Refractory mechanisms

Mototsugu Oya, Toshiaki Shinojima, Ryuichi Mizuno

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Vascular endothelial growth factor (VEGF)-targeted agents have brought significant progress in pharmacotherapy of advanced renal cell carcinoma (RCC). Some RCCs, however, appear to have innate resistance to treatment. Moreover, majority of patients who primarily respond to VEGF-targeted therapy eventually develop disease progression after prolonged treatment. The mechanism of resistance is supposed to be so multifactorial that it cannot be explained by single molecular events. Despite various factors including cytokines, bone marrowderived cells, microenvironment, and genetic or epigenetic abnormality could be involved, tumor hypoxia seems to play one of crucial roles in most of the processes. The multiple mechanism in developing drug resistance might just represent the diversity of cellular response to hypoxia and nutrient deprivation, induced by the disruption of the blood vessels. In this chapter we comprehensively review current efforts aiming to clarify these process and to develop pharmacological strategies leading to overcome the drug resistance in RCC.

Original languageEnglish
Title of host publicationRenal Cell Carcinoma
Subtitle of host publicationMolecular Features and Treatment Updates
PublisherSpringer Japan
Pages351-367
Number of pages17
ISBN (Electronic)9784431555315
ISBN (Print)9784431555308
DOIs
Publication statusPublished - 2017 Jan 1

Fingerprint

Refractory materials
Vascular Endothelial Growth Factor A
Drug therapy
Renal Cell Carcinoma
Drug Resistance
Blood vessels
Pharmaceutical Preparations
Nutrients
Cellular Microenvironment
Tumors
Bone
Cells
Cytokines
Epigenomics
Blood Vessels
Disease Progression
Therapeutics
Pharmacology
Bone and Bones
Drug Therapy

Keywords

  • Acquired resistance
  • Antiangiogenic therapy
  • Intrinsic resistance
  • Mechanisms of drug resistance
  • Renal cell carcinoma

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Oya, M., Shinojima, T., & Mizuno, R. (2017). Refractory mechanisms. In Renal Cell Carcinoma: Molecular Features and Treatment Updates (pp. 351-367). Springer Japan. https://doi.org/10.1007/978-4-431-55531-5_15

Refractory mechanisms. / Oya, Mototsugu; Shinojima, Toshiaki; Mizuno, Ryuichi.

Renal Cell Carcinoma: Molecular Features and Treatment Updates. Springer Japan, 2017. p. 351-367.

Research output: Chapter in Book/Report/Conference proceedingChapter

Oya, M, Shinojima, T & Mizuno, R 2017, Refractory mechanisms. in Renal Cell Carcinoma: Molecular Features and Treatment Updates. Springer Japan, pp. 351-367. https://doi.org/10.1007/978-4-431-55531-5_15
Oya M, Shinojima T, Mizuno R. Refractory mechanisms. In Renal Cell Carcinoma: Molecular Features and Treatment Updates. Springer Japan. 2017. p. 351-367 https://doi.org/10.1007/978-4-431-55531-5_15
Oya, Mototsugu ; Shinojima, Toshiaki ; Mizuno, Ryuichi. / Refractory mechanisms. Renal Cell Carcinoma: Molecular Features and Treatment Updates. Springer Japan, 2017. pp. 351-367
@inbook{2cc8965144d548179ee0df91c0bf4d30,
title = "Refractory mechanisms",
abstract = "Vascular endothelial growth factor (VEGF)-targeted agents have brought significant progress in pharmacotherapy of advanced renal cell carcinoma (RCC). Some RCCs, however, appear to have innate resistance to treatment. Moreover, majority of patients who primarily respond to VEGF-targeted therapy eventually develop disease progression after prolonged treatment. The mechanism of resistance is supposed to be so multifactorial that it cannot be explained by single molecular events. Despite various factors including cytokines, bone marrowderived cells, microenvironment, and genetic or epigenetic abnormality could be involved, tumor hypoxia seems to play one of crucial roles in most of the processes. The multiple mechanism in developing drug resistance might just represent the diversity of cellular response to hypoxia and nutrient deprivation, induced by the disruption of the blood vessels. In this chapter we comprehensively review current efforts aiming to clarify these process and to develop pharmacological strategies leading to overcome the drug resistance in RCC.",
keywords = "Acquired resistance, Antiangiogenic therapy, Intrinsic resistance, Mechanisms of drug resistance, Renal cell carcinoma",
author = "Mototsugu Oya and Toshiaki Shinojima and Ryuichi Mizuno",
year = "2017",
month = "1",
day = "1",
doi = "10.1007/978-4-431-55531-5_15",
language = "English",
isbn = "9784431555308",
pages = "351--367",
booktitle = "Renal Cell Carcinoma",
publisher = "Springer Japan",

}

TY - CHAP

T1 - Refractory mechanisms

AU - Oya, Mototsugu

AU - Shinojima, Toshiaki

AU - Mizuno, Ryuichi

PY - 2017/1/1

Y1 - 2017/1/1

N2 - Vascular endothelial growth factor (VEGF)-targeted agents have brought significant progress in pharmacotherapy of advanced renal cell carcinoma (RCC). Some RCCs, however, appear to have innate resistance to treatment. Moreover, majority of patients who primarily respond to VEGF-targeted therapy eventually develop disease progression after prolonged treatment. The mechanism of resistance is supposed to be so multifactorial that it cannot be explained by single molecular events. Despite various factors including cytokines, bone marrowderived cells, microenvironment, and genetic or epigenetic abnormality could be involved, tumor hypoxia seems to play one of crucial roles in most of the processes. The multiple mechanism in developing drug resistance might just represent the diversity of cellular response to hypoxia and nutrient deprivation, induced by the disruption of the blood vessels. In this chapter we comprehensively review current efforts aiming to clarify these process and to develop pharmacological strategies leading to overcome the drug resistance in RCC.

AB - Vascular endothelial growth factor (VEGF)-targeted agents have brought significant progress in pharmacotherapy of advanced renal cell carcinoma (RCC). Some RCCs, however, appear to have innate resistance to treatment. Moreover, majority of patients who primarily respond to VEGF-targeted therapy eventually develop disease progression after prolonged treatment. The mechanism of resistance is supposed to be so multifactorial that it cannot be explained by single molecular events. Despite various factors including cytokines, bone marrowderived cells, microenvironment, and genetic or epigenetic abnormality could be involved, tumor hypoxia seems to play one of crucial roles in most of the processes. The multiple mechanism in developing drug resistance might just represent the diversity of cellular response to hypoxia and nutrient deprivation, induced by the disruption of the blood vessels. In this chapter we comprehensively review current efforts aiming to clarify these process and to develop pharmacological strategies leading to overcome the drug resistance in RCC.

KW - Acquired resistance

KW - Antiangiogenic therapy

KW - Intrinsic resistance

KW - Mechanisms of drug resistance

KW - Renal cell carcinoma

UR - http://www.scopus.com/inward/record.url?scp=85019468637&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85019468637&partnerID=8YFLogxK

U2 - 10.1007/978-4-431-55531-5_15

DO - 10.1007/978-4-431-55531-5_15

M3 - Chapter

AN - SCOPUS:85019468637

SN - 9784431555308

SP - 351

EP - 367

BT - Renal Cell Carcinoma

PB - Springer Japan

ER -