Correction to: The proliferation marker pKi-67 becomes masked to MIB-1 staining after expression of its tandem repeats.

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Effect of cyclooxygenase-2 antisense oligodeoxyribonucleotides in A-549 lung cancer cells.

Background: Cyclooxygenase (COX)-2 is overexpressed in several tumor entities and seems to play a key role in carcinogenesis. This makes it a potential target in cancer therapy.

Materials And Methods: Twelve phosphorothioate-modified antisense oligonucleotides (asODNs) against six targets of COX-2 mRNA were transfected to A-549 lung carcinoma cells.

High-level mRNA quantification of proliferation marker pKi-67 is correlated with favorable prognosis in colorectal carcinoma.

Purpose: The present study retrospectively examines the expression of pKi-67 mRNA and protein in colorectal carcinoma and their correlation to the outcome of patients.

Methods: Immunohistochemistry and quantitative RT-PCR were used to analyze the expression of pKi-67 in 43 archival specimens of patients with curatively resected primary colorectal carcinoma, who were not treated with neo-adjuvant therapy.

Results: We determined a median pKi-67 (MIB-1) labeling index of 31.

Detection of mutations in the cDNA of the proliferation marker Ki-67 protein in four tumor cell lines.

The Ki-67 protein has an essential role in cell proliferation. It is present in all dividing cells of normal and tumor tissues, but absent in resting cells. At present, no data are available about any alterations in the gene of this protein that could contribute to its altered structure and function, resulting in tumor development.

Proliferation marker pKi-67 occurs in different isoforms with various cellular effects.

The Ki-67 antigen, pKi-67, is a commonly used proliferation marker in research and pathology. It has been recognized that the protein exists in two different splice variants that differ in one exon. In the current work, we present three new splice variants of human pKi-67 consisting of two naturally occurring isoforms and one atypical version.

Diagnosis and monitoring of colorectal cancer by L6 blood serum polymerase chain reaction is superior to carcinoembryonic antigen-enzyme-linked immunosorbent assay.

Purpose: The aim of this study was to compare carcinoembryonic antigen levels with detection of messenger ribonucleic acid coding for the tumor-associated antigen L6 in patients with colorectal cancer. Not only are carcinoembryonic antigens expressed by the corresponding tumor cell, but the messenger ribonucleic acid of tumor-associated antigens, in contrast, is produced exclusively by viable tumor cells.

Methods: L6 messenger ribonucleic acid was determined by reverse-transcription polymerase chain reaction.

The proliferation marker pKi-67 organizes the nucleolus during the cell cycle depending on Ran and cyclin B.

The proliferation marker pKi-67 ('Ki-67 antigen') is commonly used in clinical and research pathology to detect proliferating cells, as it is only expressed during cell-cycle progression. Despite the fact that this antigen has been known for nearly two decades, there is still no adequate understanding of its function. This study has therefore identified proteins that interact with pKi-67, using a yeast two-hybrid system.

The proliferation marker pKi-67 becomes masked to MIB-1 staining after expression of its tandem repeats.

The Ki-67 antigen, pKi-67, is one of the most commonly used markers of proliferating cells. The protein can only be detected in dividing cells (G(1)-, S-, G(2)-, and M-phase) but not in quiescent cells (G(0)). The standard antibody to detect pKi-67 is MIB-1, which detects the so-called 'Ki-67 motif' FKELF in 9 of the protein's 16 tandem repeats.

Proliferation marker pKi-67 affects the cell cycle in a self-regulated manner.

The proliferation marker pKi-67 is commonly used in research and pathology to detect proliferating cells. In a previous work, we found the protein to be associated with regulators of the cell cycle, controlling S-phase progression, as well as entry into and exit from mitosis. Here we investigate whether pKi-67 has a regulative effect on the cell cycle itself.

VEGF isoforms and mutations in human colorectal cancer.

We wished to demonstrate vascular endothelial growth factor (VEGF) transcript polymorphism in human colon cancer. RNA was extracted from 25 primary human colorectal adenocarcinomas followed by VEGF transcript amplification, fragment elution, subcloning, positive selection via insert analysis and sequencing. Four distinct splice variants were consistently expressed in cancer, including VEGF121, VEGF165, VEGF189 and the newly identified truncated splice variant VEGF145.