Advances in Cancer Research ( Volume 121 )

Publication series :Volume 121

Author: Tew   Kenneth D.;Fisher   Paul B.  

Publisher: Elsevier Science‎

Publication year: 2014

E-ISBN: 9780128003176

P-ISBN(Paperback): 9780128002490

P-ISBN(Hardback):  9780128002490

Subject: R73 Oncology

Language: ENG

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Description

Advances in Cancer Research provides invaluable information on the exciting and fast-moving field of cancer research. Here, once again, outstanding and original reviews are presented on a variety of topics.

  • Provides information on cancer research
  • Outstanding and original reviews
  • Suitable for researchers and students

Chapter

4.1. Regulation of DNA methylation by K27 and G34 H3F3A mutations

4.2. Chromosome and Myc aberrations in H3F3A mutant glioblastoma

4.3. Delineating the cell of origin for K27 and G34 H3F3A mutant glioblastoma

5. Gliomagenesis and Mutations in Isocitrate Dehydrogenase Genes

5.1. Models of IDH-mutant gliomas

5.2. Glial progenitor-origin for IDH-mutant gliomas

6. Proneural-to-Mesenchymal Transition in Glioma

6.1. Mesenchymal phenotype as a function of glioma subgroup

6.2. Transcriptional master regulators of PMT in glioma

6.3. Influence of the tumor microenvironment on the mesenchymal phenotype

7. Relationship Between GSCs and Glial Progenitors

7.1. Polycomb gene family

7.2. NOTCH

7.3. Sonic hedgehog

7.4. Wingless

8. Targeted Therapy in Glioma

8.1. Epidermal growth factor gene family

8.2. Targeting the proneural subgroup by PDGFR inhibition

8.3. Targeting the mesenchymal phenotype through c-MET inhibition

8.4. Treatment-resistance associated with RTK inhibition

8.4.1. RTK cooperativity

8.4.2. Redundant activation of PI3K/mTOR

8.4.3. Feedback loops

8.4.4. Activation of alternative survival pathways

8.5. Therapeutic targeting of IDH-mutant gliomas

9. Concluding Remarks and Future Perspectives

Acknowledgments

References

Further Reading

Chapter Two: Therapeutic Cancer Vaccines

1. Introduction

2. Cancer Vaccine Targets

3. Spectrum of Current Therapeutic Cancer Vaccine Platforms

3.1. An example of optimizing vaccine potency

3.2. Vaccine/vaccine combinations

4. Animal Models to Evaluate Cancer Vaccines: Pros and Cons

5. Types of Immunotherapy

5.1. Vaccine therapy and adoptive T-cell transfer: A study in contrasts

6. The Importance of Antigen Cascade in Vaccine-Mediated Therapeutic Responses

7. TRICOM-Based Vaccines: Clinical Studies

8. Prostate Cancer Clinical Trials

8.1. PSA-TRICOM (PROSTVAC) studies

8.2. Vaccines and tumor growth rates

8.3. A case report: Analysis of a prostate cancer patient over an 18-year period

9. Vaccine Combination Therapies

10. Combination Therapies-Preclinical Studies

10.1. Vaccine and radiation synergy

10.2. Vaccines in combination with chemotherapy

10.3. Vaccine in combination with small molecule targeted therapies

10.4. The effect of nonimmune therapeutic interventions on immune cells

11. Influence of the Tumor Microenvironment and Immunosuppressive Factors

12. Vaccine Combination Therapies—Clinical Studies

13. Biomarkers

14. Vaccine Targets Involved in Tumor Progression and Drug Resistance

15. Concluding Remarks

References

Chapter Three: IKK/Nuclear Factor-kappaB and Oncogenesis: Roles in Tumor-Initiating Cells and in the Tumor Microenvironment

1. Introduction

1.1. NF-κB family members

1.2. NF-κB regulation

1.3. NF-κB-independent functions for IKK

1.4. NF-κB and cancer

2. Tumor Microenvironment

2.1. Background on the tumor microenvironment

2.2. NF-κB and tumor-associated macrophages

2.2.1. Macrophage phenotypes

2.2.2. NF-κB and TAMs

2.2.3. Noncanonical NF-κB signaling in TAM promotion of cancer

2.2.4. Tumor inhibiting role for NF-κB signaling in the tumor microenvironment?

2.3. NF-κB and tumor-associated T lymphocytes

2.4. NF-κB promotes recruitment of regulatory T lymphocytes in lung cancer

2.5. NF-κB and cancer-associated fibroblasts

3. TICs/Cancer Stem Cells

3.1. TICs and NF-κB

3.2. TICs, cytokines, and tumor microenvironment

4. Conclusions

Acknowledgments

References

Chapter Four: The Rb–E2F Transcriptional Regulatory Pathway in Tumor Angiogenesis and Metastasis

1. Introduction

2. Rb–E2F Pathway in Angiogenesis

2.1. E2F-mediated regulation of vascular endothelial growth factor

2.2. Rb-E2F and Id proteins in angiogenesis

2.3. Rb and HIF-1α

2.4. E2F-mediated transcriptional regulation of angiogenic factors and their receptors

2.5. Raf-1-mediated inactivation of Rb contributes to VEGF-induced angiogenesis

2.6. Atypical E2Fs and angiogenesis

2.7. E2Fs in miRNA-mediated regulation of angiogenesis

3. Rb–E2F Pathway and Tumor Metastasis

3.1. Expression of Rb and E2F in metastatic cancers

3.2. Rb and E2F in metastasis-Mouse models

3.3. Rb- and E2F-mediated regulation of metastatic properties of cancer cells

3.4. Rb-E2F pathway in cancer stem cells

3.5. Rb-E2F pathway in energy metabolism

4. Conclusions

Acknowledgments

References

Chapter Five: ATP-Dependent Chromatin Remodeling Complexes as Novel Targets for Cancer Therapy

1. Introduction-The Importance of Gene Expression to Cancer Biology

2. An Overview of Epigenetic Regulatory Mechanisms

3. ATP-Dependent Chromatin Remodeling

4. Evidence of Widespread Roles for Chromatin Remodeling in Human Cancer

5. A Review of the Literature on Chromatin Remodeling and Cancer

5.1. SWI/SNF family of chromatin remodeling complexes

5.1.1. BRG1/BRM

5.1.2. INI1

5.1.3. ARID1A

5.1.4. BAF180

5.1.5. BAF53/BAF57

5.2. INO80 family of chromatin remodeling complexes

5.2.1. TRAAP/p400

5.2.2. INO80

5.2.3. RUVBL1/RUVBL2

5.3. CHD family of chromatin remodeling complexes

5.3.1. CHD3/CHD4

5.3.2. MTA1

5.3.3. HDAC1/HDAC2

5.3.4. MBD2

5.3.5. pRBAP48

5.3.6. CHD5

5.3.7. CHD1/CHD2/CHD7

5.4. ISWI family of chromatin remodeling complexes

5.4.1. SNF2H/SNF2L

5.4.2. BPTF

5.4.3. RSF1

6. Therapeutic Potential of Chromatin Remodeling Complexes in Human Cancer

7. Concluding Remarks

Acknowledgments

References

Chapter Six: Diffuse Intrinsic Pontine Gliomas

1. Introduction

2. Diagnosis

3. Historical Perspectives

4. Current Treatments

5. Recent Developments

5.1. Diagnosis and prognosis

5.2. Molecular analysis

5.3. Therapeutic approaches

6. Conclusion

References

Chapter Seven: In Vivo Modeling of Malignant Glioma: The Road to Effective Therapy

1. Introduction

2. Malignant Glioma

3. Notable Aberrant Signaling Pathways in Malignant Glioma

3.1. Activating kinases

3.1.1. EGFR/EGFRvIII

3.1.2. Platelet-derived growth factor receptor

3.1.3. c-Met

3.1.4. Src-family kinases

3.1.5. PI3K-related signaling

3.2. Tumor suppressor pathways

3.2.1. PTEN

3.2.2. NF1

3.3. IDH mutations

4. Molecular Classification of GBM

5. Progression of Glioblastoma

5.1. Invasion

5.2. Angiogenesis

6. Introduction to Animal Modeling in Glioma

7. Non-Mammalian Models of Glioma

7.1. Drosophila

7.2. Zebrafish

8. Mammalian Models of Glioma

8.1. Rat

8.2. Mouse

8.2.1. Tumor implantation techniques

8.2.2. Syngeneic mouse models

8.2.3. GEM models

8.2.4. Approaches to mouse modeling of glioma

8.2.4.1. Loss or inhibition of key tumor suppressors

8.2.4.2. Expression of oncogenes

8.2.4.3. Somatic gene transfer by viral vector

8.2.5. Investigating glioma pathology

8.2.5.1. Stromal interactions

8.2.5.2. Cell of origin

8.2.5.3. Modeling interplay between standard and novel therapies

9. Conclusions and Future Perspectives

Acknowledgments

References

Chapter Eight: Genetically Engineered Mice as Experimental Tools to Dissect the Critical Events in Breast Cancer

1. Introduction

1.1. Development of the mouse mammary gland and human breast

1.2. Genetically engineering mouse models of breast cancer

1.3. Mammary-specific promoters

2. Modeling Various Aspects of Human Breast Cancer Initiation and Progression in Mice

2.1. Modeling effects of oncogenes on cell proliferation, survival, and apoptosis in breast cancer

2.1.1. c-Myc transgenic models

2.1.2. v-Ha-ras transgenic models

2.1.3. Cyclin D1 transgenic and knockout models

2.1.4. TGFα transgenic models

2.1.5. SV40 T antigen transgenic models

2.2. Modeling breast tumor metastasis

2.2.1. ERBB2/NEU transgenic models

2.2.2. EGFR transgenic models

2.2.3. PyVmT transgenic models

2.2.4. Wnt transgenic models

2.3. Modeling angiogenesis through the vascular endothelial growth factor family

2.3.1. VEGF transgenic models

2.4. Modeling tumor suppression mediated by tumor suppressor genes

2.4.1. BRCA1 knockout models

2.4.2. p53 Transgenic and knockout models

3. Developing Novel Therapeutics and Imaging Techniques Using Transgenic Animals

3.1. Evaluating the use of novel therapeutics using transgenic animals

3.2. Imaging using transgenic animals

4. Conclusions and Future Perspectives

Acknowledgments

References

Chapter Nine: Life is Three Dimensional—As In Vitro Cancer Cultures Should Be

1. 3D Cell Culture Methods and Scaffolding Materials

1.1. Spontaneous cell aggregation into multicellular spheroids

1.1.1. Nonadhesive surface

1.1.2. External force

1.1.3. Liquid overlay

1.2. Natural and synthetic hydrogels

1.3. Natural and synthetic solid materials

1.3.1. Natural solid materials

1.3.2. Synthetic solid materials

2. Cell Morphology

3. Cell Proliferation

4. Cell Viability and Drug Metabolism Effects

5. Cell Response to External Stimuli

6. Differentiation

7. Cancer Stem Cells

8. Gene and Protein Expression

9. Future Perspectives

References

Index

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