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Lecture 2 Cancer and Immunotherapy

The lecture discussed cancer immunotherapy. It began by covering hallmarks of cancer like independent growth signals, ignoring growth stop signals, and defective tumor suppressor genes. It then discussed tumor classification and metastasis. The remainder of the lecture focused on specific immunotherapy methods like peptide vaccines, dendritic cell vaccines, monoclonal antibodies, and cytokine therapies. It concluded by outlining considerations for active versus passive immunotherapy and specific versus non-specific approaches.
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0% found this document useful (0 votes)
54 views

Lecture 2 Cancer and Immunotherapy

The lecture discussed cancer immunotherapy. It began by covering hallmarks of cancer like independent growth signals, ignoring growth stop signals, and defective tumor suppressor genes. It then discussed tumor classification and metastasis. The remainder of the lecture focused on specific immunotherapy methods like peptide vaccines, dendritic cell vaccines, monoclonal antibodies, and cytokine therapies. It concluded by outlining considerations for active versus passive immunotherapy and specific versus non-specific approaches.
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Lecture 2

MEDICAL BIOTECHNOLOGY
(BIOT 412)

Cancer Immunotherapy
Dr. Muhammad Mustafa

Department of Biological
Sciences FC College
University
Prevalence of Cancer
Factors Believed to Contribute to
Global Causes of Cancer
Hall Marks of Cancer
1. Independent of GROWTH signal from other cells often, oncogenes.
2. Ignores STOP signal defective damage control, so problems not corrected.
3. Often, tumor suppressor genes. Ex. p53
Cell cycle and control of cell division
Growth factors bind to specific receptors
on the plasma membrane to trigger cell
division
Growth factor

Plasma membrane

Relay
Receptor proteins G1 checkpoint
protein
Signal
transduction Cell cycle
pathway control
system
Role of Tumor suppressors in
cancers
 Caner is defined as the continuous
uncontrolled growth of cells.
 A tumor is a any abnormal proliferation of
cells.
 Benign tumors stays confined to its original
location
 Malignant tumors are capable of invading
surrounding tissue or invading the entire
body
 Tumors are classified as to their cell type
 Tumors can arise from any cell type in the
body
 Carcinomas; constitute 90% of cancers, are
cancers of epithelial cells
 Sarcomas; are rare and consist of tumors
of connective tissues (connective tissue,
muscle, bone etc.)
 Leukemias and lymphomas; constitute 8%
of tumors. Sometimes referred to as liquid
tumors. Leukemias arise from blood
forming cells and lymphomas arise from
cells of the immune system (T and B cells).
Normal cells show Cancer cells lack
contact inhibition contact inhibition
They keep growing

And growing

And growing

And growing
• Benign: localized and of small
size
• Cells that closely resemble,
and may function, like normal
cells
• May be delineated by a fibrous
(Basal lamina) capsule
• Become problems due to sheer
bulk or due to secretions (e.g.
hormones)
Malignant tumors: high rate of division, properties may vary compared to
cells of origin. Most malignant cells become metastatic
Invade surrounding tissue and establishment of secondary areas of
growth: Metastasis
Metastasis
Carcinoma: derived from endoderm or
ectoderm
Explore and Learn
1. Growth Factor Receptor Increased numbers in 20 percent of breast cancers

2. Ras Protein Activated by mutations in 20 to 30 percent of cancers

3. Abl Kinase Activated by abnormal chromosomes in chronic myelogenous leukemia

4. Src Kinase Activated by mutations in 2 to 5 percent of cancers

5. p53 Protein Mutated or deleted in 50 percent of cancers


 1. Independent of GROW signal from other cells
often, oncogenes. Ex. ras
 2. Ignores STOP signal
defective damage control, so problems not
corrected.
Often, tumor suppressor genes. Ex. p53
 3. No cell suicide (apoptosis)
If this occurs, treatments which damage
dividing cells may not work.
 4. No limit to cell divisions
telomeres rebuilt on ends of xsomes
new treatment target: telomerase
 5. Angiogenesis - formation of blood vessels

 6. Metastasis - ability to move to other tissues


benign: do not move from tumor site
malignant: invasive cells, can travel in
blood and lymph system
p53 Signaling Cascade
DNA damage,
HOXA10 Stress or other Ref 1 CTCF
Ref 2

Bcl2
p53
Ref 3 Ref 4 Bax
Ref 5
VDAC
CTCF p21
Mitochondria

Cell Migration G1/S cell Cytochrome c


and invasion cycle arrest

Caspase 9

Caspase 3-7

Ref 1. Claudia F.M et.al.,Neoplasia. Aug 2013


Ref 2. Micheline C. Chu et. al., Cancer Biology & Therapy, Jun 2004 Apoptosis
Ref 3. Chen Y et.al., BMC Cancer. 2012
Ref 4. Mustafa, Lee et al.BBRC 2015
Ref 5. Mustafa et.al., J Cancer 2017
p-53 Signaling Pathway
Peptide tumor or cell vaccines
Trastuzumab mechanism of action
Activity 2

Write a response (2 pages maximum) of any one of the method of


immunotherapy you studied in earlier slide

Grading criteria
Pros and cones
How much sense the references made in your description
Assignment given date : TBD
Electronic and hard copy submission deadline: TBD
Fresh Thoughts
 Non-Specific: Generalized, Non-Antigen-Specific Im
mune Activation

 Specific: Antigen-specific Response Induced in the


Mouse or Patient or Passively Transferred in from D
onor Source
Active: Induced Directly in the Tumor-Bearing Animal
or in the Patient
 Can be Specific or Non Specific

Passive or Adoptive: Immunologically Active Material


Transferred into Mouse or Patient as a Passive Recip
ient
 Can be Specific (Antibodies, T-Cells, Antigen-presenting cel
ls – Dendritic Cell Vaccines)
 Or Non-Specific (Non-specifically-activated T-Cells; Cytoki
nes
Induced in the Patient or Mouse: Non-Antigen-specific

Bacterial Extracts: Non-Specific Immune Adjuvants


 BCG: Bacillus Calmette-Guerin (Attenuated Bovine Tuberculo
sis Bacterium)
 Membrane Extracts of BCG
 C Parvum: Corynebacterium parvum (related to diphtheria ba
cillus)
Bacterial Endotoxins: Muramyl Dipeptide
Chemical Adjuvants:
 Levamisole
 Poly IC (Poly-inosinic-Poly-cytidyllic acid)
Cytokines: (Can be actively induced or passively transferred)
 Interferons
 Interleukin 2 (IL2)
 Tumor Necrosis Factor (TNF)

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