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Letters To The Editor

In Reply

^aDivision of Clinical Pharmacology, Department of Medical Oncology, and ^bDepartment of Nuclear Medicine, The Netherlands Cancer Institute, Amsterdam, The Netherlands; ^cUtrecht University, Faculty of Science, Department of Pharmaceutical Sciences, Section of Biomedical Analysis, Division of Drug Toxicology, Utrecht, The Netherlands; ^dDepartment of Pharmacy and Pharmacology, Slotervaart Hospital, Amsterdam, The Netherlands

Correspondence: D. S. Boss, MSC, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands. Telephone: 31-20-512-4657; Fax: 31-20-512-2572; e-mail: d.boss{at}nki.nl

Received April 4, 2008; accepted for publication April 15, 2008.

Disclosure: No potential conflicts of interest were reported by the authors.

We read with interest the letter entitled ¹⁸F-Fluorodeoxyglucose Positron Emission Tomography for Monitoring Response to Sorafenib Treatment in Patients with Hepatocellular Carcinoma by Siemerink et al.

Because of a lack of tumor uptake, there is as yet no defined role for ¹⁸F-FDG-PET in the staging of HCC, but ¹⁸F-FDG-PET might be valuable for the assessment of therapy response in patients with demonstrated tumor uptake at baseline. This is stated in the review by Hain and Fogelman [1]. However, we have found no prospective study in which ¹⁸F-FDG-PET scans were made at baseline and early in the course of therapy in patients with HCC. The studies that Hain and Fogelman [1] refer to in their review include one retrospective study [2] and one study in which baseline ¹⁸F-FDG uptake levels were correlated with clinical outcome [3]. In other words, at this moment there is no evidence that ¹⁸F-FDG-PET is valuable for early response measurements in patients with HCC. Perhaps this makes the findings of Siemerink et al. even more interesting.

Sorafenib is, in our opinion, an attractive drug for evaluation of its antitumor activity by ¹⁸F-FDG-PET. It is a multikinase inhibitor, with platelet-derived growth factor receptor, vascular endothelial growth factor receptor, Raf kinase, and c-Kit as predominant targets. The latter is of importance when considering ¹⁸F-FDG-PET response measurements. It has been shown that c-Kit inhibition leads to a downregulation of Glut-1, the most important transporter of glucose into the cell [4]. Consequently, treatment with sorafenib, as with imatinib, might lead to reduced ¹⁸F-FDG uptake.

In the letter by Siemerink et al., ¹⁸F-FDG-PET scans were made at baseline and after 3 weeks of treatment. After treatment with imatinib, ¹⁸F-FDG-PET responses can already be observed after 1 week of therapy, or even earlier [5]. Perhaps responses to sorafenib can also be seen after 1 week of therapy. In our opinion, it would be valuable to study ¹⁸F-FDG-PET uptake even earlier in the course of treatment, for example, after 1 week of drug treatment.

In conclusion, the use of ¹⁸F-FDG-PET for assessment of response to sorafenib therapy might be valuable, as stated by Siemerink et al. We share their opinion that these results should be confirmed in a larger population. We suggest measuring the response to sorafenib treatment even earlier in the course of therapy.

	AUTHOR CONTRIBUTIONS

Top Author Contributions References

 
Conception/design: D. S. Boss, J. H. Schellens

Manuscript writing: D. S. Boss, J. H. Schellens

Final approval of manuscript: D. S. Boss, R. V. Olmos, M. Sinaasappel, J. H. Beijnen, J. H. Schellens

	REFERENCES

Top Author Contributions References

 

1. Hain SF, Fogelman I. Recent advances in imaging hepatocellular carcinoma: Diagnosis, staging and response assessment: Functional imaging. Cancer J 2004;10:121–127.[CrossRef][Medline]
2. Wudel LJ Jr, Delbeke D, Morris D et al. The role of [18F]fluorodeoxyglucose positron emission tomography imaging in the evaluation of hepatocellular carcinoma. Am Surg 2003;69:117–124; discussion 124–126.[Medline]
3. Shiomi S, Nishiguchi S, Ishizu H et al. Usefulness of positron emission tomography with fluorine-18-fluorodeoxyglucose for predicting outcome in patients with hepatocellular carcinoma. Am J Gastroenterol 2001;96:1877–1880.[CrossRef][Medline]
4. Culinane C, Dorow DS, Kansara M et al. An in vivo tumor model exploiting metabolic response as a biomarker for targeted drug development. Cancer Res 2005;65:9633–9636.[Abstract/Free Full Text]
5. Van den Abbeele, for the GIST Collaborative PET study group, F18-FDG PET provides early evidence of biological response to STI571 in patients with malignant gastrointestinal stromal tumors (GIST). the 2001 American Society of Clinical Oncology Annual Meeting; May 12–15, 2001; San Francisco, CA, Presented at.

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