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Table of Contents
Year : 2019  |  Volume : 6  |  Issue : 4  |  Page : 200-202

Liquefaction of metastatic radioactive iodine-refractory follicular thyroid carcinoma following radiotherapy and sorafenib

1 Department of Hematology and Oncology, China Medical University Hospital, Taichung, Taiwan
2 Department of Hematology and Oncology; School of Pharmacy, China Medical University, Taichung, Taiwan

Date of Submission18-Apr-2019
Date of Decision14-Aug-2019
Date of Acceptance26-Aug-2019
Date of Web Publication22-Nov-2019

Correspondence Address:
Dr. Chen-Yuan Lin
Department of Hematology and Oncology, China Medical University Hospital, No. 2, Yu-Der Rd., Taichung City 40447
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCRP.JCRP_19_19

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Sorafenib was approved for radioactive iodine (RAI)-refractory metastatic differentiated thyroid carcinoma in 2013. Herein, we describe the first case of metastatic RAI-refractory follicular thyroid carcinoma that markedly improved with liquefaction after radiotherapy and low-dose sorafenib use (200 mg twice daily).

Keywords: Liquefaction, radiotherapy, sorafenib, thyroid cancer

How to cite this article:
Tien JZ, Lin CY. Liquefaction of metastatic radioactive iodine-refractory follicular thyroid carcinoma following radiotherapy and sorafenib. J Cancer Res Pract 2019;6:200-2

How to cite this URL:
Tien JZ, Lin CY. Liquefaction of metastatic radioactive iodine-refractory follicular thyroid carcinoma following radiotherapy and sorafenib. J Cancer Res Pract [serial online] 2019 [cited 2023 Feb 2];6:200-2. Available from: https://www.ejcrp.org/text.asp?2019/6/4/200/271497

  Introduction Top

Liquefaction is an independent prognostic factor for patients with osteosarcoma, but it has yet to be reported in thyroid carcinoma. This is the first published English language case report of treatment-induced tumor necrosis in metastatic-differentiated thyroid carcinoma.

  Case Report Top

A 37-year-old female visited a plastic surgery outpatient clinic with a subcutaneous mass (7 cm × 7 cm) at the left occipital area which had been growing for 7 months. Approximately 5 years previously, she had undergone right thyroidectomy due to goiter, and the pathology showed no malignancy. Brain magnetic resonance imaging showed an extraaxial mass measuring 7.3 cm × 6 cm × 7 cm at the left parietal region with some necrosis and hemorrhages [Figure 1]a and [Figure 1]b.
Figure 1: (a) Axial T1 fluid-attenuated inversion recovery with contrast and fat suppression revealed a hypervascular extra-axial tumor. (b) Axial T2* gradient recalled echo exhibited some hemorrhages

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She underwent left parietal-occipital craniectomy with removal of the brain tumor. The pathology revealed metastatic follicular thyroid carcinoma with skull bone [Figure 2]a and meninx invasion [Figure 2]b. Left thyroidectomy was performed to find the primary site [Figure 2]c and [Figure 2]d of the thyroid carcinoma, but the pathology revealed a benign thyroid tissue without evidence of malignancy. She underwent adjuvant radioactive iodine (RAI) therapy four times with 200 mCi in each cycle. However, she complained of worsening left thigh pain. Abdominal computed tomography (CT) revealed a large metastatic tumor up to 8.8 cm in size in the left L1–L4 paraspinal region [Figure 3]a, and positron emission tomography (PET) revealed a large hypermetabolic mass [Figure 3]b.
Figure 2: (a) Metastatic follicular thyroid carcinoma with skull invasion, ×10. (b) Metastatic follicular thyroid carcinoma with meninx invasion, ×10. (c) Positive thyroid transcription factor-1, ×10. (d) Negative galectin-3, ×10

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Figure 3: (a) A large metastatic tumor up to 8.8 cm in size in the left L1–L4 paraspinal region. (b) A large hypermetabolic mass

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Her serum thyroid-stimulating hormone and thyroglobulin levels were <0.005 mIU/L and 1564.9 ng/mL, respectively, at that time. We initiated palliative radiotherapy with 30 Gy/15 Fx to the left L1–L4 paraspinal mass for symptom relief and also started low-dose sorafenib treatment (200 mg twice daily) to minimize the risk of sorafenib-related toxicity. Her left thigh pain improved gradually. Three months later, her serum thyroglobulin level decreased to 433.8 ng/mL. Abdominal CT showed a smaller lumbar paraspinal metastatic tumor (up to 6 cm in size) with central liquefaction and peripheral contrast enhancement [Figure 4]a. A PET image revealed decreased fluorodeoxyglucose uptake in the tumor periphery and a central cold zone [Figure 4]b. She experienced only a Grade 1–2 hand–foot skin reaction and diarrhea.
Figure 4: (a) Smaller lumbar paraspinal metastatic tumor (up to 6 cm in size) with central liquefaction and peripheral contrast enhancement. (b) Decreased fluorodeoxyglucose uptake in the periphery of the tumor and the central cold zone

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  Discussion Top

According to the 2015 American Thyroid Association guidelines, external-beam radiotherapy (EBRT) is indicated for locoregional control and symptoms relief in metastatic thyroid carcinoma if RAI-resistance occurs.[1] The first case report[2] about concurrent EBRT with sorafenib or doxorubicin included five patients with bulky differentiated thyroid carcinoma and demonstrated tolerable toxicity (two patients experienced G2 mucositis and two patients experienced G1 palmoplantar erythrodysesthesia) and acceptable antitumor activity (all had a partial response). The total dose of radiotherapy ranged from 50 to 64.8 Gy and four of the five patients received concurrent sorafenib. The dose of sorafenib in two patients was 400 mg twice daily and the other two received 400 mg daily. Despite a lower radiotherapy dose (total 30 Gy) and low-dose sorafenib (200 mg twice daily), our case had a similar partial response as in the previous research. In addition, this is the first case to show a significant improvement with treatment-related liquefaction.

Tumor necrosis is considered to be a consequence of several complex processes, including tumor cell apoptosis, insufficient blood supply, and tissue-lysing substances released from inflammatory cells. Three mechanisms underlying radiation-induced cell death have been proposed: apoptosis, mitotic catastrophe, and senescence.[3] Sorafenib inhibits cell proliferation by inducing cell cycle arrest and caspase activation.[4] The spectrum of multikinase inhibition of sorafenib may have a synergistic effect with radiation.[5] Tang et al.[6] observed that Raf-1 was overexpressed in radiation-resistant hepatocellular carcinoma cells and that targeting Raf-1 with sorafenib may resensitize these cells to radiation in vitro. Based on these studies, we hypothesize that the intensity of radiation-induced cell death can be strengthened with the use of sorafenib, which led to a partial response with liquefactive changes in our patient. Nevertheless, additional studies are required to confirm this hypothesis.

Ethical statement

This case report is approved by the Research Ethics Committee of CMUH with approval number: CMUH108-REC3-048.

The patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Haugen BR, Alexander EK, Bible KC, Doherty GM, Mandel SJ, Nikiforov YE, et al. 2015 American thyroid association management guidelines for adult patients with thyroid nodules and differentiated thyroid cancer: The American thyroid association guidelines task force on thyroid nodules and differentiated thyroid cancer. Thyroid 2016;26:1-133.  Back to cited text no. 1
Cortés-Mateus KS, Holub K, Racca F, Grau JJ, Capdevila J. Concurrent palliative external radiotherapy with sorafenib or doxorubicin for bulky differentiated thyroid carcinoma: A case report. Oncol Lett 2018;16:4085-9.  Back to cited text no. 2
Eriksson D, Stigbrand T. Radiation-induced cell death mechanisms. Tumour Biol 2010;31:363-72.  Back to cited text no. 3
Broecker-Preuss M, Müller S, Britten M, Worm K, Schmid KW, Mann K, et al. Sorafenib inhibits intracellular signaling pathways and induces cell cycle arrest and cell death in thyroid carcinoma cells irrespective of histological origin or BRAF mutational status. BMC Cancer 2015;15:184.  Back to cited text no. 4
Ibrahim N, Yu Y, Walsh WR, Yang JL. Molecular targeted therapies for cancer: Sorafenib mono-therapy and its combination with other therapies (review). Oncol Rep 2012;27:1303-11.  Back to cited text no. 5
Tang WY, Chau SP, Tsang WP, Kong SK, Kwok TT. The role of raf-1 in radiation resistance of human hepatocellular carcinoma hep G2 cells. Oncol Rep 2004;12:1349-54.  Back to cited text no. 6


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

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