Clinical Aspects of Genetic Variability in &lt;EMPH TYPE="ITAL"&gt;Helicobacter pylori&lt;/EMPH&gt;

Spechler, Stuart J.

doi:10.1001/jama.283.10.1264

Cited by 19 publications

(11 citation statements)

References 26 publications

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“…Simultaneous infection with multiple strains of H. pylori that can exchange genetic sequences is common [49]. The development of clinically manifest disease during chronic infection seems to result from complex and poorly understood interactions among a number of factors, including the susceptibility of the host and the virulence of the infecting strains [50].…”

Section: H Pylori Flavodoxin As a New Drug Targetmentioning

confidence: 99%

Towards a new therapeutic target: Helicobacter pylori flavodoxin

Cremades

Bueno

Toja³

et al. 2005

Biophysical Chemistry

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Section: H Pylori Flavodoxin As a New Drug Targetmentioning

confidence: 99%

Towards a new therapeutic target: Helicobacter pylori flavodoxin

Cremades

Bueno

Toja³

et al. 2005

Biophysical Chemistry

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“…For example, while H. pylori 's urease activity is vital for its survival, an enhanced immunological response to the enzyme may decrease the bacteria's persistence and sequelae [17]. The gene products of cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) are associated with a robust production of cytokines and tissue inflammation [18, 19]. The presence or absence of the aforementioned proteins assists in classifying the distinct strains of H. pylori as well as providing further information as to its association with disease [20].…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pyloriInfection and Light Chain Gammopathy

Giron

Shah

2013

Clinical and Developmental Immunology

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Objective. Helicobacter pylori provokes a host of immune alterations upon colonizing the gastric mucosa. Design. We report 22 individuals with confirmed Helicobacter pylori infection who were also managed for the concurrent elevation of immunoglobulin free light chain (kappa and lambda) levels. Result. Of the 22 patients, 15 patients (68.2%) had elevated free light chain levels: 6 patients (40%) had only kappa chain elevation, 2 patients (13.3%) had only lambda chain elevation, and 7 patients (46.7%) had both kappa and lambda chain elevation. Twenty out of the 22 patients (90.9%) were microbiologically confirmed cured with 3 patients being lost to follow-up for repeat levels. Of the 3 patients who were lost to follow-up, 1 patient had only kappa chain elevation, 1 patient had only lambda chain elevation, and 1 patient had both kappa and lambda chain elevation. For those who were cured (19 patients), 5 patients with kappa elevation had normalized values, 4 patients with lambda elevation had normalized values, and 2 patients with combined kappa and lambda elevation had normalized values. For 6 out of the 19 patients, the light chain levels remained elevated. Conclusion. We speculate that the Helicobacter pylori infection disrupts the immunoglobulin system with potential implications being discussed below.

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“…29 The virulence of individual strains of H. pylori may depend on expression of putative virulence factors such as CagA protein. 30 It appears that infection with H. pylori, particularly with the CagAϩ strains, actually reduces the risk for these tumors, whereas minimal association has been found between these tumors and CagAstrains. 31 Although H. pylori infection clearly causes carditis that would be expected to predispose to cancer development, current data suggest an inverse association between H. pylori and the development of gastric cardia adenocarcinoma.…”

Section: Helicobacter Pylorimentioning

confidence: 99%

Concepts in the Prevention of Adenocarcinoma of the Distal Esophagus and Proximal Stomach

Souza

Spechler

2005

CA: A Cancer Journal for Clinicians

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For decades, the incidence rates for squamous cell carcinoma of the esophagus and adenocarcinoma of the distal stomach have been declining while the rates for adenocarcinomas of the esophagus and gastric cardia have increased profoundly. Recent studies have shown that the gastroesophageal junction (GEJ) is regularly exposed to concentrated gastric acid and to a variety of nitrosating species, noxious agents that may contribute to carcinogenesis in this region. For adenocarcinomas that straddle the GEJ, it can be difficult to determine whether the tumor originated in the esophagus or in the gastric cardia. This classification problem hampers studies on the epidemiology and pathogenesis of GEJ tumors. Current concepts in the prevention of cancers of the distal esophagus and proximal stomach have emerged from advances in our understanding of the specific molecular events that occur during the evolution of these tumors. This report reviews those events and focuses on current concepts in the prevention of adenocarcinomas at the GEJ. The similarities and differences in risk factors, molecular pathogenesis, and in preventive strategies for adenocarcinomas of the esophagus and gastric cardia are highlighted. (CA Cancer J Clin 2005;55:334-351.)

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Clinical Aspects of Genetic Variability in <EMPH TYPE="ITAL">Helicobacter pylori</EMPH>

Cited by 19 publications

References 26 publications

Towards a new therapeutic target: Helicobacter pylori flavodoxin

Towards a new therapeutic target: Helicobacter pylori flavodoxin

Helicobacter pyloriInfection and Light Chain Gammopathy

Concepts in the Prevention of Adenocarcinoma of the Distal Esophagus and Proximal Stomach

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