Lymphatic spread in squamous cell carcinoma of the penis is independent of elevated lymph vessel density.

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Lymphatic spread in squamous cell carcinoma of the penis is independent of elevated lymph vessel density. / Naumann, Carsten Maik; Al-Najar, Amr; Alkatout, Ibrahim; Hegele, Axel; Korda, Joanna Beate; Bolenz, Christian; Kalthoff, Holger; Sipos, Bence; Juenemann, Klaus-Peter; van der Horst, Christof.

In: BJU INT, Vol. 103, No. 12, 12, 2009, p. 1655-1659.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Naumann, CM, Al-Najar, A, Alkatout, I, Hegele, A, Korda, JB, Bolenz, C, Kalthoff, H, Sipos, B, Juenemann, K-P & van der Horst, C 2009, 'Lymphatic spread in squamous cell carcinoma of the penis is independent of elevated lymph vessel density.', BJU INT, vol. 103, no. 12, 12, pp. 1655-1659. <http://www.ncbi.nlm.nih.gov/pubmed/19220258?dopt=Citation>

APA

Naumann, C. M., Al-Najar, A., Alkatout, I., Hegele, A., Korda, J. B., Bolenz, C., Kalthoff, H., Sipos, B., Juenemann, K-P., & van der Horst, C. (2009). Lymphatic spread in squamous cell carcinoma of the penis is independent of elevated lymph vessel density. BJU INT, 103(12), 1655-1659. [12]. http://www.ncbi.nlm.nih.gov/pubmed/19220258?dopt=Citation

Vancouver

Naumann CM, Al-Najar A, Alkatout I, Hegele A, Korda JB, Bolenz C et al. Lymphatic spread in squamous cell carcinoma of the penis is independent of elevated lymph vessel density. BJU INT. 2009;103(12):1655-1659. 12.

Bibtex

@article{4e524d3af647464d81f9b6c0f95c1f6e,
title = "Lymphatic spread in squamous cell carcinoma of the penis is independent of elevated lymph vessel density.",
abstract = "OBJECTIVE: To examine the potential effect of tumour-induced lymphangiogenesis in squamous cell carcinoma of the penis as a possible mechanism responsible for lymphatic spread. PATIENTS AND METHODS: Specimens from 65 patients with invasive tumours (31 with and 34 without metastases) were evaluated for lymphatic vessel density (LVD) by the 'hot-spot' method as the density of lymphatic endothelium hyaluronan receptor (LYVE-1)-positive lymphatic vessels per unit area of tissue. LVD was examined in peritumoral, intratumoral and normal tissue areas. The LVD of each tumour in these locations was calculated as the mean of the three highest lymph vessel counts in three to five hot-spots. The nodal status was based on histopathological examination or an uneventful follow-up of >or=2 years. RESULTS: In all patients the mean (SD) peritumoral LVD of 8.05 (3.14)/0.75 mm(2) was significantly higher than for intratumoral and normal tissue, of 4.67 (2.58) and 5.20 (1.87), respectively (P <0.001). The slightly lower intratumoral LVD than in normal tissue was not significant. The peritumoral LVD was 8.07 (3.29) in metastatic and 8.03 (3.03) in non-metastatic carcinomas. The intratumoral LVD was 5.13 (3.01) in node-positive carcinomas and 4.28 (2.15) in tumours with no lymphatic node metastasis (LNM). Comparing tumours with and without LNM, there was no statistically significant difference between intra- and peritumoral LVD. CONCLUSION: Increased LVD does not significantly affect the lymphatic spread in penile carcinomas, indicating that there must be alternative mechanisms that selectively enable tumour cells to invade lymph vessels and to metastasize into the lymph nodes.",
author = "Naumann, {Carsten Maik} and Amr Al-Najar and Ibrahim Alkatout and Axel Hegele and Korda, {Joanna Beate} and Christian Bolenz and Holger Kalthoff and Bence Sipos and Klaus-Peter Juenemann and {van der Horst}, Christof",
year = "2009",
language = "Deutsch",
volume = "103",
pages = "1655--1659",
journal = "BJU INT",
issn = "1464-4096",
publisher = "Wiley-Blackwell",
number = "12",

}

RIS

TY - JOUR

T1 - Lymphatic spread in squamous cell carcinoma of the penis is independent of elevated lymph vessel density.

AU - Naumann, Carsten Maik

AU - Al-Najar, Amr

AU - Alkatout, Ibrahim

AU - Hegele, Axel

AU - Korda, Joanna Beate

AU - Bolenz, Christian

AU - Kalthoff, Holger

AU - Sipos, Bence

AU - Juenemann, Klaus-Peter

AU - van der Horst, Christof

PY - 2009

Y1 - 2009

N2 - OBJECTIVE: To examine the potential effect of tumour-induced lymphangiogenesis in squamous cell carcinoma of the penis as a possible mechanism responsible for lymphatic spread. PATIENTS AND METHODS: Specimens from 65 patients with invasive tumours (31 with and 34 without metastases) were evaluated for lymphatic vessel density (LVD) by the 'hot-spot' method as the density of lymphatic endothelium hyaluronan receptor (LYVE-1)-positive lymphatic vessels per unit area of tissue. LVD was examined in peritumoral, intratumoral and normal tissue areas. The LVD of each tumour in these locations was calculated as the mean of the three highest lymph vessel counts in three to five hot-spots. The nodal status was based on histopathological examination or an uneventful follow-up of >or=2 years. RESULTS: In all patients the mean (SD) peritumoral LVD of 8.05 (3.14)/0.75 mm(2) was significantly higher than for intratumoral and normal tissue, of 4.67 (2.58) and 5.20 (1.87), respectively (P <0.001). The slightly lower intratumoral LVD than in normal tissue was not significant. The peritumoral LVD was 8.07 (3.29) in metastatic and 8.03 (3.03) in non-metastatic carcinomas. The intratumoral LVD was 5.13 (3.01) in node-positive carcinomas and 4.28 (2.15) in tumours with no lymphatic node metastasis (LNM). Comparing tumours with and without LNM, there was no statistically significant difference between intra- and peritumoral LVD. CONCLUSION: Increased LVD does not significantly affect the lymphatic spread in penile carcinomas, indicating that there must be alternative mechanisms that selectively enable tumour cells to invade lymph vessels and to metastasize into the lymph nodes.

AB - OBJECTIVE: To examine the potential effect of tumour-induced lymphangiogenesis in squamous cell carcinoma of the penis as a possible mechanism responsible for lymphatic spread. PATIENTS AND METHODS: Specimens from 65 patients with invasive tumours (31 with and 34 without metastases) were evaluated for lymphatic vessel density (LVD) by the 'hot-spot' method as the density of lymphatic endothelium hyaluronan receptor (LYVE-1)-positive lymphatic vessels per unit area of tissue. LVD was examined in peritumoral, intratumoral and normal tissue areas. The LVD of each tumour in these locations was calculated as the mean of the three highest lymph vessel counts in three to five hot-spots. The nodal status was based on histopathological examination or an uneventful follow-up of >or=2 years. RESULTS: In all patients the mean (SD) peritumoral LVD of 8.05 (3.14)/0.75 mm(2) was significantly higher than for intratumoral and normal tissue, of 4.67 (2.58) and 5.20 (1.87), respectively (P <0.001). The slightly lower intratumoral LVD than in normal tissue was not significant. The peritumoral LVD was 8.07 (3.29) in metastatic and 8.03 (3.03) in non-metastatic carcinomas. The intratumoral LVD was 5.13 (3.01) in node-positive carcinomas and 4.28 (2.15) in tumours with no lymphatic node metastasis (LNM). Comparing tumours with and without LNM, there was no statistically significant difference between intra- and peritumoral LVD. CONCLUSION: Increased LVD does not significantly affect the lymphatic spread in penile carcinomas, indicating that there must be alternative mechanisms that selectively enable tumour cells to invade lymph vessels and to metastasize into the lymph nodes.

M3 - SCORING: Zeitschriftenaufsatz

VL - 103

SP - 1655

EP - 1659

JO - BJU INT

JF - BJU INT

SN - 1464-4096

IS - 12

M1 - 12

ER -