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BASICS OF
TARGET THERAPY
MOHAMED ABDULLA
PROF. OF CLINICAL ONCOLOGY
CAIRO UNIVERSITY
NEMROCK – CAIRO
PFIZER TRAINING COURSE
SUNDAY: 22/11/2015
SPEAKER DISCLOSURES
Member of Advisory Board, Consultant, and Speaker for:
Amgen, Astellas, AstraZeneca, Hoffman la Roche, Janssen
Cilag, Merck Serono, Novartis, Pfizer
THE NORMAL CELL
CYCLE
Class Example Method of Action Cycle
Specific
Alkylating agents Cytoxan Effects DNA chemically All
Antimetabolites 5-FU
Gemzar
Substitutes for normal cell
building blocks
S
Anthracyclines Adriamycin DNA damage or inhibit
topoisomerase
All
Anti-tumor
Antibiotics
Bleomycin DNA damage All
Topoisomerase
Inhibitors
Irinotecan Complex DNA and
topoisomerase together
S
G-2
Vinca Alkaloids Vincristine Binds to tubulin, interferes
with mitosis
M
Taxanes Taxol
Taxotere
Prevents microtubules from
disassociating
M
CLASSES OF CYTOTOXIC
THERAPIES
COULD WE DO
BETTER?
CHEMOTHERAPY VS TARGETED
THERAPY
Chemotherapy:
• Drugs that effect cells that are doubling
• Not very specific
• Mostly intravenous, some oral agents
• Cytotoxic
Targeted therapy:
• Drugs that inhibit a more specific target in cells
• Many are oral agents
• Mixture of cytostatic and cytotoxic
BIOGRAPHY OF
CANCER:
Normal Mother Cells Normal Daughter Cells
Abnormal Daughter Cells
Programed Cell Death:
APOPTOSIS
RESISTANCE TO
APOPTOSIS
Continued Un-opposed
Proliferation
Malignant Tumor PROGRESSIONANGIOGENESIS
• Life
• Growth
• Maintenance
P53
+++Growth Signals
BIOGRAPHY OF
CANCER:
CANCER = ARREST OF APOPTOSIS + ANGIOGENESIS
P53
GROWTH
SIGNALS
Repair of Critical Damage
Growth Factor  Receptor  Biological Path 
Nuclear Material  Proliferation, Angiogenesis ..
BIOGRAPHY OF
CANCER:
Growth Factor
Monoclonal
Antibody
Normally
Existing
++ By The
Tumor
TK
1
2
3
Formation of
New Blood
Vessels
Physiological
Wound Healing
Placental Implantation
Growth
Pathological
Pre-Eclampsia
Diabetic Retinopathy
Tumors
ANGIOGENESIS:
THE WHOLE MARK OF
MALIGNANCY:
Proliferation Invasion Metastases
VEGF +
+
TK
+
m-TOR
ANGIOGENESIS:
THE WHOLE MARK OF
MALIGNANCY:
New Blood
Vessel 
Proliferation
Release of GFs
Receptor
Activation
Degradation &
Proteolytic Enz.
Disruption of
ECM & Wall
Invasion &
Migration
ANGIOGENESIS:
THE WHOLE MARK OF
MALIGNANCY:
VEGF
R
AKT
Grb SOS
mTOR
Protein Synthesis
HIF-1@
Metabolism
Growth
Angiogenesis
RAS
RAF
Mek
Erk
Cell Cycle Progression &
Proliferation
1. Avastin [package insert]. South San Francisco, CA: Genentech; 2009. 2. Escudier B et al; TARGET Study Group. N Engl J
Med. 2007;356:125-134. 3. Escudier B et al. J Clin Oncol. 2009;27:3312-3318. 4. Nexavar [package insert]. Wayne, NJ: Bayer
Healthcare Pharmaceuticals; 2007.
Bevacizumab
RAD 001
ANGIOGENESIS:
THE WHOLE MARK OF
MALIGNANCY:
Tyrosine Kinase Receptors
VEGFR - 1 VEGFR - 2 VEGFR - 3 NRP - 1 NRP - 2
VEGFs
VEGF - A VEGF - B VEGF - C VEGF - D PlGF
ANGIOGENESIS:
THE WHOLE MARK OF
MALIGNANCY:
Hypoxia
HIF
VEGF Gene
VEGFVEGFR on Nearby Vessels VEGFR on Tumor Vessels
ANGIOGENESIS:
THE WHOLE MARK OF
MALIGNANCY:
ANGIOGENESIS:
THE WHOLE MARK OF
MALIGNANCY:
Possible
Targets for
Treatment
Growth Factors
Extracellular
Receptor
Domain
Tyrosine Kinase
Receptor
Domain
Critical Protein
in Biological
Cascade
Blocking VEGF Small Molecule
TKI
EGFR Inhibitors Soluble VEGF
Decoy Receptor
Bevacizumab Sorafinib, Sunitinib,
Pazopanib,
Axitinib,
Regorafinib
Erlotinib,
Gefitinib
Aflibercept
Blocking 100% of
VEGF-A  Anti-
angiogenic Activity
Wide Range:
PDGFR,
C-kit,
EGFR,
FGFR  Both Anti-
angiogenic & Anti-
mitogenic Activity
Blocking ERB-1
Receptors  Both
Anti-angiogenic
and Anti-mitogenic
Activity
Blocking VEGF –
A and B, PlGF 
Anti-angiogenic
Activity
IV Bioavailability Oral Bioavailability Oral Bioavailability IV Bioavailability
17 – 21 HLT Short Lived Short Lived Higher Affinity to
VEGF-A than
other MAB.
ANGIOGENESIS:
THE WHOLE MARK OF
MALIGNANCY:
BREAKTHROUGHS:
1. Trastuzumab in Breast Cancer.
2. Rituximab in B-Cell NHL.
3. Bevacizumab in Colon and Ovarian Cancer.
4. Cetuximab and Panitumumab in Colon Cancer.
5. Denosumab in GCTB and Metastatic Bone Disease.
6. Imatinib in GIST.
7. Everolimus in NET and RCC.
8. Sunitinib in RCC.
9. Erlotinib and Gefitinib in Non Squamous NSCLC.
10. Crizotinib in Non Squamous NSCLC.
11. ………
THE ART OF TODAY:
• Chemotherapy is still the backbone of most of cancer
treatment protocols.
• Targeted Therapies could represent an opened era of
being more personalized and specific in cancer
management when added to conventional therapies.
• Some of the TARGETED THERAPIES represent a
breakthrough in management (Combo and Sole)
• Others pave the way of pessimistic disease entities.
• Still we need to understand much of the molecular events
playing in the back-stage of disease.
THANK YOU

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Introduction to Targeted Therapies in Oncology

  • 1. BASICS OF TARGET THERAPY MOHAMED ABDULLA PROF. OF CLINICAL ONCOLOGY CAIRO UNIVERSITY NEMROCK – CAIRO PFIZER TRAINING COURSE SUNDAY: 22/11/2015
  • 2. SPEAKER DISCLOSURES Member of Advisory Board, Consultant, and Speaker for: Amgen, Astellas, AstraZeneca, Hoffman la Roche, Janssen Cilag, Merck Serono, Novartis, Pfizer
  • 4. Class Example Method of Action Cycle Specific Alkylating agents Cytoxan Effects DNA chemically All Antimetabolites 5-FU Gemzar Substitutes for normal cell building blocks S Anthracyclines Adriamycin DNA damage or inhibit topoisomerase All Anti-tumor Antibiotics Bleomycin DNA damage All Topoisomerase Inhibitors Irinotecan Complex DNA and topoisomerase together S G-2 Vinca Alkaloids Vincristine Binds to tubulin, interferes with mitosis M Taxanes Taxol Taxotere Prevents microtubules from disassociating M CLASSES OF CYTOTOXIC THERAPIES
  • 6. CHEMOTHERAPY VS TARGETED THERAPY Chemotherapy: • Drugs that effect cells that are doubling • Not very specific • Mostly intravenous, some oral agents • Cytotoxic Targeted therapy: • Drugs that inhibit a more specific target in cells • Many are oral agents • Mixture of cytostatic and cytotoxic
  • 7. BIOGRAPHY OF CANCER: Normal Mother Cells Normal Daughter Cells Abnormal Daughter Cells Programed Cell Death: APOPTOSIS RESISTANCE TO APOPTOSIS Continued Un-opposed Proliferation Malignant Tumor PROGRESSIONANGIOGENESIS • Life • Growth • Maintenance P53 +++Growth Signals
  • 8. BIOGRAPHY OF CANCER: CANCER = ARREST OF APOPTOSIS + ANGIOGENESIS P53 GROWTH SIGNALS Repair of Critical Damage Growth Factor  Receptor  Biological Path  Nuclear Material  Proliferation, Angiogenesis ..
  • 10. Formation of New Blood Vessels Physiological Wound Healing Placental Implantation Growth Pathological Pre-Eclampsia Diabetic Retinopathy Tumors ANGIOGENESIS: THE WHOLE MARK OF MALIGNANCY:
  • 11. Proliferation Invasion Metastases VEGF + + TK + m-TOR ANGIOGENESIS: THE WHOLE MARK OF MALIGNANCY:
  • 12. New Blood Vessel  Proliferation Release of GFs Receptor Activation Degradation & Proteolytic Enz. Disruption of ECM & Wall Invasion & Migration ANGIOGENESIS: THE WHOLE MARK OF MALIGNANCY:
  • 13. VEGF R AKT Grb SOS mTOR Protein Synthesis HIF-1@ Metabolism Growth Angiogenesis RAS RAF Mek Erk Cell Cycle Progression & Proliferation 1. Avastin [package insert]. South San Francisco, CA: Genentech; 2009. 2. Escudier B et al; TARGET Study Group. N Engl J Med. 2007;356:125-134. 3. Escudier B et al. J Clin Oncol. 2009;27:3312-3318. 4. Nexavar [package insert]. Wayne, NJ: Bayer Healthcare Pharmaceuticals; 2007. Bevacizumab RAD 001 ANGIOGENESIS: THE WHOLE MARK OF MALIGNANCY:
  • 14. Tyrosine Kinase Receptors VEGFR - 1 VEGFR - 2 VEGFR - 3 NRP - 1 NRP - 2 VEGFs VEGF - A VEGF - B VEGF - C VEGF - D PlGF ANGIOGENESIS: THE WHOLE MARK OF MALIGNANCY:
  • 15. Hypoxia HIF VEGF Gene VEGFVEGFR on Nearby Vessels VEGFR on Tumor Vessels ANGIOGENESIS: THE WHOLE MARK OF MALIGNANCY:
  • 16. ANGIOGENESIS: THE WHOLE MARK OF MALIGNANCY: Possible Targets for Treatment Growth Factors Extracellular Receptor Domain Tyrosine Kinase Receptor Domain Critical Protein in Biological Cascade
  • 17. Blocking VEGF Small Molecule TKI EGFR Inhibitors Soluble VEGF Decoy Receptor Bevacizumab Sorafinib, Sunitinib, Pazopanib, Axitinib, Regorafinib Erlotinib, Gefitinib Aflibercept Blocking 100% of VEGF-A  Anti- angiogenic Activity Wide Range: PDGFR, C-kit, EGFR, FGFR  Both Anti- angiogenic & Anti- mitogenic Activity Blocking ERB-1 Receptors  Both Anti-angiogenic and Anti-mitogenic Activity Blocking VEGF – A and B, PlGF  Anti-angiogenic Activity IV Bioavailability Oral Bioavailability Oral Bioavailability IV Bioavailability 17 – 21 HLT Short Lived Short Lived Higher Affinity to VEGF-A than other MAB. ANGIOGENESIS: THE WHOLE MARK OF MALIGNANCY:
  • 18. BREAKTHROUGHS: 1. Trastuzumab in Breast Cancer. 2. Rituximab in B-Cell NHL. 3. Bevacizumab in Colon and Ovarian Cancer. 4. Cetuximab and Panitumumab in Colon Cancer. 5. Denosumab in GCTB and Metastatic Bone Disease. 6. Imatinib in GIST. 7. Everolimus in NET and RCC. 8. Sunitinib in RCC. 9. Erlotinib and Gefitinib in Non Squamous NSCLC. 10. Crizotinib in Non Squamous NSCLC. 11. ………
  • 19. THE ART OF TODAY: • Chemotherapy is still the backbone of most of cancer treatment protocols. • Targeted Therapies could represent an opened era of being more personalized and specific in cancer management when added to conventional therapies. • Some of the TARGETED THERAPIES represent a breakthrough in management (Combo and Sole) • Others pave the way of pessimistic disease entities. • Still we need to understand much of the molecular events playing in the back-stage of disease.