A renowned cancer researcher at the Massachusetts Institute of Technology (MIT) has retracted a highly cited paper published ten years ago because of "inadvertent sloppiness."
In the now retracted 2003 paper published in Cancer Cell, MIT researcher Robert Weinberg and his colleagues described the role of the thrombospondin-1 (TSP-1) protein in tumor growth (1). Since then, the article has been cited 233 times by other authors, according to Thomson Scientific’s Web of Knowledge.
Weinberg told the blog Retraction Watch that he withdrew the paper from the journal because of errors in the figures that occurred during their electronic preparation. He explained that a team member compiled the internal loading controls with the wrong experimental channels, a mistake affecting the immunoblot data shown in the paper.
Overall, Weinberg maintains that the conclusions of the paper are accurate, but although the errors "do not and did not affect the major conclusions of the paper, the journal nevertheless requested that we retract this paper because there were multiple errors in assembling these figures," he said. He also explained that no indication of scientific misconduct exists and that the errors were based on "inadvertent sloppiness" in the rush to assemble figures for the publication.
Weinberg's lab is known for the discovery of the first human oncogene, ras, which causes normal cells to form tumors. The team also isolated the first known tumor suppressor gene, which encodes the retinoblastoma (RB) protein.
In the 2003 Cancer Cell paper, Weinberg’s group "use a genetically defined tumor model system to evaluate the molecular regulators of the angiogenic switch," wrote Northwestern cancer researcher Olga Volpert and Johns Hopkins cancer researcher Rhoda M. Alani in a commentary article published in the same issue (2).
The paper showed that repression of TSP-1 is a critical step for enabling human cells to perform angiogenesis, the process through which new blood vessels form. The TSP-1 protein is a molecular organizer that brings together growth factors and other cellular components to regulate the phenotype of the cell during tissue development and repair.
In the study, repression of TSP-1 was essential for engineered mammalian epithelial and kidney cells to form tumors. The group also identified a signaling pathway that coordinated the activity of TSP-1, ras, and another oncogene, myc, and demonstrated its role in angiogenesis and tumor development.
Based on the results, the team argued that it had successfully created a model system for studying tumor dormancy, which they wrote was a "critical yet poorly understood phenomenon affecting both the diagnosis and treatment of human cancers."
According to their retraction statement, the researchers stand by their conclusions and plan to republish the data with corrected figures, plus results from new experiments that verify and advance the original findings. But for now, the paper and its findings will live on through its numerous citations.
1. Watnick, R. S., Y.-N. N. Cheng, A. Rangarajan, T. A. Ince, and R. A. Weinberg. 2003. Ras modulates myc activity to repress thrombospondin-1 expression and increase tumor angiogenesis. Cancer cell 3(3):219-231.
2. Volpert, O. and Alani, R. (2003) "Wiring the angiogenic switch: Ras, Myc, and Thrombospondin-1." Cancer Cell, 3: 199-200.