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TKTL1 is overexpressed in a large portion of non-small cell lung cancer specimens

Holger Schultz1, Daniel Kähler1, Detlev Branscheid2, Ekkehard Vollmer1, Peter Zabel34 and Torsten Goldmann1*

Author affiliations

1 Research Center Borstel, Clinical and Experimental Pathology, Parkallee 3a, D-23845, Borstel, Germany

2 Hospital Großhansdorf, Department of Thoracic Surgery, Wöhrendamm 80, D-22927, Großhansdorf, Germany

3 Medical University Hospital III Lübeck/Department of Clinical Medicine, Research Center Borstel, Parkallee 35, D-23845 Borstel, Germany

4 Ratzeburger Allee 160, D-23562 Lübeck, Germany

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Citation and License

Diagnostic Pathology 2008, 3:35  doi:10.1186/1746-1596-3-35

Published: 12 August 2008


In several tumors the transketolase activity, controlled inter alia by enzymes of the pentose phosphate pathway which is an alternative, energy generating reaction-cascade to glycolysis, has been correlated with proliferation. The increase of thiamine-dependant transketolase enzyme reactions is induced especially through upregulated transketolase-like enzyme 1 (TKTL1)-activity; that shows TKTL1 to be a causative enzyme for tumors enhanced, anaerobic glucose degradation. We investigated TKTL1-expression in 88 human, formalin-fixed non-small cell lung cancer tissues and 24 carcinomas of the breast by immunohistochemical stainings applying a 0 to 3 staining-score system (3 = strongest expression). For means of validation we additionally stained 40 NSCLC fixed and paraffin-embedded utilizing the HOPE-technique; showing comparable results to the formalin-fixed, paraffin-embedded specimens (not shown). Potential correlations with age, sex, TNM-classification parameters and tumor grading as well as tumor transcription factor 1 (TTF1) and surfactant protein A (SPA) expression were investigated. 40.9% of the analyzed lung tumors expressed TKTL1 weakly (Score 1), 38.6% moderately (score 2) and 17.1% strongly (score 3). 3 tumors were diagnosed TKTL1-negative (3.4%; score 0). All Breast cancer specimen stainings were positive and scored 1: 32%; scored 2: 36%; scored 3: 32%. Alveolar macrophages and Alveolar Epithelial Cells Type II were also found to be TKTL1-positive.

None of the listed clinical parameters could be found to show a significant correlation to TKTL1 signal appearance.

Although we describe the expression of TKTL1 in lung cancers, we need to state that up till now there is no scientific indication for any treatment regimens based upon these findings.