Prognostic significance of endogenous adhesion/growth-regulatory lectins in lung cancer
vor 21 Jahren
Podcast
Podcaster
Beschreibung
vor 21 Jahren
Objective: To determine the expression of endogenous
adhesion/growth-regulatory lectins and their binding sites using
labeled tissue lectins as well as the binding profile of hyaluronic
acid as an approach to define new prognostic markers. Methods:
Sections of paraffin-embedded histological material of 481 lungs
from lung tumor patients following radical lung excision processed
by a routine immunohistochemical method (avidin-biotin labeling,
DAB chromogen). Specific antibodies against galectins-1 and - 3 and
the heparin-binding lectin were tested. Staining by labeled
galectins and hyaluronic acid was similarly visualized by a routine
protocol. After semiquantitative assessment of staining, the
results were compared with the pT and pN stages and the
histological type. Survival was calculated by univariate and
multivariate methods. Results: Binding of galectin-1 and its
expression tended to increase, whereas the parameters for
galectin-3 decreased in advanced pT and pN stages at a
statistically significant level. The number of positive cases was
considerably smaller among the cases with small cell lung cancer
than in the group with non-small-cell lung cancer, among which
adenocarcinomas figured prominently with the exception of
galectin-1 expression. Kaplan-Meier computations revealed that the
survival rate of patients with galectin-3-binding or
galectin-1-expressing tumors was significantly poorer than that of
the negative cases. In the multivariate calculations of survival
lymph node metastases ( p < 0.0001), histological type ( p =
0.003), galectin-3-binding capacity ( p = 0.01), galectin-3
expression ( p = 0.03) and pT status ( p = 0.003) proved to be
independent prognostic factors, not correlated with the pN stage.
Conclusion: The expression and the capacity to bind the
adhesion/growth regulatory galectin-3 is defined as an unfavorable
prognostic factor not correlated with the pTN stage. Copyright (C)
2005 S. Karger AG, Basel.
adhesion/growth-regulatory lectins and their binding sites using
labeled tissue lectins as well as the binding profile of hyaluronic
acid as an approach to define new prognostic markers. Methods:
Sections of paraffin-embedded histological material of 481 lungs
from lung tumor patients following radical lung excision processed
by a routine immunohistochemical method (avidin-biotin labeling,
DAB chromogen). Specific antibodies against galectins-1 and - 3 and
the heparin-binding lectin were tested. Staining by labeled
galectins and hyaluronic acid was similarly visualized by a routine
protocol. After semiquantitative assessment of staining, the
results were compared with the pT and pN stages and the
histological type. Survival was calculated by univariate and
multivariate methods. Results: Binding of galectin-1 and its
expression tended to increase, whereas the parameters for
galectin-3 decreased in advanced pT and pN stages at a
statistically significant level. The number of positive cases was
considerably smaller among the cases with small cell lung cancer
than in the group with non-small-cell lung cancer, among which
adenocarcinomas figured prominently with the exception of
galectin-1 expression. Kaplan-Meier computations revealed that the
survival rate of patients with galectin-3-binding or
galectin-1-expressing tumors was significantly poorer than that of
the negative cases. In the multivariate calculations of survival
lymph node metastases ( p < 0.0001), histological type ( p =
0.003), galectin-3-binding capacity ( p = 0.01), galectin-3
expression ( p = 0.03) and pT status ( p = 0.003) proved to be
independent prognostic factors, not correlated with the pN stage.
Conclusion: The expression and the capacity to bind the
adhesion/growth regulatory galectin-3 is defined as an unfavorable
prognostic factor not correlated with the pTN stage. Copyright (C)
2005 S. Karger AG, Basel.
Weitere Episoden
vor 21 Jahren
Kommentare (0)
Melde Dich an, um einen Kommentar zu schreiben.