Enrichment of epithelial cells for molecular studies

Maitra, Anirban; Wistuba, Ignacio I.; Virmani, Arvind K.; Sakaguchi, Masahiro; Park, Inwon; Stucky, Amy; Milchgrub, Sara; Gibbons, David; Minna, John D.; Gazdar, Adi F.

doi:10.1038/7458

Cited by 59 publications

(41 citation statements)

References 16 publications

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“…cells were significantly enriched by the procedure. 25 A similar approach using SAGE and cDNA-microarray databases may allow the identification of molecules specific for other organs or cancers that are applicable for tumors of unknown origin.…”

Section: Discussionmentioning

confidence: 99%

Identification of MGB1 as a Marker in the Differential Diagnosis of Lung Tumors in Patients with a History of Breast Cancer by Analysis of Publicly Available SAGE Data

Koga

Horio

Mitsudomi

et al. 2004

The Journal of Molecular Diagnostics

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The risk of developing second primary cancers is increased in patients with breast cancer. The lung is one of the major target organs, and therefore a differential diagnosis between primary and metastatic cancers is required for the treatment of lung tumors in patients with a history of breast cancer. However, biopsy specimens frequently result in small, fragmented tissues containing only a few, degenerated cancer cells. We attempted to find a useful marker for differential diagnosis, using the online SAGE database. We selected three molecules, small breast epithelial mucin (SBEM), prostate epithelium-specific Ets transcription factor (PDEF), and mammaglobin (MGB1), as potential markers for breast cancer. SBEM and PDEF proved of no use for practical differential diagnosis because they are expressed in the normal bronchus. In contrast, expression of MGB1 was detected in all 22 primary breast cancers, but not in 22 normal lung tissues. Furthermore, all 12 metastatic breast cancers examined demonstrated positive MGB1 transcripts, whereas one of 48 primary lung adenocarcinomas expressed MGB1. This suggests that MGB1 can serve as a differential molecular marker. In practice, prospective examination, using the nine cases with a history of breast cancer, confirmed the usefulness of MGB1 in differential diagnosis.

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Section: Discussionmentioning

confidence: 99%

Identification of MGB1 as a Marker in the Differential Diagnosis of Lung Tumors in Patients with a History of Breast Cancer by Analysis of Publicly Available SAGE Data

Koga

Horio

Mitsudomi

et al. 2004

The Journal of Molecular Diagnostics

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“…We initially attempted to use the primer sequences identified, which span the mutation and give an amplified product of 640 bp (10). Unfortunately, we did not obtain DNA of a sufficient length to amplify this relatively long product from our samples because DNA fragmentation, which occurs with tissue fixation (11). Therefore, we designed our primers to amplify a short DNA fragment of 128 bp that included the G1528C mutation.…”

Section: Discussionmentioning

confidence: 99%

Absence of the G1528C (E474Q) Mutation in the α-Subunit of the Mitochondrial Trifunctional Protein in Women with Acute Fatty Liver of Pregnancy

et al. 2002

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Acute fatty liver of pregnancy (AFLP) is a rare and dreaded complication of pregnancy, almost exclusively seen in the third trimester. The histopathologic features of AFLP closely resemble those seen in metabolic disorders characterized by deficiency of fatty acid oxidative enzymes. Several reports have established a strong association between AFLP in the mother and fetal deficiency of the enzyme long-chain L-3-hydroxyacyl-CoA dehydrogenase (LCHAD). However, these studies have an inevitable selection bias resulting from ascertainment through an affected infant, rather than an unselected population of patients with AFLP. We retrospectively examined a series of 10 women with pregnancies complicated by AFLP to determine the prevalence of the common LCHAD mutation (G1528C) in this population. The existing LCHAD primers, which produce a 640-bp amplicon (IJlst L, Ruiter JP, Hoovers JM, Jakobs ME, Wanders RJ: J Clin Invest 98: 1028 -1033, 1996), were modified to make them amenable to analysis of fragmented DNA obtained from microdissected formalin-fixed material. None of the patients were found to harbor the common G1528C mutation. It is likely that AFLP arising in the context of fetal LCHAD deficiency represents only one of the possible etiologies for this uncommon disorder, and the metabolic basis of AFLP is more heterogeneous than previously believed. A spectrum of maternal liver disorders can occur during pregnancy. Many, such as hepatitis or drug-induced hepatotoxicity, can also be seen in nonpregnant individuals, whereas others, including preeclampsia and intrahepatic cholestasis of pregnancy, are unique to the gravid state (1). AFLP is an uncommon but clinically severe form of hepatopathy that is seen almost exclusively in the third trimester of pregnancy. AFLP manifests with jaundice, which can rapidly progress to severe coagulopathy, fulminant hepatic failure, and death of both mother and fetus. Approximately 50% of affected patients have preeclampsia with high blood pressure, proteinuria, and peripheral edema, and up to 20% may have AFLP coexisting with the HELLP syndrome (1). AFLP derives its name from the presence of marked microvesicular steatosis in the liver, often with involvement of the heart, kidneys, and pancreas. Recent studies have reported a maternal mortality rate of 10 -20% with AFLP, underscoring the need for early diagnosis and intervention. The cornerstone of therapy is delivery of the fetus, and the clinical condition dramatically ameliorates in the postpartum period.In recent years, investigators have speculated that AFLP/ HELLP syndrome and certain inherited fatty acid oxidation disorders, specifically LCHAD deficiency, may share a common pathogenic mechanism, based on striking similarities in hepatic pathology. This empirical association was strengthened by reports of AFLP or HELLP syndrome occurring during the third trimester in mothers bearing children with LCHAD deficiency. For example, Wilcken et al. (2) were the first to report the occurrence of AFLP and HELLP syndrome in six of six...

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“…3,5,[25][26][27][28][29][30] Furthermore, genotyping of tumor-derived cell lines 31 is possible since the selected cells are viable after sorting. Reculturing was successful after negative CD45 MACS selection in spiking experiments with both cell lines (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Detection and enrichment of disseminated renal carcinoma cells from peripheral blood by immunomagnetic cell separation

et al. 2001

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Enrichment of epithelial cells for molecular studies

Cited by 59 publications

References 16 publications

Identification of MGB1 as a Marker in the Differential Diagnosis of Lung Tumors in Patients with a History of Breast Cancer by Analysis of Publicly Available SAGE Data

Identification of MGB1 as a Marker in the Differential Diagnosis of Lung Tumors in Patients with a History of Breast Cancer by Analysis of Publicly Available SAGE Data

Absence of the G1528C (E474Q) Mutation in the α-Subunit of the Mitochondrial Trifunctional Protein in Women with Acute Fatty Liver of Pregnancy

Detection and enrichment of disseminated renal carcinoma cells from peripheral blood by immunomagnetic cell separation

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