Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

43 Cards in this Set

  • Front
  • Back
Tumors are the result of what?
DYSregulated growth- a clone of cells that replicate
Cancer and tumors
uncontrolled tumor growth

Malignant vs. Bening Tumor
Not invasive, not capable of indefinite growth
What are the three types of cancer?
1) Carcinoma
2) Lymphoma/Leukemia Cells
3) Sarcomas
Endodermal or ectodermal tissue

Skin, epithelial lining of organs- breast, colon, lung, prostate (~80%)
from HEMATOPOIETIC CElls (myeloid vs. lymphoid leukemia)

Lymph nodes
lymphode cell
From mesodermic tissue- BONE
What are 3 causes of cancer?
1) Induce cell proliferation
2) loss of tumor suppressor gene function
3) loss of control of cell death- bcl2
Cancer is a result of
1) spontaneous or inherited mutation
2) Chemical carcinogens
3) virus transformation
Genes that were normal before them became an ONCOGENES
PROTO oncogenes
What are mutations that induce cell proliferation
A) Growth factor receptors (NEU)

Breast cancer- is over production of NEU

B) Tyrosine kinases in GF signaling (Src, abl)

C) GTP-binding proteins involved in growth induction
Proteins involved in mutation in tumor suppressor genes (mutates to lose inhibition of cell growth)
p53, RB

These normally regulate cell growth- but don't regulate as they should
Gene amplification of genes controlling cell death mutation involves what protein
Anti-apoptotic protein
Inhibits apoptosis and promotes growth

Increase bcl2, increase tumor generation (Lymphoma)
The development of cancer requires
15% of all cancers are from
Viruses that integrate into genome and induce transformation
What are examples of viruses that cause TUMOR
HPV- cervical
Epstein Barr Virus
nasopharyngeal carcinoma
Burkitt lymphoma
Hepatitis B virus- Liver cancer
Human T-lymphotropic virus (HTLV)
human, single-stranded RNA retrovirus that causes T-cell leukemia and T-cell lymphoma in adult
How do we know that a protective response can be mounted against tumors?
Tumor rejection antigens
Tumor specific antigens
Tumor associated antigens
Why won't response to irradiated tumor will not eliminate unrelated tumors of different cell types?
Response to UNIQUE tumor rejection ANTIGENS elmiminates tumor
Response to unique tumor rejection antigen
Tumor antigen CEA
reactivates embroynic gene xpression in tumor cell- present new antigens to adult immun esystem
Overexpress normal self-peptide by a tumor cell changes peptide presentation density allowing T cell recognition
HIGHER levels of expression
If you have mutated peptide, then you have
alterations in CHO

Alteration in glycosylation machinery- alter structure, making it susceptible to different ways of cleaving.

Different cleaves, different MHC T cell presentation (foreign)
underglycosylated mucin

Different kinds: Over and differently glycosylated

Exposure of cleavage site for processing, recognition by acid residue sequences
Three immune responses to tumors?
CTL killing
Nk Killing
Macropahges secreting stuff
CTL killing involves what?
LAK cells
LAK cells
Lymphokine activated killer cells are white blood cells that help to identify and destroy cancer cells in the body.
Nk killing occurs
directly or via FCR
direct or ADCC (FcR)
What do macrophages secrete
lyctic enzymes, NO, Ros, TNF alpha
Mechanisms by which tumors escape immune recognition
1) Antigenic modulation

Antibody against tumor-cell surface antigens can induce ENDOCYTOSIS and DEGRADATION of antigen

Immune selection of antigen-loss variants
Antigenic moduation
down regulate

now the immune system can no longer see it
So ab' is not enough to generate Complement activation
Not in right place to allow for phagocyte or NK mediated killing
Immune may also generate proteases
ECTOpreateases that cleave up antigen
Tumors have low immunogenicity
Down regulate
Loss of HLA class I expression in prostate gland
Tumors and HLA class I
lymphocytes coming in to combat tumor

No HLA 1 to present foreign peptide
Must have CD8s to work
Macrophages and low immunogenicity of tuomrs
The successful Macrophages against tumor cells secrete soluble TNF receptor

Kill tumors by secreting TNF alpha, induces apoptosis in tumor cells
Tumor cells clip that off by clipping protease
No longer have receptor- no apoptosis
TNF-alpha binding- neutralize
Low immunogenicity of Tumors because they don't have
MHC ligand
Adhesion molecules
Co-stimulatory molecules
Tumors escape immune suppression DIRECTLY via
TGF-beta by tumor cells inhibits T cells directly

Blocking factors- like sTNF alpha receptor
How are NK cells activated?
Tumor specific antibody
binds to tumor cell

NK cells with Fc receptors (CD16) activated to kill tumor cells
If tumor specific Ab has CONJUGATED
Cojugate is internalized, killing the cell
Tumor specific antibody conjugated to RADIONUCLIDE
radioactive antibody binds to the tumor cell

Radiation kills tumor cell and neighbor tumor cell
Monoclonal Antibodies-

Presence of TRA and no accompanying costimulatory molecules
Tumor rejection antigen

Can't turn on naive CD8 T cells
Tumor grows progressively