Activated leukocyte cell adhesion molecule (CD166/ALCAM): Developmental and mechanistic aspects of cell clustering and cell migration

Swart, Guido W.M.

doi:10.1078/0171-9335-00256

Cited by 231 publications

(212 citation statements)

References 55 publications

Supporting

Mentioning

202

Contrasting

Unclassified

Order By: Relevance

“…ALCAM is an adhesion molecule that acts through both homophylic and heterophylic interaction by CD6 binding. 23 In vitro experiments in articular chondrocytes have demonstrated that the expression of ALCAM and other cell adhesion molecules correlates with efficient cartilage formation, 24 and we have demonstrated high expression in CMF, specifically in the spindle-cell component at the periphery of the lobules. This pattern of distribution is strikingly similar to what was observed previously for the adhesion molecule N-cadherin in CMF.…”

Section: Discussionmentioning

confidence: 99%

The role of noncartilage‐specific molecules in differentiation of cartilaginous tumors

Romeo

Oosting

Rozeman

et al. 2007

Cancer

View full text Add to dashboard Cite

BACKGROUND.Chondroblastoma (CB) and chondromyxoid fibroma (CMF) are benign tumors of bone morphologically recapitulating cartilage differentiation. CMF can resemble high‐grade central chondrosarcoma (HGCCS) because of its cellular atypia. The mechanism that drives this morphologic spectrum of cartilage differentiation is unclear.METHODS.CMFs and CBs were hybridized on a complementary DNA microarray that was enriched for cartilage‐specific genes. Data were analyzed by Linear Model for Microarray Analysis and were compared with previous data on osteochondromas and HGCCS. Verification was performed in an extended series.RESULTS.None of the 68 genes that were differentially expressed in CB versus CMF, including several extracellular matrix (ECM) and ECM‐degradation genes, were related specifically to cartilage. Perlecan, versican, collagen 4A2 (Col4A2), and cell‐cell adhesion genes, such as CD166, were significantly higher in CMF. Sixty genes were expressed differentially in CMF versus HGCCS. Higher expression levels of CD166, cyclin D1 (CCND1), and p16INK4A were observed in CMF.CONCLUSIONS.The current findings indicated that differential expression of adhesion and ECM molecules, such as CD166, versican, perlecan, and Col4A2, may interfere with cartilaginous differentiation. The decreased expression of CCND1, p16INK4A, and CD166 in HGCCS reflects impairment of cell cycle progression and of cell‐cell adhesions in malignant tumors and is of use in the differential diagnosis of CMF. Cancer 2007. © 2007 American Cancer Society.

show abstract

Section: Discussionmentioning

confidence: 99%

The role of noncartilage‐specific molecules in differentiation of cartilaginous tumors

Romeo

Oosting

Rozeman

et al. 2007

Cancer

View full text Add to dashboard Cite

show abstract

“…ALCAM is a cell adhesion molecule expressed by epithelial cells in several organs and is involved in embryogenesis, angiogenesis, hematopoiesis (1), immune response (2) and, of course, cell adhesion (3). Cell adhesion molecules can be involved in tumor cell-tumor cell adhesion, tumor cellendothelial cell adhesion and tumor cell-matrix adhesion, which are all essential during primary tumor formation or metastasis at different times.…”

Section: Introductionmentioning

confidence: 99%

Loss of ALCAM expression is linked to adverse phenotype and poor prognosis in breast cancer: A TMA-based immunohistochemical study on 2,197 breast cancer patients

et al. 2014

View full text Add to dashboard Cite

Abstract. Activated leukocyte cell adhesion molecule (ALCAM) is a membranous cell adhesion protein that is often expressed in breast cancer. Data on the prognostic impact of ALCAM expression is highly controversial in this cancer. To evaluate the clinical impact of ALCAM expression in a sufficiently large patient cohort, we utilized a tissue microarray (TMA) containing more than 2,100 primary breast cancers with clinical follow-up data by immunohistochemistry. TMA spots containing normal breast epithelium showed moderate to strong membranous ALCAM staining. ALCAM staining was strong in 66.2%, moderate in 10.9%, weak in 11.1% and absent in 11.8% of 1,778 (80.9%) interpretable breast cancer tissue spots. Decreased ALCAM expression was significantly associated with advanced tumor size (p=0.0017), unfavorable tumor grade (p<0.0001), negative ER and PR status (p<0.0001 each) as well as high Ki67 labeling index (p<0.0001). Cancers with ACLAM expression loss had a significantly poorer overall (p<0.0001) and disease-specific survival (p= 0.0088). This association also held true in the subset of nodal positive cancers (p<0.0001). In conclusion, these data demonstrate that ALCAM is generally expressed in normal and cancerous breast epithelium and that a marked reduction of ALCAM expression characterizes a subset of breast cancer patients with adverse tumor characteristics and unfavorable clinical outcome.

show abstract

“…ALCAM (activated leucocyte cell adhesion molecule, synonym CD166) belongs to the Ig superfamily and mediates both heterophilic (ALCAM-CD6) and homophilic (ALCAM-ALCAM) cell -cell interactions (Swart, 2002). It is considered a prognostic marker in melanoma (van Kempen et al, 2000), prostate cancer (Kristiansen et al, 2005), breast cancer (King et al, 2004;Weichert et al, 2004;Burkhardt et al, 2006), colorectal cancer (Weichert et al, 2004), bladder cancer (Tomita et al, 2003), oesophageal squamous cell carcinoma (Verma et al, 2005) and ovarian cancer (Mezzanzanica et al, 2008).…”

mentioning

confidence: 99%

Increased expression of ALCAM/CD166 in pancreatic cancer is an independent prognostic marker for poor survival and early tumour relapse

et al. 2009

View full text Add to dashboard Cite

BACKGROUND: ALCAM (activated leucocyte cell adhesion molecule, synonym CD166) is a cell adhesion molecule, which belongs to the Ig superfamily. Disruption of the ALCAM-mediated adhesiveness by proteolytic sheddases such as ADAM17 has been suggested to have a relevant impact on tumour invasion. Although the expression of ALCAM is a valuable prognostic and predictive marker in several types of epithelial tumours, its role as a prognostic marker in pancreatic cancer has not yet been reported. METHODS: In this study, paraffin-embedded samples of 97 patients with pancreatic cancer undergoing potentially curative resection were immunostained against ALCAM, ADAM17 and CK19. Expression of ALCAM and ADAM17 was semiquantitatively evaluated and correlated to clinical and histopathological parameters. RESULTS: We could show that in normal pancreatic tissue, ALCAM is predominantly expressed at the cellular membrane, whereas in pancreatic tumour cells, it is mainly localised in the cytoplasm. In addition, univariate and multivariate analyses show that increased expression of ALCAM is an adverse prognostic factor for recurrence-free and overall survival. Overexpression of ADAM17 in pancreatic cancer, however, failed to be a significant prognostic marker and was not coexpressed with ALCAM. CONCLUSIONS: Our findings support the hypothesis that the disruption of ALCAM-mediated adhesiveness is a relevant step in pancreatic cancer progression. Moreover, ALCAM overexpression is a relevant independent prognostic marker for poor survival and early tumour relapse in pancreatic cancer.

show abstract

Activated leukocyte cell adhesion molecule (CD166/ALCAM): Developmental and mechanistic aspects of cell clustering and cell migration

Cited by 231 publications

References 55 publications

The role of noncartilage‐specific molecules in differentiation of cartilaginous tumors

The role of noncartilage‐specific molecules in differentiation of cartilaginous tumors

Loss of ALCAM expression is linked to adverse phenotype and poor prognosis in breast cancer: A TMA-based immunohistochemical study on 2,197 breast cancer patients

Increased expression of ALCAM/CD166 in pancreatic cancer is an independent prognostic marker for poor survival and early tumour relapse

Contact Info

Product

Resources

About