An edition of CANCER. Targeting Killer Cells
(2009)
CANCER. Targeting Killer Cells
Finding New tactics To Win The Guerrilla War
by Gilbert Mertens
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The book is written by the author of „The Molecular Revolution“ (Raider Publishing International), „From Quackery to Credibility“ (Financial Times Ltd.), „Beyond Blockbusters“ (Reuters Business Insight), „Direct-to-Consumer Advertising for Prescription Medicines“ (Financial Times Ltd.), „Mastering the Complexities of Women’s Health“ (Nicholas Hall & Co), „Targeted Cancer Therapies“ (Reuters Business Insight), and many more global medical community bestsellers. It says that scientists all over the world are coming up with treatments not imagined even a decade ago. In this new book on CANCER, Gilbert Mertens explains the developments in Cancer Therapies and focuses on innovative medicines and their impact on the future of oncology.
Currently, treatment for cancer depends on the type of cancer, tumor size, localization and stage of disease; and the person's general health. Advances in research have meant that treatment will depend less on cancer type (organ location, histology) and be more driven by molecular features, the author notes.
Innovatives are the most promising area for all cancers and may create the answer to reduced side effects associated with cancer treatment and have the vast potential of dramatically increasing disease free survival and overall survival rates. The promise behind innovative medicines and reduced side effects arises from the potential of specifically targeting cancer cells, thus avoiding killing normal healthy cells, a common problem associated with cytotoxics and anti-metabolites. There has been a clear move away from cytotoxics in favor of cytostatic drugs, which has been integral to the development of targeted cancer therapies. While traditional chemotherapy agents kill cancer cells by being cytotoxic, many new agents work mostly by interrupting their growth.
We will see new medicines that can offer significant extension in survival and, ideally, extended disease-free survival. We will see improved second-line treatments for patients who fail to respond to first-line treatments, or suffer a relapse after receiving first-line therapy. Improved diagnostic tests and appropriate tumor markers, which are critical to the future success of Cancer Therapies, will allow the new medicines to be appropriately targeted and therefore demonstrate cost-effectiveness for cancer patients.
The author describes the numerous emerging therapies and how they will create a targeted medicines sector and, in time, lead to the development of personalized cancer therapy programs.
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Book Details
Table of Contents
Visit: www.Cancer.com.ag
Scientists all over the world are coming up with treatments not imagined even a decade ago.
In this new book on CANCER, Gilbert Mertens explains the developments in Cancer Therapies and focuses on innovative medicines and their impact on the future of oncology.
Currently, treatment for cancer depends on the type of cancer, tumor size, localization and stage of disease; and the person's general health. Advances in research have meant that treatment will depend less on cancer type (organ location, histology) and be more driven by molecular features.
The promise behind innovative medicines and reduced side effects arises from the potential of specifically targeting cancer cells, thus avoiding killing normal healthy cells, a common problem associated with cytotoxics and anti-metabolites.
We will see new medicines that can offer significant extension in survival and, ideally, extended disease-free survival. We will see improved second-line treatments for patients who fail to respond to first-line treatments, or suffer a relapse after receiving first-line therapy. Improved diagnostic tests and appropriate tumor markers, which are critical to the future success of targeted cancer therapies, will allow the new medicines to be appropriately targeted and therefore demonstrate cost-effectiveness for cancer patients.
The author describes the numerous emerging therapies and how they will create a targeted medicines sector and, in time, lead to the development of personalized cancer therapies.
Contents
Introduction:
I.1. Expect and prepare for exciting times in a health care environment with new dimensions.
I.2. Comparing individual variations against a blueprint for the human race.
I.3. Integrated Therapeutic Providers. The ‘value chain of health’ to take a place at the center of all activities.
I.4. Global innovative medicines research.
I.5. A scientific revolution transforms the practice of medicine.
I.6. Coming up with medicines not imagined even a decade ago.
I.7. The emergence of therapies based on New Biology.
I.8. By 2020, the impact of personalized medicine is likely to be far more important than any of
us can envision today.
I.9. Oncogenics can provide one of the key routes to the development of successful targeted
therapies.
I.10. The cost factor: Preparing for a future of unseen opportunity in healthcare requires a profound shift in thinking from all the stakeholders.
Chapter I: A new dimension in healthcare.
II.1. The new era of personalized healthcare.
II.2. Understanding disease in ways never before possible.
II.3. The right medicine, the right dose, the right patient: Achieving optimal medical outcomes.
II.4. The right drug at the right time.
II.5. Far-reaching mental and structural transformation is inevitably going to happen.
Chapter II: Progress brings with it new expectations.
III.1. An ongoing search for better medicines.
III.2. Increase in longevity: A tremendous responsibility.
III.3. Representing the ingredients of life.
III.4. Driving the discovery of genes associated with a host of common diseases.
III.5. How does a stem cell decide what specialized identity to adopt?
III.6. Stem cell future shaped by epigenetics.
III.7. Jumonji enzymes and cell regulation.
III.8. Generating cancer stem cells for study purposes.
III.9. Accurate and effective cell division is one of the most critical of all life functions.
III.10. The importance of Apc and its role in switching off Wnt signaling.
III.10. Test of maturity for stem cells.
III.11. CD133 stem cells can initiate metastatic disease and could redirect cancer research.
III.12. More cancer stem cell discoveries.
III.13. Understanding the association of autophagy with cell death.
III.14. Unequivocal demonstration that tumor blood vessel cells are far from normal.
III.15. Studying telomerase.
III.16. Battling cancer, one cell at a time.
III.17. Cancer cells: uncovering their cover.
Chapter III: Genes, genes, genes...
IV.1. The relevance of small RNA molecules for gene regulation.
IV.2. Novel Inhibitor of Human microRNA: Discovery points to new avenue for cancer treatment.
IV.3. Engineering RNA for medical purposes.
IV.4. A role for dueling RNAs.
IV.5. RNAi shows promise in gene therapy.
IV.6. Fighting cancer with siRNAs.
IV.7. siRNA therapeutic candidate CALAA-01.
IV.8. ddRNAi technology.
IV.9. An expressed interfering RNA (eiRNA) approach.
IV.10. siRNA delivery into human T cells and primary cells with carbon-nanotube transporters.
IV.11. ncRNA and its ability to block a group of genes of the HOX family: another novel therapeutic strategy.
IV.12. Studying HOX expression patterns...finding ncRNAs influence on gene expression
patterns at distant locations.
IV.13. Characterizing the aggressiveness of cancer cells.
IV.14. Understanding genome stability in humans.
IV.15. Regulation of the nuclear architecture of the cell fails..
IV.16. Visualization of the structure of topo II as a help in the development of anticancer
medicines.
V.17. Fixing broken DNA
IV.18. The role of XPD in cancer and aging.
IV.19. A new approach to modelling RNA structure.
IV.20. Reintroducing miR-200 into late cancer cells.
IV.21. Paving the way for the future of identifying proteins inside cells.
IV.22. The dream of personalized medicine may be on the verge of being expanded beyond the
wealthiest of nations with state-of-the-art clinics.
IV.23. Revolutionary progress in biomedical science changes paradigm of discovery and
development.
Chapter IV: Nanotech fights cancer.
V.1. Nanotechnology promises to have a profound impact on society. The benefits of
nanomedicine.
V.2. NIH Nanomedicine Roadmap.
V.3. New drug-delivery system using nanomaterials.
V.4. Nanoparticles and Liposomes
V.5. Tumor-targeting capability of nanoparticles.
V.6. Developing nanomedicine techniques for cancer medicines delivery.
V.7. Using nanotechnology to localize and control drug delivery.
V.8. A new nanoparticle-approach to treating intractable tumors.
V.9. Nanocytes.
V.10. Delivering light-activated medicines to tumors.
V.11. Nanobialys.
V.12. “Cargo ships”: Constructing the next generation of smart tumor-targeting nanodevices.
V.13. Nanorods.
V.14. Medicines are most helpful when they directly affect the diseased organs or cells.
V.15. Nanoparticles: shape matters
V.16. Implanted magnetic sensing.
V.17. Magnetic nanocrystals carry and release anticancer agents.
V.18. Human cells as delivery vehicles for anti-cancer gene therapy.
V.19. Increasing the in-vivo lifetime of polymeric nanoparticles.
V.20. Nanobodies: the race to develop a new class of drugs.
Chapter V: Unlocking the mysteries of cancer: curious scientists.
VI.1. Results of new treatments in phase III trials compared with standard treatments.
VI.2. Research progresses by continuously putting itself into question.
VI.3. Molecular 'cages' to deliver medicines.
VI.4. One more step closer to tailor-made molecular medicine for patients.
VI.5. Microarrays: Making a family tree for disease.
VI.6. Microarrays: cancer to get personal.
VI.7. Tackling diseases influenced by different types of T cells.
VI.8. Specifically killing tumor cells by harnessing the power of P53.
VI.9. The missing piece of the puzzle that explains how p53 can inhibit the mTOR pathway and
thereby negatively regulate cell growth.
VI.10. Nutlin-3a can activate the cancer suppressor gene p53.
VI.11. Using bi-functionalized dendrimers to discover disease-causing proteins.
VI.12. Quantum dots and quantum rods.
VI.13. lipidomic based therapeutics.
VI.14. Cyclomodulins.
VI.16. The naturally occurring enzyme Fbx4 and its role in early stages of cancer.
VI.17. Altering lymphocytes, a new type of gene therapy.
VI.18. A cell surface profiling technique with potential for science to create a simple blood test for detecting the onset of cancer.
VI.19. The potential of antidepressants for cancer.
VI.20. Breaking the mucus barrier.
VI.21. The importance of interactions between tissue types.
VI.21. How do infections and toxins launch a cell's self-destruct and alarm system?
VI.22. Notch inhibitors.
VI.23. Combining innovative radiation techniques with translational research.
VI.23.1 Image guided Radiotherapy.
VI.23.2.Stereotactic Body radiotherapy (SBRT) in advanced lung cancer as an adjunctive to
pharmaceutical treatment.
VI.23.3.Inhibition of the PI3-kinase/AKT/mTOR axis during Radiotherapy.
VI.24. Long-lived rodents may know a cure for cancer.
VI.25. Needle-track device to locate the exact position of tumors during treatment.
VI.26. Of mice and men: tumorgrafts.
VI.27. When a bodyguard protein turns into an assassin.
VI.28. What happens when the Scribble protein is missing?
VI.29. A challenge to the fundamental tenet of cancer biology.
VI.30. New discovery about growth factor can open up an entirely new landscape for future
research.
Chapter VI: The cost of hope: Ethics and solidarity vs. economics of care.
VII.1. A burning issue to society.
VII.2. The cost of patient time associated with cancer care.
VII.3. Healthcare as a human right.
VII.4. Rational drug therapy.
VII.5. Challenges to health and equity.
VII.6. The dictate of economics.
VII.7. Is ‘efficiency’ synonymous with ‘economy’?
VII.8. The “consequences” of individual responsibility.
VII.9. Americans: paying more for getting less.
VII.10. The price of solidarity: Everyone wants the best available medical treatment, provided
someone else pays for it.
VII.11. An infantilizing social democratic grip on the active individual.
VII.12. The time has come to abandon disease as the focus of medical care.
VII.13. The overlooked economic impact of two types of health improvements.
VII.14. The reimbursement issue of new cancer therapies
VII. 15. Access to cancer care will depend on cost and political will.
Chapter VII: Accelerating the progress across cancer research and drug delivery.
VIII.1. Clinical development times are increasing.
VIII.2. Winning medicinal product approval: increasingly stringent regulatory requirements.
VIII.3. A new generation clinical trials to save time and money, improve patient care.
VIII.4. Shorter effective patent protection time.
VIII.5. Using the tools and concepts of the last century to assess this century’s drug candidates.
Chapter VIII: Constraining tumor progression. There is no “one cure for all” in cancer treatment.
IX.1. Tumorigenesis.
IX.2. Drivers and Passengers on the Road to Cancer.
IX.3. An essential precursor for targeted medicines.
IX.4. Advances in diagnosing infections and tumors.
IX.5. Screening tools.
IX.6. Progress in oncogenics.
IX.7. A veritable pandemic.
IX.8. Natural selection as a driver of the evolution of cancer?
IX.9. Valuable insights into how cancer cells develop and mutate.
IX.10. How molecules out of balance lead to human multiple myeloma and other cancers.
IX.11. The aging population...chances of surviving a death sentence. Will cancer screening help?
IX.12. New types of cancer treatments.
IX.13. Scientific research efforts stimulates hope for new targeted medicines.
IX.13.1.Opening a window on new therapeutic strategies.
IX.13.2.A new way to control cell growth, potential targets for cancer treatments.
IX.14. The level of a gene and its protein (RBM3) in cancerous cells.
IX.15. Understanding tumor growth in cancer: an interdisciplinary approach.
IX.16. Which pathways to target?
IX.17. Ensuring that the novel therapeutic modality will achieve its full potential.
IX.18. A promising therapeutic field to the medical research community.
IX.19. A highly innovative drug that continues to surprise.
IX.20. Disrupting the balance of cellular signals.
IX.21. Targeted cancer cells have the tendency to fight back...
IX.22. Molecularly targeted therapies.
IX.23. Regulatory risk-benefit evaluation vs. pharmaceutical industry’s use of surrogate
endpoints for clinical efficacy…
IX.24. Efficacy criteria.
IX.25. Access to cancer therapy in various geographies.
IX.26. Finding the mechanism by which cells resist chemotherapy.
IX.27. Chemotherapy drugs often never reach the tumors they're intended to treat...
IX.28. Why chemo works for some people and not others: predicting individuals' responses.
IX.29. New synthetic molecules appear to be synergistic with chemotherapeutic drugs, while
having no toxic effects on normal tissue.
IX.30. Many chemotherapeutic drugs which are used to cure cancer are themselves powerful
carcinogens that can also cause cancer.
IX.31. From cytotoxic to cytostatic.
IX.32. Fragmentation of the oncology therapeutic treatment segment.
IX.33. A huge unmet need for oncology drugs with prolonged survival rates.
IX.34. Mathematics driven oncology research.
Chapter IX: Fighting cancer: The battle intensifies.
X.1. Angiogenesis: a promising new approach to cancer treatment?
X.2. Bevacizumab (Avastin): first in class; first line indications.
X.3. Chemotherapy-stimulated tumor recovery impeded by anti-angiogenic medicines.
X.4. VEGF: new medicines development.
X.5. Angiocept (CT-322)
X.6. Axitinib (AG-013736)
X.7. Vargatef (BIBF-1120)
X.8. CDP-791
X.9. E7080
X.10. IMC-1121b
X.11. Motesanib diphosphate (AMG 706)
X.12. OSI-930
X.13. Pazopanib
X.14. PTC-299
X.15. Recentin (Cediranib, or AZD2171)
X.16. Vatalanib
X.17. Aflibercept (VEGF-Trap)
X.18. Vandetanib (Zactima)
X.19. Sorafenib (Nexavar) targets two important processes that enable cancer growth.
X.20. TKI1258, an oral, multitargeted receptor tyrosine kynase inhibitor.
X.21. Sunitinib: counting on new evidence to support the routine use of systemic treatment.
X.22. RAF265 inhibits VEGFR2, and also RAF kinases.
X.23. Cost effectiveness of sunitinib vs. other treatments.
X.24. mTOR inhibitors Temsorilus, Deferolimus (AP23573)
X.25 Temsorilus (Torisel): superior therapy vs. Cytokines in first-line therapy of RCC.
X.26. Deferolimus (AP23573)
X.27. Everolimus (RAD001): blocking mTOR, a central regulator of cancer-cell growth and
metabolism.
X.28. OSI-027
X.29. Combining mitogen-activated protein kinase inhibitors MTORC1 Inhibitors.
X.30. Syndecan-4 appears to activate mTORC2.
X.31. Changes in the PI3K-mTOR Pathway.
X.32. Targets to go after in humans to improve “health span” in a person’s life.
X.33. Selective MMP inhibitors BMS 275291, BAY12-9566, Marimastat, Prinomastat.
X.34. Integrin inhibitors Vitaxin and Cilengitide.
X.35. Signal transduction inhibitors.
X.36. Cetuximab (Erbitux): especially effective when used in combination with other therapy
forms.
X.37. Erlotinib (Tarceva) reversibly and selectively inhibits tyrosine kynase activity.
X.38. Gefitinib (Iressa): a once a day pill designed to shrink tumors without the side effects of
chemotherapy.
X.39. Panitumumab (Vectibix, ABX-EGF): the 1st fully human monoclonal antibody to target the
EGFr.
X.40. Nimotuzumab
X.41. Bavituximab’s specific tumor blood vessel targeting properties.
X.42. Lapatinib (Tykerb, GW-572016): the ability to cross the blood-brain barrier.
X.43. U3-1287, a fully human HER3 antibody, becomes a promising novel first-in-class HER
familyinhibitor.
X.44. Dasatinib (Sprycel, BMS 354825).
X.45. Bosutinib (SKI606).
X.46. Farnesyltransferase inhibitor Tipifarnib (Zarnestra), lonafarnib (Sarasar): making
chemotherapy more effective.
X.47. Proteasome inhibitor Bortezomib: showing impressive activity in patients with relapsed
multiple myeloma.
X.48. Signal transductor inhibitors: bexaroten (targretine), perifosine (KRX0401).
X.49. Apoptosis stimulators: oblimersen (Genasense), aprinocarsen (Affinitak, Isis 3521, LY900003),
exisulind (Aptosyn).
X.50. Cell cycle regulators: Seliciclib (CYC-202; R-roscovitine), Indisulam (E-7070), UCN –01.
X.51. Monoclonal antibodies targeting unprecedented receptors: MLN2704, ibritumomab (Zevalin).
Chapter X: Exploring intelligent investigational treatment options.
XI.1. Tovok (BIBW2992)
XI.2. Alvocidib (Flavopiridol, HMR1275),
XI.3. Bryostatin1 (NSC339555),
XI.4. Depsipeptide (FK 228),
XI.5. Denosumab
XI.6. AMG 655: Targeting apoptosis via death receptors.
XI.7: AMG 479, targeting growth regulation in cancer.
XI.8 An investigational HGF/SF:c-Met therapy.
XI.9. Lomeguatrib (Patrin-2)
XI.10. Cortistatin A
XI.11. Azixa (MPC6827)
XI.12. Ipilimumab
XI.13. Adecatumumab (MT201)
XI.14. Mapatumumab (HGS-ETR1) and the TRAIL-receptor antibody program.
XI.15. Pioneering work: scientists sequence the genome of leukemia cells.
XI.16. IMC-A12, IMC 1121B
XI.17. MAGE-A3 ASCI
XI.18. Epratuzumab
XI.19. PI-88
XI.20. Catumaxomab (Removab): trifunctional antibody therapy.
XI.21. WX-G250 (Rencarex)
XI.22. Mesupron
XI.23. Panzem (2ME2)
XI.24. Combretastatin A4 Prodrug
XI.25. Fosbretabulin (Zybrestat),the first therapeutic product in a novel class of vasucular
disrupting agents (VDAs).
XI.26. Tavocept (dimesna)
XI.27. Dual mechanism anti-cancer therapeutic 3PO
XI.28. Vasostatin-Apo2L
XI.29. MORAb-009, a monoclonal antibody to mesothelin.
XI.30. Karenitecin
XI.31. PPM1D inhibitors (protein phosphatase magnesium-dependent 1 d inhibitors).
XI.32. Angiolix
XI.33. EndoTAG-1
XI.34. P13K-C2alpha, an enzyme that sensitizes cells to chemotherapeutics, to become a potential new anti-cancer target.
XI.35. Silencing HSP proteins.
XI.36. AUY922 inhibits the ATPase activity of HSP90.
XI.37. Motesanib Diphosphate.
XI.38. Trabectedin
XI.39. Oral CP-4126, a novel Lipid vector Technology analogue of gemcitabine.
XI.40. Panobinostat, potent pan-DAC inhibitor-targeting epigenetic and multiple oncogenic
pathways.
XI.41. Pazopanib
XI.42. Tasigna, a next-generation tyrosine kinase inhibitor.
XI.43. NTX-010, a tumor-selective oncolytic virus for the treatment of neuroendocrine cancer.
XI.44. Elesclemol, killing cells by elevating oxidative stress levels.
XI.45. Degarelix
XI.46. Apomab
XI.47. NuBCP-9 peptide.
XI.48. Prolarix, targeted combination chemotherapy.
XI.49. Vitor and cachexia in cancer
XI.50. Natural THIAA analogs found to be potent and selective, multi-target, protein kinase
inhibitors.
XI.51. Testing Benzoylphenylurea (BPU) against Biomerk Tumorgrafts: Enhancing the value of
oncology medicines.
XI.52. Lumiliximab
XI.53. AP 12009, a TGF-beta 2 inhibitor.
XI.54. EPO906 (Patupilone)
XI.55. Differentiation therapy of cancer: developing HDAC inhibitors as anti-cancer drugs.
G2M777, suberanilohydroxamic acid, LBH589, Romidepsin, Pivanex, belinostat, MGCD0103.
XI.56. HDAC Inhibitor MGCD0103 in Hodgkin's lymphoma, Myelodysplastic Syndromes and acute
myelogenous leukemia.
XI.57. Cooperation response genes.
XI.58. Making cancer vulnerable to “good” viruses.
XI.58.1. Oncolytic Virus CG0070.
XI.58.2. AdD24-RGD
XI.58.3. OncoVEXGM-CSF
XI.58.4. HSV1716
XI.58.5. Reolysin
XI.59. A Brain Tumor Drug Derived From Herpes Virus?
XI.60. Safer virus therapy as a possible cancer treatment with the help of microRNAs.
Chapter XI: Cancer of female reproductive organs -- breast, ovary and uterus
XII.1. Breast cancer
XII.2. Risk factors, key predictors.
XII.3. SATB1. A nuclear protein that triggers aggressive breast cancer.
XII.4. Tissue geometry in breast cell invasion.
XII.5. A landmark therapeutic.
XII.6. Trastuzumab (Herceptin), Lapatinib (Tykerb) target breast cancer stem cells.
XII.7. Tumor cell resistance to Trastuzumab (Herceptin).
XII.8. Which women with breast cancers will respond to tamoxifen, and which will not.
XII.9. Regulating the effectiveness of Taxol chemotherapy.
XII.10. New evidence that breast cancer can derive from stem cells.
XII.11. A protein in embryonic stem cells may have potential to prevent metastasis.
XII.12. Genes set scene for metastasis.
XII.13. Increasing potential of the E1A Gene: found to downregulate HER2/neu gene, and... having powerful anti-tumor activity.
XII.14. Combining Paclitaxel with albumin to deliver the chemotherapy.
XII.15. No two patients are identical. Each cancer has a different blueprint.
XII.16. New research results explain the recurrence of breast cancer tumor cells; why dormant
tumor cells become active in later years.
XII.17. Reverting cancer cells back to a pre-malignant state.
XII.18. Genetic signature predicts recurrence of cancers.
XII.19. Variation in the Caspase 8 gene.
XII.20. ‘Switching off’ a molecule, a key player in the molecular processes that trigger breast
cancer.
XII.21. A novel cellular mechanism may guide cell movement and possibly cancer invasion.
XII.22. Cancer screening: Improving anatomical imaging that targets the most lethal cancer
subtypes.
XII.23. New treatments in breast cancer: predictions.
XII.24. DeCODE, a genetic test to screen for risk of the common forms of breast cancer.
XII.25. Tailoring the therapy to the cancer.
XII.26. A potential new way for stopping tumor proliferation.
XII.27. Ovarian cancer.
XII.28. Ovarian cancer’s deadly secrets.
XII.29. RNA splicing factor implicated in ovarian tumor cell growth.
XII.30. A new culprit in cancer metastase.
XII.31. Cervical cancer.
XII.32. A novel PARP inhibitor in uterine cancer.
Chapter XII: Kidney cancer, prostate cancer: complex diseases
XIII.1. Kidney cancer.
XIII.2. A molecule that kills kidney cancer cells.
XIII.3. Derived from each individual’s tumor, Vitespen (Oncophage) reprograms the body’s
immune system to selectively target cancer cells.
XIII.4. Prostate cancer.
XIII.5 The Ras-like small GTPase, Rheb, is directly involved in prostate tumorigenesis.
XIII.6. Screening.
XIII.7. The metronomic dosing method as part of a therapeutic prostate cancer vaccine strategy.
XIII.8. Mapping of prostate cancer genes opens the door to new treatments.
XIII.9. Proton Therapy.
XIII.10. Advances in predicting the probability of developing prostate cancer.
XIII.11. Therapy options.
XIII.12. Provenge, GVAX.
Chapter XIII: When cells in the gastro-intestinal system run amok.
XIV.1. Colorectal cancer
XIV.2. The sign for progression of colorectal carcinoma.
XIV.3. Improving median survival rates.
XIV.4. Genetic testing can predict treatment response in CRC.
XIV.5. Listen to warning signs: Skin cancer may be just the first sign of colorectal cancer.
XIV.6. Potential for bispecific antibodies containing two different binding sites?
XIV.7. Regional differences in treatment preferences.
XIV.8. One more step towards a future of genetic testing.
XIV.9. Photodynamic diagnosis.
XIV.10. Peritoneal surface disease from colorectal cancer: the surgical removement option.
XIV.11. Colon cancer: gut bacterium’s involvement.
XIV.12. Early detection with new medical imaging.
XIV.13. Identification of genetic predictors of esophageal cancer.
XIV.14. Pancreatic cancer.
XIV.15. A powerful new approach to validate linkages between suspect genes and their functional contributions to liver cancer.
XIV.16. New “suicide gene” delivery approach offers potential for novel therapy.
XIV.17. TGF-beta 2 inhibitoren in pancreatic carcinoma and in other cancer types.
XIV.18. Triptolide will be the first pancreatic cancer-specific agent tested in nearly a quarter
century.
Chapter XIV: Head and Neck, Lung, Brain cancers: feverishly expecting breakthrough treatments.
XV.1. Head and neck cancer.
XV.2. More treatment options emerge as risks evolve.
XV.3. Lung cancer.
XV.4. Genetic predisposition to lung cancer.
XV.5. Lung cancer's molecular complexities: the big picture perspective opens door to
individualized treatment strategies.
XV.6. Treatment regimes.
XV.7. Is there an alternativ to cisplatin in the first-line treatment of lung cancer?
XV.8. Extension of patient survival.
XV.9. Cancer stem cells looking and behaving like normal stem cells...
XV.10. Molecular profiling of lung cancer.
XV.11. New antibody for EGFR causes lung cancer regression.
XV.12. Bcl-2 Family Protein Inhibitors.
XV.13. MAGE-A3 cancer immunotherapy.
XV.14. Prognostic tool to alter clinical decision making.
XV.15. The type of NSCLC patients have may influence a treatment regimen and survival outcome.
XV.16. Increasing incidence of gliomas,the most frequent primary malignant brain tumors in adults.
XV.17. Switch for Programmed Cell Death Promotes Spread of Glioblastoma.
XV.18. Treatment of glioblastoma multiforme.
XV.19. miR-21 in glioblastoma multiforme.
XV.20. Genetic therapy in the fight against brain tumors.
XV.21. Amphinase.
XV.22. The origin of medulloblastomas, the most malignant type of brain tumor.
XV.23. Medulloblastomas: The cell type in which a mutation happens is as important as the
mutation itself.
XV.24. Biomarker brain tumors.
Chapter XV: Biomarkers: A key to 21st century personalized cancer care.
XVI.1. The discovery of biomarkers: undervalued and under-funded.
XVI.2. Biomarkers: greatly accelerating basic and translational research.
XVI.3. Glycobiology of cancer: The search for glycan-based biomarkers.
XVI.4. The Oncology Biomarker Qualification Initiative (OBQI).
XVI.5. Testing EGFR as biomarker for non small lung cancer drug response.
XVI.6. A model to find blood biomarkers that estimate tumor size.
XVI.7. Predictive Biomarker development: Signaling pathways.
XVI.8. Microvessel Vascular (MVV) : guiding the use of new-generation angiogenesis-inhibiting
medicines.
XVI.9. Research technology for gene expression analysis.
XVI.10. Moving medicine from a curative model of today to a preemptive era.
XVI.11. Evaluating FDG-PET as a potential predictive biomarker of tumor response and patient
outcome.
XVI.12. NSBCC research concept.
XVI.13. Moving the practice of oncology from a reactive discipline to a predictive, preventive
and personalize modes.
XVI.14. Development of more effective immunitherapy approaches for cancer.
XVI.15. Improve Position Emission Tomography (PET) allowing for smaller tumors and lower
concentration disease targets to be detected.
XVI.16. Finding molecularly-based biomarkers that define disease progression, the initiating
oncogenic lesion and response to therapy.
XVI.17. Optimize and validate microfluidics integrated nanoelectronic sensors as a diagnostic tool
for cancer.
XVI.18. Revealing genetic activity of tumors.
XVI.19. Detecting key mutations in tumors.
XVI.20. Assessing all of the important genomic changes involved in cancer.
XVI.21. Genetic profiling to lead to better medicine.
XVI.22. Identifying individuals who require therapy.
XVI.23. A new era in cancer research.
List of tables/figures:
1. Reshaping the “traditional” healthcare model.
2. Towards maximum individualized patient care.
3. Transforming medicine.
4. The promise of genomics.
5. New medicines discoveries account for longer lives.
6. Drug targets
7. Diseases associated with genes in the extended MHC.
8. microRNAs present a new therapeutic approach.
9. Biochemical classes of drug targets of current therapies.
10. Type of RNA compounds.
11. The nucleolus resides within the cell nucleus, surrounded by heterochromatin.
12. The cell nuclei of Su(var)3-9 mutants exhibit multiple irregular nucleoli.
13. The formation of extrachromosomal DNA and multiple nucleoli.
14. DNA may compress and extend more than previously thought possible.
15. The binding an cleavage core of topo II interacting with DNA.
16. Two-gate model of topo II.
17. A cell nucleus after radiation by high-energy particles similar to those in cosmic rays.
18. The four domains of XPD.
19. The topology of XPD.
20. Reading DNA/RNA microarrays.
21. Molecular approach.
22. Medicines: from the past to the future.
23. The shift towards personalized medicine.
24. Polymer micelle.
25. Cancer medicine paclitaxel enters a cancer cell.
26. Nano mother ships: what they look like.
27. The speed of discovery.
28. Antibody engineering technologies that will be used in the coming years.
29. NCI Division of Cancer Prevention: Number of clinical trials by phase and fiscal year.
30. Profiling mucin-type O-linked glycoproteins.
31. Needle-size device to track tumors.
32. From phenotype to genotype.
33. New medicines development: the time it takes.
34. Average clinical development times selected by therapy area.
35. The new drug development process.
36. Expensive high technology drives the Research and Development process.
37. The time it takes to bring a substance to market and get a return on investment.
38. Making Medicines.
39. The changing medicinal discovery process.
40. Cancer is a disease of the genes.
41. DNA sequence from, top, normal and, bottom, cancer tissue from a case of
non-small-cell lung cancer (NSCLC).
42. Cancer theory timeline.
43. Cancer pathologies (selected): incidence, mortality, prevalence, 5-year survival rate.
44. SEER Cancer Incidence and US Death Rates, 2000-2004. By Cancer Site and Race.
45. New tumor-fighting targets.
46. Antibody based oncology drugs, targets, molecular function.
47. Impact of information technology on the practice of health care.
48. Targeted signaling pathways that are being pursued in oncology drug Development.
49. New therapies: effective and predicted approval dates.
50. Chronology of the development of protein kinase inhibitors.
51. Cancer market share of targeted therapy 2005-2015.
52. Currently used chemotherapeutics.
53. Currently used hormonal therapies.
54. Benefits of chemotherapy.
55. Chronology of the various cytotoxic classes.
56. Cancer survival rate 2004-2008.
57. 5-year survival rate in breast cancer, by region.
58. Reduction in death rate from testicular cancer, by region.
59. Prediction of the cancer market 2010, 2015.
60. Economic importance of cancer antibodies.
61. Antitumor and antiangiogenic activity of TKI1258.
62. RAF265, an oral, potent inhibitor of RAF and VEGFR with a highly selective profile.
63. The role of EGFR in cancer. Proposed mode of action.
64. Protein kinase inhibitor drugs: clinical trials & cancer indications.
65. Blocking the mammalian target of rapamycin (mTOR) protein.
66. Mage-A3 expression in various cancer types.
67. Blocking tumor growth by inhibiting heat shock protein 90 (HSP90).
68. pan-DAC inhbitor activity of LBH589: multiple effects in tumor cell lines.
69. Inducing cell death through microtubule stabilization.
70. HDAC inhibitors.
71. Viruses involved in Virotherapy research.
72. SATB1 and the promotion of the expression or suppression of genes.
73. The effect of reducing the expression of SATB1 in metastatic breast cancer cells.
74. Visualization of how branching morphogenesis in breast cancer is determined by tubule
geometry.
75. Breast cancer therapy market opportunities, as the medical industry sees it.
76. Showing promise in the treatment of cancer.
77. Superior survival with Xeloda/Taxotere.
78. Targeted Breast Cancer Therapies.
79. Improved cancer screening.
80. Attacking cancer on all fronts.
81. HPV vaccines’ commercial success forecast 2010.
82. Compact proton therapy concept.
83. Current treatments in colorectal cancer.
84. Treatment preferences in metastatic setting.
85. Lung cancer cell division.
86. The seven Tumor Glycome Laboratories projects.
87. Marvel study.
Edition Notes
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- Created November 23, 2010
- 6 revisions
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| September 15, 2012 | Edited by VacuumBot | Updated format 'hardcover' to 'Hardcover' |
| October 16, 2011 | Edited by Michèle Varda | The author is Gilbert Mertens, not Stefan Lievens |
| November 23, 2010 | Edited by Edith Leclercq | Edited without comment. |
| November 23, 2010 | Edited by Edith Leclercq | Added new cover |
| November 23, 2010 | Created by Edith Leclercq | Added new book. |