(Secondary) solid tumors in thyroid cancer patients treated with the multi-kinase inhibitor sorafenib may present diagnostic challenges

BMC Cancer

Volumn 16, Issue 1, 2016, Pages

  Schneider, Tatiana C ^a   Kapiteijn, Ellen ^a   van Wezel, Tom ^a   Smit, Jan W A ^b   van der Hoeven, Jacobus J M ^a   Morreau, Hans ^a  

^a LEIDEN UNIVERSITY MEDICAL CENTER   (Netherlands)

^b RADBOUD UNIVERSITY MEDICAL CENTER   (Netherlands)

Author keywords

Clonal divergence; Differentiated thyroid cancer; Sorafenib; Squamous cell carcinoma; Squamous differentiation

Indexed keywords

RADIOACTIVE IODINE; SORAFENIB; B RAF KINASE; BRAF PROTEIN, HUMAN; CARBANILAMIDE DERIVATIVE; KRAS PROTEIN, HUMAN; NICOTINAMIDE; PROTEIN KINASE INHIBITOR; PROTEIN P21;

ADULT; AGED; ARTICLE; BRAF GENE; CANCER CHEMOTHERAPY; CANCER RECURRENCE; CASE REPORT; DIARRHEA; DNA SEQUENCE; DRUG DOSE REDUCTION; DRUG SAFETY; DRUG WITHDRAWAL; FEMALE; GENE; GENE MUTATION; HAND FOOT SYNDROME; HISTOPATHOLOGY; HUMAN; HUMAN TISSUE; LARYNX CARCINOMA; LUNG ADENOCARCINOMA; LUNG METASTASIS; LYMPH NODE DISSECTION; LYMPH NODE METASTASIS; MALE; MALIGNANT PLEURA EFFUSION; MIDDLE AGED; PHASE 2 CLINICAL TRIAL (TOPIC); THYROID METASTASIS; THYROID PAPILLARY CARCINOMA; THYROIDECTOMY; TONGUE CARCINOMA; ANALOGS AND DERIVATIVES; APOPTOSIS; CARCINOGENESIS; CHEMICALLY INDUCED; DRUG EFFECTS; GENETICS; MUTATION; NEOVASCULARIZATION, PATHOLOGIC; PATHOLOGY; SECONDARY; SQUAMOUS CELL CARCINOMA; THYROID NEOPLASMS; TUMOR RECURRENCE;

AGED; APOPTOSIS; CARCINOGENESIS; CARCINOMA, SQUAMOUS CELL; FEMALE; HUMANS; MALE; MIDDLE AGED; MUTATION; NEOPLASM RECURRENCE, LOCAL; NEOVASCULARIZATION, PATHOLOGIC; NIACINAMIDE; PHENYLUREA COMPOUNDS; PROTEIN KINASE INHIBITORS; PROTO-ONCOGENE PROTEINS B-RAF; PROTO-ONCOGENE PROTEINS P21(RAS); THYROID NEOPLASMS;

EID: 84955250780     PISSN: None     EISSN: 14712407     Source Type: Journal    
DOI: 10.1186/s12885-016-2060-4     Document Type: Article

References (18)

1. Brose MS, Nutting CM, Jarzab B, Elisei R, Siena S, Bastholt L, et al. Sorafenib in radioactive iodine-refractory, locally advanced or metastatic differentiated thyroid cancer: a randomised, double-blind, phase 3 trial. Lancet epub ahead of print].
2. Schneider TC, Abdulrahman RM, Corssmit EP, Morreau H, Smit JW. Long-term analysis of the efficacy and tolerability of sorafenib in advanced radio-iodine refractory differentiated thyroid carcinoma: final results of a phase II trial. Eur J Endocrinol. 2012;167(5):643-50.
3. Arnault JP, Mateus C, Escudier B, Tomasic G, Wechsler J, Hollville E, et al. Skin tumors induced by sorafenib; paradoxic RAS-RAF pathway activation and oncogenic mutations of HRAS, TP53, and TGFBR1. Clin Cancer Res. 2012;18(1):263-72.
4. Dubauskas Z, Kunishige J, Prieto VG, Jonasch E, Hwu P, Tannir NM. Cutaneous squamous cell carcinoma and inflammation of actinic keratoses associated with sorafenib. Clin Genitourin Cancer. 2009;7(1):20-3.
5. Hong DS, Reddy SB, Prieto VG, Wright JJ, Tannir NM, Cohen PR, et al. Multiple squamous cell carcinomas of the skin after therapy with sorafenib combined with tipifarnib. Arch Dermatol. 2008;144(6):779-82.
6. Raymond AK, Puri PK, Selim MA, Tyler DS, Nelson KC. Regional squamous cell carcinomas following systemic sorafenib therapy and isolated limb infusion for regionally advanced metastatic melanoma of the limb. Arch Dermatol. 2010;146(12):1438-9.
7. Smith KJ, Haley H, Hamza S, Skelton HG. Eruptive keratoacanthoma-type squamous cell carcinomas in patients taking sorafenib for the treatment of solid tumors. Dermatol Surg. 2009;35(11):1766-70.
8. Williams VL, Cohen PR, Stewart DJ. Sorafenib-induced premalignant and malignant skin lesions. Int J Dermatol. 2011;50(4):396-402.
9. van Eijk R, van Puijenbroek M, Chhatta AR, Gupta N, Vossen RH, Lips EH, et al. Sensitive and specific KRAS somatic mutation analysis on whole-genome amplified DNA from archival tissues. J Mol Diagn. 2010;12:27-34.
10. Hoftijzer H, Heemstra KA, Morreau H, Stokkel MP, Corssmit EP, Gelderblom H, et al. Beneficial effects of sorafenib on tumor progression, but not on radioiodine uptake, in patients with differentiated thyroid carcinoma. Eur J Endocrinol. 2009;161:923-31.
11. Therasse P, Arbuck SG, Eisenhauer EA, Wanders J, Kaplan RS, Rubinstein L, et al. New guidelines to evaluate the response to treatment in solid tumors. J Natl Cancer Inst. 2009;92:205-16.
12. Lee YW. Peptide nucleic acid clamp polymerase chain reaction reveals a deletion mutation of the BRAFgene in papillary thyroid carcinoma: A case report. Exp Ther Med. 2013;6:1550-2.
13. Lee SR, Jung CK, Kim TE, Bae JS, Jung SL, Choi YJ, et al. Molecular genotyping of follicular variant of papillary thyroid carcinoma correlates with diagnostic category of fine-needle aspiration cytology: values of RAS mutation testing. Thyroid. 2013;11:1416-22.
14. Jang MA, Lee ST, Oh YL, Kim SW, Chung JH, Ki CS, et al. Identification of a rare 3 bp BRAF gene deletion in a thyroid nodule by mutant enrichment with 3'-modified oligonucleotides polymerase chain reaction. Ann Lab Med. 2012;3:238-41.
15. Su F, Viros A, Milagre C, Trunzer K, Bollag G, Spleiss O, et al. RAS mutations in cutaneous squamous-cell carcinomas in patients treated with BRAF inhibitors. N Engl J Med. 2012;366:207-15.
16. Callahan MK1, Rampal R, Harding JJ, Klimek VM, Chung YR, Merghoub T, et al. Progression of RAS-mutant leukemia during RAF inhibitor treatment. N Engl J Med. 2012;367:2316-21.
17. Chapman P, Metz D, Sepulveda AR. Development of colonic adenomas and gastric polyps in BRAF mutant melanoma patients treated with vemurafenib. Pigment Cell Melanoma Res. 2012;25:847.
18. Andrews MC, Behren A, Chionh F, Mariadason J, Vella LJ. BRAF inhibitor-driven tumor proliferation in a KRAS-mutated colon carcinoma is not overcome by MEK1/2 inhibition. J Clin Oncol. 2013;31:e448-51.