Patterning of the “Distal Esophagus” in Esophageal Atresia with Tracheo-esophageal Fistula: Is Thyroid Transcription Factor 1 a Player?

Crisera, Christopher A.; Maldonado, Thomas S.; Kadison, Alan S.; Li, Min; Longaker, Michael T.; Gittes, George K.

doi:10.1006/jsre.2000.5850

Cited by 18 publications

(13 citation statements)

References 15 publications

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“…Secondly, the lower end of the esophagus in this particular form of EA is likely different from the fistula of regular EA/TEF in which cartilage inclusions and islands of tracheal epithelial ectopia are frequent. The presence of specific respiratory transcription factors and the absence of esophageal ones in the fistula of rats with EA/TEF confirmed its respiratory origin [40,41]. This might not apply to the lower end of the esophagus in isolated EA.…”

Section: Discussionsupporting

confidence: 56%

Intrinsic esophageal innervation in esophageal atresia without fistula

et al. 2007

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Esophageal atresia and tracheo-esophageal fistula (EA + TEF) are often associated with malformations of neural crest origin. Esophageal innervation is also derived from the neural crest and it is abnormal in EA + TEF in which there is motor dysfunction. Our aim was to examine the intrinsic esophageal innervation in children with isolated EA in which different embryogenic mechanisms might be involved. Specimens from the proximal and distal esophageal segments of 6/35 patients who had esophageal replacement for isolated EA between 1965 and 2006 were suitable for the study. They were sectioned and immunostained with anti-neurofilament (NF) and anti-S-100 antibodies. The muscle and neural surfaces on each section were measured with the assistance of image processing software. The surface of the ganglia and the number of neurons per ganglion were determined at high power microscopy. The findings were compared with those of six autopsy specimens from newborns dead of other diseases by means of standard statistical tests and a significance threshold of P < 0.05. Unmatched age/size of babies in isolated EA and control groups precluded comparison of the relative surfaces occupied by neural elements. Patients with pure EA had denser fibrilar network and larger ganglia than controls. The number of neurons/ganglion were similar in both groups although the cells from EA patients were larger. The findings were similar at both esophageal levels studied. In spite of methodologic biases, it seems that intrinsic esophageal fibrilar network is denser and the intramural ganglia larger with larger cells in patients with pure EA than in controls on both esophageal ends of the organ. These neural anomalies are only in part reminiscent of those described in regular EA/TEF but may as well explain esophageal dysfunction in patients with repaired isolated EA.

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Section: Discussionsupporting

confidence: 56%

Intrinsic esophageal innervation in esophageal atresia without fistula

et al. 2007

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“…The combined BMP ligand and receptor results demonstrate that the fistula differs from both normal esophagus and lung. In terms of BMP ligand expression the fistula tract is more ''trachea-like'' which reinforces its respiratory origin, as we have previously described [7][8][9][10].…”

Section: Discussionsupporting

confidence: 52%

“…The fistula tract continues to grow caudally through the mesenchyme, fistulizing with the developing stomach on embryonic day (E) 12.5 [4,5]. While the fistula tract appears to be a ''distal esophagus'' histologically, the functional and genetic phenotype of the fistula tract is in some respect [positive thyroid transcription factor 1 (TTF-1) and fibroblast growth factor (FGF) signaling] ''respiratory-like'', which is consistent with an origin from the trifurcation of the embryonic lung bud [6][7][8][9]. In patients with EA/TEF, the distal esophagus demonstrates poor motility and contains regions of pseudostratified columnar epithelium, also consistent with a respiratory origin [4,10].…”

Section: Introductionmentioning

confidence: 92%

Bone morphogenetic protein expression patterns in human esophageal atresia with tracheoesophageal fistula

et al. 2005

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The organogenesis of esophageal atresia with tracheoesophageal fistula (EA/TEF) remains unknown. The fistula tract appears to develop from a non-branching trifurcation of the embryonic lung bud. The non-branching growth of the fistula differs from the other lung buds and suggests a deficiency in bone morphogenetic protein (BMP) signaling, since BMPs are critical to proper lung development and branching. With IRB approval, portions of newborn human proximal esophageal pouch and distal fistula samples were recovered at the time of surgical repair of EA/TEF. The tissues were processed for immunohistochemistry. Commercially available fetal tissues were used as controls. In control tissues, BMP ligands (BMP 2, 4, and 7) were all present in the esophagus but absent in the trachea. BMPRIA was absent in both tissues. BMPRIB was detected in trachea but not in esophagus and BMPRII was detected in esophagus but not in trachea. In the EA/TEF specimens, all BMP ligands were present in the proximal esophageal pouch but absent in the fistula tract. BMPRIA and BMPRIB were not detected in either tissue. However, BMPRII was found in both fistula tract and proximal pouch. The submucosa of the fistula appears to maintain a mixed (identical neither to lung, esophagus, or trachea) BMP signaling pattern, providing one mechanism which could potentially explain the esophageal dismotility and lack of lung branching seen in the fistula/distal esophagus.

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“…4 It is also expressed in rat and human tracheoesophageal fistulas. [5][6][7] Napsin A is a pepsinlike aspartic proteinase in the A1 clan of the AA clade of proteinases. Napsin A is distributed mainly in type II pneumocytes, alveolar macrophages, renal tubules, and pancreatic exocrine glands and ducts.…”

Section: Panel Proposalmentioning

confidence: 99%

TTF-1 and Napsin A Do Not Differentiate Metastatic Lung Adenocarcinomas From Primary Esophageal Adenocarcinomas: Proposal of a Novel Staining Panel

Aulakh

Chisholm

Smith

et al. 2013

Archives of Pathology &Amp; Laboratory Medicine

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Context.-When adenocarcinomas arise within the esophagus, particularly when located away from the gastroesophageal junction, it may be important in some patients to differentiate between a primary esophageal adenocarcinoma and metastasis from another site. Lung adenocarcinoma is one tumor that has been reported to frequently metastasize to the esophagus.Objectives.-To create a panel of immunohistochemical markers that can reliably distinguish between an esophageal and pulmonary primary; within the gastrointestinal pathology literature, including published articles and textbooks, common lung immunohistochemical markers, such as TTF-1, are assumed to be negative in esophageal adenocarcinoma, yet, to our knowledge, no study has yet investigated the veracity of that presumption.Design.-In this study, 24 cases each of pulmonary and esophageal adenocarcinomas were stained with TTF-1, napsin A, CDX2, 34bE12, N-cadherin, and IMP3 in an attempt to define an optimal panel for differentiation. Esophageal adenocarcinomas occurring at the gastroesophageal junction were excluded in this study because a gastric primary tumor cannot be excluded in those cases.Results.-Surprisingly, TTF-1 and napsin A were positive in similar proportions of tumors from both sites. Those markers that differentiated statistically between esophageal and pulmonary adenocarcinoma were IMP3, CDX2, and N-cadherin.Conclusions.-When differentiating the origin of a tumor as either esophageal or pulmonary, an immunohistochemical panel consisting of IMP3, CDX2, and Ncadherin is superior to either TTF-1 or napsin A.(Arch Pathol Lab Med. 2013;137:1094-1098; doi: 10.5858/arpa.2012-0305-OA) M alignant tumors frequently involve multiple organ systems, either by direct extension or by metastasis. Moreover, adenocarcinomas from various sites can be morphologically similar, necessitating immunohistochemical examination to accurately determine the site of origin. Distinguishing a primary site when adenocarcinomas involve both the esophagus and lungs can be difficult. Tumors in these organs may metastasize or can invade via direct extension because of the close proximity of the involved organs.Metastasis to the esophagus is not an uncommon occurrence. However, certain tumors have been documented to metastasize to the esophagus more frequently than others, including lung, thyroid, breast, and ovary. In a study of 1835 autopsy cases of patients who died from carcinomas, metastases to the esophagus occurred in 112 cases (6.1%). The lung was the most common primary site, representing 51 of 112 cases (45.5%) of esophageal metastases. Of these 51 cases, 32 (63%) were adenocarcinoma and 19 (37%) were squamous cell carcinoma.1 Because of the histomorphologic similarities, distinguishing the exact site of a primary tumor can be exceedingly difficult and is critical because the treatment regimens differ depending on the tissue origin.Thyroid transcription factor-1 (TTF-1) protein has historically been a reliable marker of pulmonary adenocarcinoma and thyroid malignancies. Init...

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Patterning of the “Distal Esophagus” in Esophageal Atresia with Tracheo-esophageal Fistula: Is Thyroid Transcription Factor 1 a Player?

Cited by 18 publications

References 15 publications

Intrinsic esophageal innervation in esophageal atresia without fistula

Intrinsic esophageal innervation in esophageal atresia without fistula

Bone morphogenetic protein expression patterns in human esophageal atresia with tracheoesophageal fistula

TTF-1 and Napsin A Do Not Differentiate Metastatic Lung Adenocarcinomas From Primary Esophageal Adenocarcinomas: Proposal of a Novel Staining Panel

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