Gastric Adenocarcinoma Associated With Fundic Gland Polyps in A Patient With Attenuated Familial Adenomatous Polyposis

Hofgartner, Wolfgang; Thorp, Micah L.; Ramus, Mark W.; Delorefice, Guy; Chey, William Y.; Ryan, Charlotte; Takahashi, Garry W; Lobitz, John R

doi:10.1111/j.1572-0241.1999.01312.x

Cited by 125 publications

(38 citation statements)

References 31 publications

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“…(Watanabe et al 1978;Oerhaus et al 1999;Hofgartner et al 1999). Germline mutations of the APC gene on chromosome 5q21 are responsible for this disease (Groden et al 1991).…”

Section: Familial Adenomatous Polyposis Coli (Fap)mentioning

confidence: 98%

Gastric adenocarcinoma: pathomorphology and molecular pathology

Werner

Becker

Keller

et al. 2001

Journal of Cancer Research and Clinical Oncology

120

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Two types of gastric adenocarcinoma can be distinguished histopathologically: the diffuse and the intestinal type. Molecular pathology supports this theory by showing differences in the genetic pathways of both tumor types. In addition to known pathomorphological factors of prognosis, e.g., depth of tumor infiltration, number of lymph node metastases and resection margins, a few genes have been suggested to have prognostic impact in gastric carcinoma. Clinically relevant molecules whose expression or structure is altered include the plasminogen activator (uPA) and its inhibitor PAI-1 (plasminogen activator inhibitor type 1), the cell cycle regulator cyclin E, epidermal growth factor (EGF), the apoptosis inhibitor bcl-2, the cell adhesion molecule E-cadherin, and the multifunctional protein beta-catenin. Gene amplification and protein overexpression of the growth factor receptors c-erbB-2 and K-sam may be prognostic factors for intestinal-type and diffuse-type gastric cancer, respectively. In addition, genetic instability is commonly seen. There has long been evidence for a genetic predisposition to gastric cancer by epidemiological studies and case reports. Very recently, germ line mutations of E-cadherin have been identified that are responsible for a dominantly inherited form of diffuse-type gastric cancer and could be used to identify individuals that are at high risk.

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“…(Watanabe et al 1978;Oerhaus et al 1999;Hofgartner et al 1999). Germline mutations of the APC gene on chromosome 5q21 are responsible for this disease (Groden et al 1991).…”

Section: Familial Adenomatous Polyposis Coli (Fap)mentioning

confidence: 98%

Gastric adenocarcinoma: pathomorphology and molecular pathology

Werner

Becker

Keller

et al. 2001

Journal of Cancer Research and Clinical Oncology

120

View full text Add to dashboard Cite

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“…Since the initial report by Zwick et al, 38 cases of adenocarcinoma or high-grade dysplasia occurring in FGP have been described in the literature. [39][40][41] Although Sekine et al 41 proposed APC genotype to be a predisposing factor for malignant transformation in FGP, the precise mechanism of such transformation remains unclear. Because sPLA2 has an important role in the regulation of cell cycles of the gastric epithelium via arachidonic acid synthesis, PLA2g2a may contribute to a pathway from FGP to dysplastic change.…”

Section: Discussionmentioning

confidence: 97%

Impact of Phospholipase A2 Group IIa Gene Polymorphism on Phenotypic Features of Patients with Familial Adenomatous Polyposis

Yanaru-Fujisawa¹,

Matsumoto²,

Kukita³

et al. 2007

Diseases of the Colon &Amp; Rectum

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“…[5][6][7][8] Fundic gland polyps rarely progress to cancer. [9][10][11] Similar polyps, although fewer in number, are sometimes observed in the general population and possibly associated with chronic use of proton pump inhibitors. 12,13 Adenomatous polyps in the stomach occur in approximately 10 percent of persons with FAP.…”

Section: Cancer Risk In Fapmentioning

confidence: 97%

An Evidence-Based, Multidisciplinary Approach to the Clinical Considerations, Management, and Surveillance of Adrenal Lesions in Familial Adenomatous Polyposis: Report of Three Cases

Ferrández¹,

Pho²,

Solomon³

et al. 2006

Diseases of the Colon &Amp; Rectum

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Adrenal masses are commonly discovered incidentally in patients with familial adenomatous polyposis, and adrenal malignancies have been rarely reported. Individuals with familial adenomatous polyposis frequently undergo abdominal CT-scan examinations for surveillance or symptoms. Adrenal lesions often are detected unexpectedly and are thus becoming a common clinical problem in this population. Adrenal lesions encompass a heterogeneous spectrum of pathologic entities, including primary adrenocortical and medullary tumors, benign or malignant lesions, hormonally active or inactive lesions, metastases, and infections. When an adrenal mass is detected, the clinician needs to address two crucial questions: 1) is the mass malignant? and 2) is it hormonally active? This article presents three new cases of incidental adrenal lesions in familial adenomatous polyposis, reviews the medical literature for this setting, and provides an overview of the diagnostic clinical approach and management of the adrenal findings in familial adenomatous polyposis patients.

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Gastric Adenocarcinoma Associated With Fundic Gland Polyps in A Patient With Attenuated Familial Adenomatous Polyposis

Cited by 125 publications

References 31 publications

Gastric adenocarcinoma: pathomorphology and molecular pathology

Gastric adenocarcinoma: pathomorphology and molecular pathology

Impact of Phospholipase A2 Group IIa Gene Polymorphism on Phenotypic Features of Patients with Familial Adenomatous Polyposis

An Evidence-Based, Multidisciplinary Approach to the Clinical Considerations, Management, and Surveillance of Adrenal Lesions in Familial Adenomatous Polyposis: Report of Three Cases

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