Preface

**Section 3 Parasitic Tropical Lung Diseases 141**

Ntumba Jean-Marie Kayembe

Chapter 7 **Tropical Lung Diseases 143**

**VI** Contents

In this book dealing with the lung health, the authors focus on various fields, spreading from pulmonary oncogenesis, to inflammatory and parasitic lung diseases.

The first section deals with the fundamental research on lung cancer that is mandatory for the development of novel and early biomarkers for diagnosis of the lung cancer. This devel‐ opment could be enhanced using experimental models despite the species barrier. Mouse models can help us understand the sequence of events involved in human lung neoplasia and their underlying molecular mechanisms.

The results of the research could be used to identify novel targets for the development of new biological therapies.

In the second section of this book, the role of inflammation in various respiratory diseases is outlined. The authors recall cellular mechanisms including neutrophils to improve the un‐ derstanding of the phenomenon and help develop targeted therapies.

The third section on parasitic tropical lung disease highlights the growing importance of ne‐ glected tropical diseases due to increased traffic across the continents and migration of the population. Physicians need to be aware of the symptoms and imaging findings of these diseases mainly in travelers and immigrants from tropical endemic areas.

**Jean-Marie Kayembe**

**Section 1**

**Oncogenesis and the Lung**

**Oncogenesis and the Lung**

**Chapter 1**

**Angiogenesis and Lung Cancer**

S. Vázquez, U. Anido, M. Lázaro, L. Santomé,

Additional information is available at the end of the chapter

L. A. Aparicio

**1. Introduction**

http://dx.doi.org/10.5772/54309

stimulate neoangiogenesis [6].

J. Afonso, O. Fernández, A. Martínez de Alegría and

Angiogenesis is the formation of new blood vessels from the existing vasculature, and neo‐ vascularization is a prerequisite for the growth of solid tumors beyond 1-2 mm in diameter [1]. Because of this, during tumorigenesis, tumor growth reaches a growth-limiting step

Tumors acquire blood vessels by co-option of neighboring vessels from sprouting or intus‐ suscepted microvascular growth and by vasculogenesis from endothelial precursor cells [2]. In most solid tumors the newly formed vessels are plagued by structural and functional ab‐ normalities due to the sustained and excessive exposure to angiogenic factors produced by the tumor [3]. As a result of this, the new tumor-associated vasculature is abnormal and in‐ efficient, but it is essential for tumor growth and metastasis. Despite being abnormal, these new vessels allow tumor growth at early stages of carcinogenesis and progression from in

As a result, tumors tend to become hypoxic. The normal cellular response to hypoxia is to produce growth factors such as vascular endothelial growth factor (VEGF), transforming growth factor alpha (TGF-α), and platelet derived growth factor (PDGF), by neoplastic, stro‐ mal cells or inflammatory cells [4], and may trigger an angiogenic switch to allow the tumor to induce the formation of microvessels from the surrounding host vasculature [5], that

VEGF is the most potent and specific growth factor for endothelial cells, and is associat‐ ed with tumor vessel density, cancer metastasis, and prognosis [7-10]: high levels of cir‐ culating VEGF have been reported in patients with non-small cell lung cancer (NSCLC)

and reproduction in any medium, provided the original work is properly cited.

© 2013 Vázquez et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

where oxygen and nutrient levels are insufficient to continue proliferation.

situ lesions to locally invasive, and eventually to metastatic tumors.

**Chapter 1**
