CD44 and its v6 spliced variant in lung tumors

Fasano, Maria Edvige; Sabatini, Maria T.; Wieczorek, Rosemary; Sidhu, Gurdip S.; Goswami, Sunanda; Jagirdar, Jaishree

doi:10.1002/(sici)1097-0142(19970701)80:1<34::aid-cncr5>3.0.co;2-f

Cited by 43 publications

(30 citation statements)

References 22 publications

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“…7), which are both well known secretary products of Clara cells [34]. There were also changes in the expression pattern of the membrane-bound adhesion molecule CD44v6, which has been implicated in cell-cell and cell-matrix interactions and airway epithelial repair [25,26], and which is not expressed in cells of the neuroendocrine system [27]. Changes in CC10 and SP-D were estimated by means of stereology.…”

Section: Resultsmentioning

confidence: 99%

“…In addition, BORTHWICK et al [44] reported that the potential stem cell population of the trachea, which was identified as BrdU label-retaining cells after oxygen saturation-induced injury, did not express the PNEC marker CGRP [44]. As most neuroendocrine tumours and the cells of the neuroendocrine system do not express CD44v6 [27], the increased expression of this membrane-bound adhesion molecule in response to rHuKGF further indicates that the responsive cells are not PNECs.…”

Section: Discussionmentioning

confidence: 99%

“…Nothing is known, however, about changes of the membrane-bound adhesion molecule CD44v6, which has been implicated in cell-cell and cell-matrix interactions as well as in airway epithelial repair [25,26]. Since CD44v6 is present in pulmonary stem cells of epithelial origin but not in cells of neuroendocrine lineage [27], CD44v6 may serve as an additional marker to evaluate the origin of the cells proliferating in response to KGF.…”

mentioning

confidence: 94%

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Keratinocyte growth factor-induced proliferation of rat airway epithelium is restricted to Clara cells in vivo

Fehrenbach

Fehrenbach²,

Pan³

et al. 2002

European Respiratory Journal

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Keratinocyte growth factor-induced proliferation of rat airway epithelium is restricted to Clara cells in vivo. H. Fehrenbach, A. Fehrenbach, T. Pan, M. Kasper, R.J. Mason. #ERS Journals Ltd 2002. ABSTRACT: Keratinocyte growth factor (KGF) is a potent mitogen of pulmonary bronchial and alveolar epithelial cells. However, it is unclear which type(s) of airway epithelial cells (AEC) proliferate(s) in response to KGF.AEC proliferation was induced in rats by either endobronchial instillation of 5 mg recombinant human (rHu) KGF per kg body weight or by adenoviral transfer of the human KGF gene (Ad5-HuKGF). Alterations in terminal airway AEC were followed for up to 7 days after rHuKGF, and for up to 28 days after Ad5-HuKGF.Cell proliferation, as assessed by immunohistochemistry (IHC) for incorporated 5-bromo-29-deoxyuridine (BrdU) and quantified by stereology, peaked at days 1-2 and was resolved by day 7 after rHuKGF and by day 21 after Ad5-HuKGF. Double immunofluorescence labelling for BrdU or Ki-67 on the one hand, and for Clara cell specific protein 10 (CC10) and calcitonin-gene related peptide on the other hand, demonstrated that Clara cells, not pulmonary neuroendocrine cells, proliferated in response to human KGF. TUNEL (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labelling) method in conjunction with IHC for MNF116 failed to detect significant numbers of apoptotic AEC. IHC in conjunction with stereology revealed transient phenotypic alterations with a decrease in CC10, an increase in surfactant protein D and an increase in CD44v6 in AEC.The authors conclude that Clara cells responded to human keratinocyte growth factor in vivo by proliferation as well as by changes in protein expression, whereas no significant response was observed in pulmonary neuroendocrine cells. As Clara cells are intimately involved in airway epithelial repair, ion and fluid transport, and modulate lung inflammation, the potential of human keratinocyte growth factor to protect the lung may in part rely on the response of Clara cells.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 94%

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Keratinocyte growth factor-induced proliferation of rat airway epithelium is restricted to Clara cells in vivo

Fehrenbach

Fehrenbach²,

Pan³

et al. 2002

European Respiratory Journal

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“…A nivel pulmonar, el CD44v6 ha mostrado diferencias en su comportamiento entre el pulmón fetal y del adulto. Así, en el primero modula ciertos factores de crecimiento involucrados en la morfogénesis y maduración tisular, mientras que en el adulto se asocia con células pluripotenciales e interviene en la migración celular durante la reparación y transformación tumoral 2 . Los carcinomas microcíticos de pulmón no expresan CD44v6, mientras que los no microcíticos lo hacen en un porcentaje importante de casos, siendo éste mayor en los escamosos que en los adenocarcinomas, por lo que se considera un buen marcador de la diferenciación epitelial escamosa 3 .…”

Section: Introductionunclassified

Valor clínico-biológico de la concentración citosólica de ácido hialurónico en adenocarcinomas pulmonares CD44v6 positivos

Ruibal

Salmón²,

Argibay

et al. 2005

Oncología (Barc.)

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Resumen• Propósito: El objetivo de este estudio ha sido analizar la influencia de la concentración citosóli-ca de ácido hialurónico (AH) sobre las características clínico-biológicas de adenocarcinomas de pulmón CD44v6 positivos.• Material y métodos: El grupo estudio incluyó 34 muestras tumorales. Dosificamos las concentraciones citosólicas de AH, pS2, catepsina D, t-AP, NSE, cyfra 21.1, CA125 y fracción libre de la hormona gonadotrófica coriónica. También determinamos las concentraciones de EGFR, proteína oncogénica erbB2, CD44s y CD44v5 en las membranas celulares. Se tuvo presente, asimismo, el estadio clínico, grado histológico, ploidía, índice de DNA y fase de síntesis celular (FS).• • Conclusiones: Los resultados obtenidos parecen resaltar la importancia de la concentración citosólica de AH en los adenocarcinomas pulmonares CD44v6 positivos, de tal modo que altos valores en el índice AH/CD44v6 se asocian con una mayor proliferación e indiferenciación celular, lo cual unido a mayores concentraciones de proteína oncogénica erbB2, sugiere un subgrupo de tumores con un posible diferente comportamiento. Sin embargo, dada el reducido número de enfermos incluí-dos, creemos que son necesarios más estudios para poder confirmar nuestros hallazgos.

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“…However, information regarding the utility of these data in predicting behavior is controversial (3,4). Recently, several other tumor markers such as Ki-67, Bcl-2, and p53; cell adhesion molecules; and tumor angiogenesis have been explored as possible prognostic markers (5)(6)(7)(8)(9)(10).…”

mentioning

confidence: 99%

Expression of Cell Adhesion Molecules, CD44s and E-Cadherin, and Microvessel Density in Carcinoid Tumors

Sun

Gong

Talamonti³

et al. 2002

Mod Pathol

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Although all carcinoids are potentially malignant, their biologic behavior is quite variable. Currently there are no reliable morphological criteria to predict metastatic potential. Cell adhesion molecules, such as CD44 and E-cadherin, are considered important in regulating invasion and metastasis of tumors. Also, angiogenesis has been shown to be associated with tumor growth and progression. In this study, we examined 51 carcinoids, including 13 carcinoids with known lymph node and/or visceral metastasis, for expression of CD44s (the standard form of CD44) and E-cadherin by immunohistochemistry. We found that 55% and 37% of carcinoids were negative for CD44s and E-cadherin, respectively. Carcinoids with lymph node and/or visceral metastasis were significantly more frequently negative for CD44s than were those without demonstrated metastasis (P ‫؍‬ .030). Ten of 11 tumors with lymph node metastasis lacked CD44s (P ‫؍‬ .022), whereas E-cadherin was negative in only 3 (P ‫؍‬ .975). Additionally, we analyzed microvessel density to evaluate the role of tumor angiogenesis in the tumor behavior. Carcinoid tumors in general demonstrated high microvessel density (160 ؎ 82/five 200؋ fields), irrespective of location and with and without metastasis. These results suggest that loss of CD44s, but not E-cadherin, may be a useful predictor of metastatic potential of carcinoid tumors.

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CD44 and its v6 spliced variant in lung tumors

Cited by 43 publications

References 22 publications

Keratinocyte growth factor-induced proliferation of rat airway epithelium is restricted to Clara cells in vivo

Keratinocyte growth factor-induced proliferation of rat airway epithelium is restricted to Clara cells in vivo

Valor clínico-biológico de la concentración citosólica de ácido hialurónico en adenocarcinomas pulmonares CD44v6 positivos

Expression of Cell Adhesion Molecules, CD44s and E-Cadherin, and Microvessel Density in Carcinoid Tumors

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