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Medical Genetics > FINAL - CH 11 > Flashcards

FINAL - CH 11 Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

Origin of Cancer

A

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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2
Q

Theories for metastasis

A

“Seed and soil”

Routes of blood supply theory

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3
Q

Steps to metastases

A

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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4
Q

angiogenesis

A

local blood vessel formation

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5
Q

Characteristics of Cancer Cells

A 
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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6
Q

Carcinogens

A

are substances that cause cancer by mutating DNA (mutagens)

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7
Q

Genes that control growth of cancer

A 
Proto-oncogenes (accelerators)
Tumor supressor (brakes)
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8
Q

Oncogenes

A

Mutated proto-oncogene

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9
Q

Different proto-oncogenes

A

HIST
HRAS
CDK4

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10
Q

HIST

A

Fibroblast growth factor

stomach cancer

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11
Q

HRAS

A

GTPase

Colon, lung, pancreatic cancer

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12
Q

CDK4

A

Cyclin dependent kinase

Malignant melanoma

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13
Q

Her-2/neu

A

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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14
Q

How are monoclonal antibodies made?

A

Inject animal with antigen

Get the B cells out

Fuse with myeloma from host

Make monoclonal antibody

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15
Q

How are oncogenes created?

A

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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16
Q

Examples of tumor suppressor genes invloved in cancer

A

BRCA1
XPA
NF1

17
Q

BRCA1

A

DNA repair protein complex

Familial breast/ovarian cancer

18
Q

XPA

A

Nucleotide excision repair

Xeroderma pigmentosum

19
Q

NF1

A

Down regulates ras protein

Neurofibromatosis 1

20
Q

Two Hit Hypothesis

A

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”

21
Q

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

A

DNA repair

all future daughter

22
Q

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

A

telomere length

Cell cycle

23
Q

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

A

TP53 gene

24
Q

Function of TP53

A

Determines if a cell has repaired DNA damage

If can’t repair damage, p53 induces apoptosis

25
Q

_____ human cancers involve abnormal p53

A

> 50%

26
Q

Environmental factors contributing to cancer

A 
Organic chemicals
radon gas in  homes 
foods
UV exposure from the sun
Cosmic radiation exposure in airplanes
X-rays, CAT scans, chemotherapy, drugs
27
Q

Retinoblastoma

A

Phenotype: Cancer of the retina

Etiology: Autosomal dominant mutation in Rb 1 gene, which is a tumor suppressor gene

28
Q

Chronic myelogenous leukemia

A

Phenotype: Cancer in bone marrow

Etiology: Mutation in ABL gene, protein kinase oncogene

29
Q

Li-fraumeni

A

Phenotype: causes many different types of cancer in family members at early age

Etiology: Mutation in p53 tumor supressor, transcription factor

30
Q

Breast cancer

A

Phenotype: Breast/ovarian cancer

Etiology: Mutation in BRCA1 tumor suppressor gene, DNA repair protein complex

31
Q

Colon cancer

A

Phenotype: Colon cancer

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

32
Q

Effect of translocations on cancer development

A

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

33
Q

Immunotherapy treatments for Cancer

A

Uses natural power of your immune system to fight cancer

34
Q

Different Immunotherapy treatments

A

General Immunotherapy (Non-specific)

T-Cell Transfer Therapy

Immune Checkpoints

Monoclonal Antibodies (e.g. Herceptin)

35
Q

Environment Impacts on Cancer: Diet

A

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

36
Q

Chemoprevention Foods

A

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

37
Q

Nutrigenomics

A

Branch of nutritional genomics

Studies the effects of foods and food constituents on gene expression

38
Q

Other Cancer Treatment

A

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

Medical Genetics (12 decks)

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