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- Volume 1, 2006
Annual Review of Pathology: Mechanisms of Disease - Volume 1, 2006
Volume 1, 2006
- Preface
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A PATHOLOGIST'S ODYSSEY
Vol. 1 (2006), pp. 1–22More LessI am honored to write the prefatory chapter for the inaugural volume of the Annual Review of Pathology: Mechanisms of Disease. This publishing venture signals that pathology takes its rightful place alongside the other biomedical sciences. I thought it may be of interest to some to delineate how a circuitous path led me into a career in experimental pathology and to give some of the flavor of a past era in experimental appro Read More
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IMMUNOBIOLOGY AND PATHOGENESIS OF VIRAL HEPATITIS
Vol. 1 (2006), pp. 23–61More LessAmong the many viruses that are known to infect the human liver, hepatitis B virus (HBV) and hepatitis C virus (HCV) are unique because of their prodigious capacity to cause persistent infection, cirrhosis, and liver cancer. HBV and HCV are noncytopathic viruses and, thus, immunologically mediated events play an important role in the pathogenesis and outcome of these infections. The adaptive immune response mediates Read More
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THE PATHOGENESIS OF HELICOBACTER PYLORI–INDUCED GASTRO-DUODENAL DISEASES
Vol. 1 (2006), pp. 63–96More LessHelicobacter pylori is the main cause of peptic ulceration, distal gastric adenocarcinoma, and gastric lymphoma. Only 15% of those colonized develop disease, and pathogenesis depends upon strain virulence, host genetic susceptibility, and environmental cofactors. Virulence factors include the cag pathogenicity island, which induces proinflammatory, pro-proliferative epithelial cell signaling; the cytotoxin VacA, which Read More
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MOLECULAR PATHOLOGY OF MALIGNANT GLIOMAS
Vol. 1 (2006), pp. 97–117More LessMalignant gliomas, the most common type of primary brain tumor, are a spectrum of tumors of varying differentiation and malignancy grades. These tumors may arise from neural stem cells and appear to contain tumor stem cells. Early genetic events differ between astrocytic and oligodendroglial tumors, but all tumors have an initially invasive phenotype, which complicates therapy. Progression-associated genetic Read More
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TUMOR STROMA AND REGULATION OF CANCER DEVELOPMENT
Vol. 1 (2006), pp. 119–150More LessIn the past 25 years, a majority of cancer studies have focused on examining functional consequences of activating and/or inactivating mutations in critical genes implicated in cell cycle control. These studies have taught us a great deal about the functions of oncogenes and tumor suppressor genes and the signaling pathways regulating cell proliferation and/or cell death. However, such studies have largely ignored the fact that Read More
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NEURODEGENERATIVE DISEASES: New Concepts of Pathogenesis and Their Therapeutic Implications
Vol. 1 (2006), pp. 151–170More LessNeurodegenerative diseases as diverse as Alzheimer's, Parkinson's, and Creutzfeldt-Jakob disease share a common pathogenetic mechanism involving aggregation and deposition of misfolded proteins, which leads to progressive central nervous system disease. Although the type of aggregated protein and the regional and cellular distribution of deposition vary from disease to disease, these disorders may all be linke Read More
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THE ENDOTHELIUM AS A TARGET FOR INFECTIONS
Vol. 1 (2006), pp. 171–198More LessThe endothelial cells lining vascular and lymphatic vessels are targets of several infectious agents, including viruses and bacteria, that lead to dramatic changes in their functions. Understanding the pathophysiological mechanisms that cause the clinical manifestations of those infections has been advanced through the use of animal models and in vitro systems; however, there are also abundant studies that explore the c Read More
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GENETIC REGULATION OF CARDIOGENESIS AND CONGENITAL HEART DISEASE
Vol. 1 (2006), pp. 199–213More LessDevelopmental heart disorders are the most common of all human birth defects and occur in nearly one percent of the population. Survivors of congenital heart malformations are an increasing population, and it is becoming clear that genetic mutations that cause developmental anomalies may result in cardiac dysfunction later in life. This review highlights the progress in understanding the underlying molecular basis for car Read More
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REGULATION OF LUNG INFLAMMATION IN THE MODEL OF IGG IMMUNE-COMPLEX INJURY
Vol. 1 (2006), pp. 215–242More LessModern techniques of cell and molecular biology have rapidly uncovered the mechanisms underlying inflammatory injury of the lung. This expanding knowledge (which includes an understanding of complement, cell surface receptors, cytokines and chemokines, transcription factors, oxidants, proteinases, and endogenous inhibitors, as well as the role of leukocyte adhesion-promoting molecules) has provided new insig Read More
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INTEGRATIVE BIOLOGY OF PROSTATE CANCER PROGRESSION
Vol. 1 (2006), pp. 243–271More LessProstate cancer displays considerable clinical, morphological, and biological heterogeneity. Classical genetic techniques have provided only limited information about the pathogenesis of prostate cancer progression. Nevertheless, several candidate genes and pathways have been implicated in prostate cancer development. High-throughput techniques have exponentially expanded the number of candidate genes, including som Read More
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KSHV INFECTION AND THE PATHOGENESIS OF KAPOSI'S SARCOMA
Vol. 1 (2006), pp. 273–296More LessKaposi's sarcoma (KS) has long been suspected of having an infectious etiology on the basis of its unusual epidemiology, histopathology, and natural history. Nearly a decade ago, a novel herpesviral genome was discovered in KS biopsies, and since that time strong epidemiologic evidence has accumulated correlating infection with this KS-associated herpesvirus (KSHV, also known as human herpesvirus 8) with the develop Read More
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INFLAMMATION AND ATHEROSCLEROSIS
Vol. 1 (2006), pp. 297–329More LessAtherosclerosis, the cause of myocardial infarction, stroke, and ischemic gangrene, is an inflammatory disease. The atherosclerotic process is initiated when cholesterol-containing low-density lipoproteins accumulate in the intima and activate the endothelium. Leukocyte adhesion molecules and chemokines promote recruitment of monocytes and T cells. Monocytes differentiate into macrophages and upregulate p Read More
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LUNG CANCER PRENEOPLASIA
Vol. 1 (2006), pp. 331–348More LessFrom histological and biological perspectives, lung cancer is a complex neoplasm. Although the sequential preneoplastic changes have been defined for centrally arising squamous carcinomas of the lung, they have been poorly documented for the other major forms of lung cancers, including small cell lung carcinoma and adenocarcinomas. There are three main morphologic forms of preneoplastic lesions recognized Read More
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PATHOGENESIS OF NONIMMUNE GLOMERULOPATHIES
Vol. 1 (2006), pp. 349–374More LessNonimmune glomerulopathies are an area of significant research. This review discusses the development of focal segmental glomerulosclerosis, with particular attention to the role of the podocyte in the initiation of glomerulosclerosis and the contribution to glomerulosclerosis from capillary hypertension and soluble factors such as transforming growth factor beta, platelet-derived growth factor, vascular endothelial growth fa Read More
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SPECTRUM OF EPSTEIN-BARR VIRUS–ASSOCIATED DISEASES
J.L. Kutok, and F. WangVol. 1 (2006), pp. 375–404More LessThe association between Epstein-Barr virus (EBV) and a large number of benign and malignant diseases is unique among DNA viruses. Within infected tissues, proteins that are expressed during the normal lytic and latent viral life cycle lead to cellular alterations that contribute to these EBV-associated diseases. Although the early events of EBV infection are poorly understood, increasing knowledge of the viral processes Read More
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CALCIUM IN CELL INJURY AND DEATH*
Vol. 1 (2006), pp. 405–434More LessLoss of Ca2+ homeostasis, often in the form of cytoplasmic increases, leads to cell injury. Depending upon cell type and the intensity of Ca2+ toxicity, the ensuing pathology can be reversible or irreversible. Although multiple destructive processes are activated by Ca2+, lethal outcomes are determined largely by Ca2+-induced mitochondrial permeability transition. This form of damage is primarily dependent upon mitoch Read More
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GENETICS OF SOFT TISSUE TUMORS
Vol. 1 (2006), pp. 435–466More LessSarcomas form a highly diverse group of rare tumors that are derived from connective tissue. More than 100 different malignant and benign soft tissue neoplasms can be recognized by histologic examination. Few diagnostic markers exist, and the cell of origin for many soft tissue tumors is unknown. The accurate diagnosis of many of these tumors therefore remains a challenge. The study of sarcomas has yielded many insi Read More
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SEVERE SEPSIS AND SEPTIC SHOCK: The Role of Gram-Negative Bacteremia
Vol. 1 (2006), pp. 467–496More LessAlthough Gram-negative bacteria have often been implicated in the pathogenesis of severe sepsis and septic shock, how they trigger these often lethal syndromes is uncertain. In particular, the role played by blood-borne bacteria is controversial. This review considers two alternatives. In the first, circulating Gram-negative bacteria induce toxic reactions directly within the vasculature; in the second, the major inflammatory sti Read More
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PROTEASES IN PARASITIC DISEASES
Vol. 1 (2006), pp. 497–536More LessParasitic diseases represent major global health problems of immense proportion. Schistosomiasis, malaria, leishmaniasis, Chagas disease, and African sleeping sickness affect hundreds of millions of people worldwide, cause millions of deaths annually, and present an immense social and economic burden. Recent advances in genomic analysis of several of the major global parasites have revealed key factors involved in th Read More
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Previous Volumes
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Volume 19 (2024)
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Volume 18 (2023)
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Volume 17 (2022)
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Volume 16 (2021)
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Volume 15 (2020)
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Volume 14 (2019)
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Volume 13 (2018)
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Volume 12 (2017)
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Volume 11 (2016)
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Volume 10 (2015)
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Volume 9 (2014)
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Volume 8 (2013)
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Volume 7 (2012)
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Volume 6 (2011)
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Volume 5 (2010)
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Volume 4 (2009)
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Volume 3 (2008)
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Volume 2 (2007)
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Volume 1 (2006)
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Volume 0 (1932)