor suppressor gene, DNA repair protein complex

Colon cancer

Phenotype: Colon cancer Etiology: Loss of APC gene, activation of the KRAS proto-oncogene, loss of the SMAD4 gene, Loss of the TP53 gene

Effect of translocations on cancer development

Displace genes so that they are under NEW regulatory control, so they can be improperly up or down regulated

Immunotherapy treatments for Cancer

Uses natural power of your immune system to fight cancer

Different Immunotherapy treatments

General Immunotherapy (Non-specific) T-Cell Transfer Therapy Immune Checkpoints Monoclonal Antibodies (e.g. Herceptin)

Environment Impacts on Cancer: Diet

Fatty diets are correlated with increased estrogen and increased breast cancer Red meat and processed meat increases colon cancer risk Grilled red meat releases carcinogen called heterocyclic aromatic amines

Chemoprevention Foods

Lycopene (Tomatoes) cruciferous vegetables (e.g broccoli, brussell sprouts, cauliflower) decrease risk of colon cancer) Vitamin C (antioxidant that deactivate DNA damaging free radicals) anti-inflammatory foods, e.g. flaxseed

Nutrigenomics

Branch of nutritional genomics Studies the effects of foods and food constituents on gene expression

Other Cancer Treatment

Targeted therapies – e.g. Gleevac for CML Angiogenesis inhibitors – inhibits blood vessel formation e.g. Avastin helps treat colon cancer Drugs that stimulate cells to regain specialized cell fxn e.g. retinoic acid Induce apoptosis of cancer cells