Adhesion molecules in human pancreatic cancer

Adrien A. Tempia-Caliera, Laszlo Zs Horvath, Arthur Zimmermann, Tibor T. Tihanyi, Murray Korc, Helmut Friess, Murray Korc

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

Background and Objectives: Adhesion molecules are cell surface glycoproteins that are important in cell-to-cell and cell-to-extracellular matrix interactions. In the present study, we analyzed the adhesion molecules ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1), and ELAM-1 (endothelial leukocyte adhesion molecule-1) in human pancreatic cancer. Methods: ICAM-1, VCAM-1, and ELAM-1 were analyzed in 20 pancreatic cancer specimens and 20 normal pancreatic tissues, mRNA expression encoding ICAM-1, VCAM-1, and ELAM-1 was assessed with Northern blot analysis. The distribution and localization of ICAM-1, VCAM-1, and ELAM-1 was determined in the pancreatic specimens by immunohistochemistry. Results: Northern blot analysis revealed a 5.4-fold increase of ICAM-1 (P <0.01) and a 3.7-fold increase in VCAM-1 (P <0.01) mRNA expression in cancer samples in comparison with normal controls. In contrast, ELAM-1 mRNA levels did not show significant differences between the cancer and the normal tissues. Immunohistochemical analysis of cancer tissues showed strong immunostaining for ICAM-1 and VCAM-1, and faint immunostaining for ELAM-1 in the pancreatic cancer cells. Fibrotic or noncancerous pancreatic tissue adjacent to the cancer mass was devoid of any immunoreactivity for ICAM-1, ELAM-1, and VCAM-1. In contrast, the normal pancreas exhibited no immunoreactivity of ICAM-1, ELAM-1, and VCAM-1. Conclusions: Enhanced expression of ICAM-1 and VCAM-1 in human pancreatic cancers suggests a role in tumor pathogenesis. The increase of these adhesion molecules might influence the detachment of cancer cells in the primary tumor, might contribute to cancer cell migration and the spread of cancer cells to distant organs, or both.

Original languageEnglish (US)
Pages (from-to)93-100
Number of pages8
JournalJournal of Surgical Oncology
Volume79
Issue number2
DOIs
StatePublished - 2002
Externally publishedYes

Fingerprint

Vascular Cell Adhesion Molecule-1
E-Selectin
Intercellular Adhesion Molecule-1
Pancreatic Neoplasms
Neoplasms
Northern Blotting
Messenger RNA
Membrane Glycoproteins
Cell Movement
Extracellular Matrix
Pancreas
Immunohistochemistry

Keywords

  • Adhesion molecules
  • ELAM-1
  • ICAM-1
  • Metastasis
  • Pancreatic cancer
  • VCAM-1

ASJC Scopus subject areas

  • Surgery
  • Oncology

Cite this

Tempia-Caliera, A. A., Horvath, L. Z., Zimmermann, A., Tihanyi, T. T., Korc, M., Friess, H., & Korc, M. (2002). Adhesion molecules in human pancreatic cancer. Journal of Surgical Oncology, 79(2), 93-100. https://doi.org/10.1002/jso.10053

Adhesion molecules in human pancreatic cancer. / Tempia-Caliera, Adrien A.; Horvath, Laszlo Zs; Zimmermann, Arthur; Tihanyi, Tibor T.; Korc, Murray; Friess, Helmut; Korc, Murray.

In: Journal of Surgical Oncology, Vol. 79, No. 2, 2002, p. 93-100.

Research output: Contribution to journalArticle

Tempia-Caliera, AA, Horvath, LZ, Zimmermann, A, Tihanyi, TT, Korc, M, Friess, H & Korc, M 2002, 'Adhesion molecules in human pancreatic cancer', Journal of Surgical Oncology, vol. 79, no. 2, pp. 93-100. https://doi.org/10.1002/jso.10053
Tempia-Caliera AA, Horvath LZ, Zimmermann A, Tihanyi TT, Korc M, Friess H et al. Adhesion molecules in human pancreatic cancer. Journal of Surgical Oncology. 2002;79(2):93-100. https://doi.org/10.1002/jso.10053
Tempia-Caliera, Adrien A. ; Horvath, Laszlo Zs ; Zimmermann, Arthur ; Tihanyi, Tibor T. ; Korc, Murray ; Friess, Helmut ; Korc, Murray. / Adhesion molecules in human pancreatic cancer. In: Journal of Surgical Oncology. 2002 ; Vol. 79, No. 2. pp. 93-100.
@article{7fa6d95dd5004bfaa0c9cb4cc685bb86,
title = "Adhesion molecules in human pancreatic cancer",
abstract = "Background and Objectives: Adhesion molecules are cell surface glycoproteins that are important in cell-to-cell and cell-to-extracellular matrix interactions. In the present study, we analyzed the adhesion molecules ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1), and ELAM-1 (endothelial leukocyte adhesion molecule-1) in human pancreatic cancer. Methods: ICAM-1, VCAM-1, and ELAM-1 were analyzed in 20 pancreatic cancer specimens and 20 normal pancreatic tissues, mRNA expression encoding ICAM-1, VCAM-1, and ELAM-1 was assessed with Northern blot analysis. The distribution and localization of ICAM-1, VCAM-1, and ELAM-1 was determined in the pancreatic specimens by immunohistochemistry. Results: Northern blot analysis revealed a 5.4-fold increase of ICAM-1 (P <0.01) and a 3.7-fold increase in VCAM-1 (P <0.01) mRNA expression in cancer samples in comparison with normal controls. In contrast, ELAM-1 mRNA levels did not show significant differences between the cancer and the normal tissues. Immunohistochemical analysis of cancer tissues showed strong immunostaining for ICAM-1 and VCAM-1, and faint immunostaining for ELAM-1 in the pancreatic cancer cells. Fibrotic or noncancerous pancreatic tissue adjacent to the cancer mass was devoid of any immunoreactivity for ICAM-1, ELAM-1, and VCAM-1. In contrast, the normal pancreas exhibited no immunoreactivity of ICAM-1, ELAM-1, and VCAM-1. Conclusions: Enhanced expression of ICAM-1 and VCAM-1 in human pancreatic cancers suggests a role in tumor pathogenesis. The increase of these adhesion molecules might influence the detachment of cancer cells in the primary tumor, might contribute to cancer cell migration and the spread of cancer cells to distant organs, or both.",
keywords = "Adhesion molecules, ELAM-1, ICAM-1, Metastasis, Pancreatic cancer, VCAM-1",
author = "Tempia-Caliera, {Adrien A.} and Horvath, {Laszlo Zs} and Arthur Zimmermann and Tihanyi, {Tibor T.} and Murray Korc and Helmut Friess and Murray Korc",
year = "2002",
doi = "10.1002/jso.10053",
language = "English (US)",
volume = "79",
pages = "93--100",
journal = "Journal of Surgical Oncology",
issn = "0022-4790",
publisher = "Wiley-Liss Inc.",
number = "2",

}

TY - JOUR

T1 - Adhesion molecules in human pancreatic cancer

AU - Tempia-Caliera, Adrien A.

AU - Horvath, Laszlo Zs

AU - Zimmermann, Arthur

AU - Tihanyi, Tibor T.

AU - Korc, Murray

AU - Friess, Helmut

AU - Korc, Murray

PY - 2002

Y1 - 2002

N2 - Background and Objectives: Adhesion molecules are cell surface glycoproteins that are important in cell-to-cell and cell-to-extracellular matrix interactions. In the present study, we analyzed the adhesion molecules ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1), and ELAM-1 (endothelial leukocyte adhesion molecule-1) in human pancreatic cancer. Methods: ICAM-1, VCAM-1, and ELAM-1 were analyzed in 20 pancreatic cancer specimens and 20 normal pancreatic tissues, mRNA expression encoding ICAM-1, VCAM-1, and ELAM-1 was assessed with Northern blot analysis. The distribution and localization of ICAM-1, VCAM-1, and ELAM-1 was determined in the pancreatic specimens by immunohistochemistry. Results: Northern blot analysis revealed a 5.4-fold increase of ICAM-1 (P <0.01) and a 3.7-fold increase in VCAM-1 (P <0.01) mRNA expression in cancer samples in comparison with normal controls. In contrast, ELAM-1 mRNA levels did not show significant differences between the cancer and the normal tissues. Immunohistochemical analysis of cancer tissues showed strong immunostaining for ICAM-1 and VCAM-1, and faint immunostaining for ELAM-1 in the pancreatic cancer cells. Fibrotic or noncancerous pancreatic tissue adjacent to the cancer mass was devoid of any immunoreactivity for ICAM-1, ELAM-1, and VCAM-1. In contrast, the normal pancreas exhibited no immunoreactivity of ICAM-1, ELAM-1, and VCAM-1. Conclusions: Enhanced expression of ICAM-1 and VCAM-1 in human pancreatic cancers suggests a role in tumor pathogenesis. The increase of these adhesion molecules might influence the detachment of cancer cells in the primary tumor, might contribute to cancer cell migration and the spread of cancer cells to distant organs, or both.

AB - Background and Objectives: Adhesion molecules are cell surface glycoproteins that are important in cell-to-cell and cell-to-extracellular matrix interactions. In the present study, we analyzed the adhesion molecules ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1), and ELAM-1 (endothelial leukocyte adhesion molecule-1) in human pancreatic cancer. Methods: ICAM-1, VCAM-1, and ELAM-1 were analyzed in 20 pancreatic cancer specimens and 20 normal pancreatic tissues, mRNA expression encoding ICAM-1, VCAM-1, and ELAM-1 was assessed with Northern blot analysis. The distribution and localization of ICAM-1, VCAM-1, and ELAM-1 was determined in the pancreatic specimens by immunohistochemistry. Results: Northern blot analysis revealed a 5.4-fold increase of ICAM-1 (P <0.01) and a 3.7-fold increase in VCAM-1 (P <0.01) mRNA expression in cancer samples in comparison with normal controls. In contrast, ELAM-1 mRNA levels did not show significant differences between the cancer and the normal tissues. Immunohistochemical analysis of cancer tissues showed strong immunostaining for ICAM-1 and VCAM-1, and faint immunostaining for ELAM-1 in the pancreatic cancer cells. Fibrotic or noncancerous pancreatic tissue adjacent to the cancer mass was devoid of any immunoreactivity for ICAM-1, ELAM-1, and VCAM-1. In contrast, the normal pancreas exhibited no immunoreactivity of ICAM-1, ELAM-1, and VCAM-1. Conclusions: Enhanced expression of ICAM-1 and VCAM-1 in human pancreatic cancers suggests a role in tumor pathogenesis. The increase of these adhesion molecules might influence the detachment of cancer cells in the primary tumor, might contribute to cancer cell migration and the spread of cancer cells to distant organs, or both.

KW - Adhesion molecules

KW - ELAM-1

KW - ICAM-1

KW - Metastasis

KW - Pancreatic cancer

KW - VCAM-1

UR - http://www.scopus.com/inward/record.url?scp=0036154774&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036154774&partnerID=8YFLogxK

U2 - 10.1002/jso.10053

DO - 10.1002/jso.10053

M3 - Article

C2 - 11815996

AN - SCOPUS:0036154774

VL - 79

SP - 93

EP - 100

JO - Journal of Surgical Oncology

JF - Journal of Surgical Oncology

SN - 0022-4790

IS - 2

ER -