VOLUME
33
䡠
NUMBER
17
䡠
JUNE
10
2015
JOURNAL OF CLINICAL ONCOLOGY
Follicular Dendritic Cell Sarcoma Presenting As a Thyroid Mass Case Report A 44-year-old white woman with a history of Hashimoto’s thyroiditis presented to her primary care physician for routine evaluation. A palpable right-sided thyroid nodule was noted. Ultrasound demonstrated heterogeneous enlargement of the thyroid with two 1 cm thyroid nodules (one hypoechoic, one isoechoic) in the lower pole of the right thyroid lobe. A 6-month follow-up ultrasound revealed a hypoechoic nodule measuring 2.7 ⫻ 1.7 ⫻ 2.2 cm (Fig 1A, gold arrow) with peripheral nodularity (Fig 1A, white arrowheads) and Doppler flow (Fig 1B)—all features of malignancy. Fine-needle aspiration suggested anaplastic thyroid carcinoma.
A
B
Fig 1. e74
© 2014 by American Society of Clinical Oncology
D I A G N O S I S
I N
O N C O L O G Y
The patient underwent a total thyroidectomy, central compartment dissection, and parathyroid reimplantation. Pathology revealed a 2.5 cm extranodal follicular dendritic cell sarcoma (FDCS) (Figs 2A and 2B, inset) in a background of a lymphocytic infiltrate. The tumor was described as high grade due to significant cytological atypia and nuclear pleomorphism. One intrathyroidal parathyroid gland was involved by tumor, as were three of 11 lymph nodes in the central compartment (Fig 2C). Surgical margins of the tumor were negative. Immunostains for CD21 (Fig 2D), CD23 (Fig 2E), vimentin, clusterin (Fig 2F), fascin, podoplanin, and CXCL13 were positive. No features of Castleman’s disease were seen within the tumor specimen or lymph nodes removed. Epstein-Barr virus (EBV) in situ hybridization was negative, as was calcitonin. Adjuvantly, our patient received parotidsparing intensity-modulated radiation therapy (IMRT) to the bilateral neck and tumor bed with 54 Gy. She did not receive adjuvant chemotherapy due to the lack of benefit in reported series.1 Because of the rarity of the tumor, lack of benefit with known systemic agents, and absence of genomic characterization in the literature, we analyzed the genomic profile of the tumor utilizing the Foundation One genomic analysis developed by the Broad Institute (Cambridge, MA). The assay uses next-generation sequencing to evaluate the status of 236 cancer-related genes. Discussion FDCS has been defined by the World Health Organization as a low-grade sarcoma with follicular dendritic cell differentiation.2 The disease was first described by Monda et al in 1986.3 Pathology is characterized by spindle to ovoid cells in fascicular, whorled, or storiform patterns with occasional multinucleated giant cells. Here we report only the third case of extranodal FDCS involving the thyroid.4,5 Interestingly, all three cases (including ours) of FDCS involving the thyroid were in the background of Hashimoto’s thyroiditis (ie, lymphocytic thyroiditis). The etiology is unknown but some studies have identified FDCS in association with hyaline vascular Castleman’s disease to suggest that Castleman’s may be a precursor.6,7 Because of a possible association with EBV and Castleman’s disease,8,9 EBV in situ hybridization testing has been previously performed in FDCS.10-12 Only one of twenty seven cases had positive EBV in situ hybridization and this case did have evidence of Castleman’s disease. Immunohistochemistry of FDCS typically identifies one or more of the following markers: CD21, CD23, CD35, podoplanin,13 and CXCL-13.14 In the two largest published series (51 and 54 patients), FDCS has a median age of 41 and 53 years with no gender predilection.1,15 It usually presents as cervical or axillary lymphadenopathy; however, up to one third may present with extranodal disease.1 Extranodal presentation is usually in the head, neck, and abdominal regions.15 Due to its rarity, FDCS is often initially misdiagnosed. Duan et al12 reported that of the 36 cases they reviewed, 21 (58%) were initially misdiagnosed. An adequate biopsy specimen is crucial to making the correct diagnosis. Our patient’s initial biopsy showed large atypical cells suggestive of a poorly differentiated carcinoma. In the setting of a thyroid mass the Journal of Clinical Oncology, Vol 33, No 17 (June 10), 2015: pp e74-e76
Information downloaded from jco.ascopubs.org and provided by at CAMBRIDGE UNIV MEDICAL LIBRARY on September Copyright © 2015 American Society Clinical Oncology. All rights reserved. 12, 2015 from of 131.111.164.128
Diagnosis in Oncology
A
B
C
500 µm
D
500 µm
E
500 µm
F
500 µm
500 µm
500 µm
Fig 2.
diagnosis of anaplastic thyroid carcinoma was considered. Some features that would help the clinician differentiate FDCS from poorly differentiated carcinomas is negative immunohistochemistry (IHC) for cytokeratin and epithelial membrane antigen, lack of irregular infiltrative tumor islands, lack of crowded nuclei, and the presence of excess cytoplasm and multinucleated giant cells. Tumors that have been confused with FDCS (especially extranodal FDCS) include: melanoma, soft tissue sarcoma, squamous cell carcinoma, meningioma, and inflammatory pseudotumor. Outcomes of this malignancy were analyzed in 54 patients with FDCS using a SEER database.15 While patients with localized disease had a median overall survival that was not reached, the median overall survival for those who presented with distant disease was 48 months. The largest review of extranodal FDCS by Duan et al12 included 39 cases with pharyngeal presentations. They reported recurrence, metastasis, and mortality rates of 23%, 21%, and 3%, respectively (27month median follow-up). The results were consistent with this malignancy being a low-grade sarcoma, as classically described. In contrast, a series of 17 patients (10 extranodal, 7 nodal) described by Chan et al10 reported recurrence, metastasis, and mortality rates of 43%, 24%, and 17%, respectively (36-month median follow-up). Case series have suggested predictors of poorer outcomes including intraabdominal presentation, high mitotic count (ⱖ 5 per 10 HPF), coagulative necrosis, and cytologic atypia.10,11 The mainstay of treatment for this disease is complete surgical resection, if feasible. Adjuvant radiation has not been shown to improve survival.15 We decided to use localized radiation therapy for our patient because of the cytological atypia suggesting a worse prognosis, along with the 20% to 40% local recurrence rate reported in previous studies cited above. The benefit of chemotherapy in this malignancy remains in question namely because of the small number of cases and lack of uniform indications for use. Reports have described chemowww.jco.org
therapy used for bulky tumors,1 incomplete surgical resections,6,11 and misdiagnosis. Cyclophosphamide, doxorubicin, vincristine, and prednisone (ie, lymphoma-based treatment) is the most commonly reported regimen that has been used with this neoplasm.1,16 There is also reported experience with sarcoma-based regimens (ie, gemcitabine, ifosfamide, etoposide).1,16 Little is known of molecular drivers of FDCS, particularly extranodal FDCS of the thyroid. Using polymerase chain reaction on a FDCS tumor of the thyroid in a patient with a history of Hashimoto’s thyroiditis, Yu and Yang5 revealed clonality of immunoglobulin (Ig) H and Ig in both the tumor and adjacent inflamed thyroid suggesting that FDCS arose in the setting of chronic inflammation. In another study, Sun et al17 evaluated eight FDCS cases for epidermal growth factor receptor (EGFR) expression using IHC. Results revealed seven out of eight tumors expressed EGFR in a variable fashion suggesting that agents that inhibit the EGFR pathway may be useful for subsets of this patient population. In order to detect potential mutations in the DNA for our patient’s tumor, we utilized the Foundation One assay to sequence all exons of 236 cancer-related genes. This analysis revealed mutations in the genes the following three genes: PTEN, RET, and TP53. Both mutations in phosphatase and tensin homolog (PTEN), E40* and K267fs*9, are nonsense mutations, resulting in a truncated and nonfunctional protein, and have previously been described in endometrial, colorectal, and breast cancers.18 PTEN is a tumor suppressor that negatively regulates the P13K/Akt/mTOR pathway, and loss of PTEN leads to uncontrolled cell growth and suppression of apoptosis.19 The rearranged during transfection (RET) mutation (M1109T) is a missense mutation that has not been described previously. RET encodes a receptor tyrosine kinase involved in transmitting growth and differentiation signals in tissues derived from the neural crest.20 Constitutive activation of RET leads to increased cell proliferation, decreased © 2014 by American Society of Clinical Oncology
Information downloaded from jco.ascopubs.org and provided by at CAMBRIDGE UNIV MEDICAL LIBRARY on September Copyright © 2015 American Society Clinical Oncology. All rights reserved. 12, 2015 from of 131.111.164.128
e75
Starr et al
apoptosis, increased cell migration, and altered cell adhesion.21 RET mutations have been well characterized as a driver mutation in medullary thyroid cancer; however, the functional significance of the reported mutation in our patient sample remains unknown.22 Tumor protein (TP) 53, the most common mutation noted in malignancies, was reported to be a missense mutation (I254V) that is well described as a loss of function mutation in other malignancies. No mutation of EGFR was identified in this tumor, despite a previous study17 suggesting overexpression of EGFR with IHC staining. Whether we can use the genetic information to guide therapy in this patient remains unknown as the functional significance of these mutations in this sample remains unclear. With that being said, should the patient develop a recurrence, treatment options that inhibit the PI3K/AKT/mTOR and RET pathways should be at least considered given the limited active agents available for this malignancy. In conclusion, we describe a case of high-grade extranodal FDCS of the thyroid arising in the inflammatory background of Hashimoto’s thyroiditis. To our knowledge, this is the first report to characterize DNA mutations in this disease. The clinical significance of these mutations remains unknown.
Jason S. Starr, Steven Attia, Richard W. Joseph, David Menke, John Casler, and Robert C. Smallridge Mayo Clinic, Jacksonville, FL
ACKNOWLEDGMENT
This work was supported by the Mayo Clinic Center for Individualized Medicine and a generous gift from Alfred D. and Audrey M. Petersen. AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST
The author(s) indicated no potential conflicts of interest. REFERENCES 1. Fonseca R, Yamakawa M, Nakamura S, et al: Follicular dendritic cell sarcoma and interdigitating reticulum cell sarcoma: A review. Am J Hematol, 59:161-167, 1998 2. S. Swerdlow, Campo E, Harris NL, et al: WHO Classification of Tumours of Hematopoeitic and Lymphoid Tissue (ed 4), 2008 3. Monda L, Warnke R, Rosai J: A primary lymph node malignancy with features suggestive of dendritic reticulum cell differentiation: A report of 4 cases. Am J Pathol, 122:562-572, 1986
4. Galati LT, Barnes EL, Myers EN: Dendritic cell sarcoma of the thyroid. Head Neck, 21:273-275, 1999 5. Yu L, Yang SJ: Primary follicular dendritic cell sarcoma of the thyroid gland coexisting with Hashimoto’s thyroiditis. Int J Surg Pathol, 19:502-505, 2011 6. Chan JK, Tsang WY, Ng CS: Follicular dendritic cell tumor and vascular neoplasm complicating hyaline-vascular Castleman’s disease. Am J Surg Pathol 18:517-525, 1994 7. Chan AC, Chan KW, Chan JK, et al: Development of follicular dendritic cell sarcoma in hyaline-vascular Castleman’s disease of the nasopharynx: Tracing its evolution by sequential biopsies. Histopathology 38:510-518, 2001 8. Gomes, H, Huyett, Laver N, et al: A unique presentation of Epstein-Barr virus-associated Castleman’s disease. Am J Otolaryngol 3:262-264, 2013 9. Chen, CH, Liu HC, Hung TT, et al: Possible roles of Epstein-Barr virus in Castleman disease. J Cardiothorac Surg 4:31, 2009 10. Chan JK, Fletcher CD, Nayler SJ, et al: Follicular dendritic cell sarcoma: Clinicopathologic analysis of 17 cases suggesting a malignant potential higher than currently recognized. Cancer 79:294-313, 1997 11. Perez-Ordonez B, Erlandson RA, Rosai J: Follicular dendritic cell tumor: Report of 13 additional cases of a distinctive entity. Am J Surg Pathol, 20:944955, 1996 12. Duan GJ, Wu F, Zhu J, et al: Extranodal follicular dendritic cell sarcoma of the pharyngeal region: A potential diagnostic pitfall, with literature review. Am J Clin Pathol, 133:49-58, 2010 13. Yu H, Gibson JA, Pinkus GS, et al: Podoplanin (D2-40) is a novel marker for follicular dendritic cell tumors. Am J Clin Pathol, 128:776-782, 2007 14. Vermi W, Lonardi S, Bosisio D, et al: Identification of CXCL13 as a new marker for follicular dendritic cell sarcoma. J Pathol, 216:356-364, 2008 15. Perkins SM, Shinohara ET: Interdigitating and follicular dendritic cell sarcomas: A SEER analysis. Am J Clin Oncol 36:395-398, 2013 16. Soriano AO, Thompson MA, Admirand JH, et al: Follicular dendritic cell sarcoma: A report of 14 cases and a review of the literature. Am J Hematol, 82:725-728, 2007 17. Sun X, Chang KC, Abruzzo LV, et al: Epidermal growth factor receptor expression in follicular dendritic cells: A shared feature of follicular dendritic cell sarcoma and Castleman’s disease. Hum Pathol, 34:835-840, 2003 18. My Cancer Genome. 2013. www.mycancergenome.com 19. Simpson L, Parsons R: PTEN: Life as a tumor suppressor. Exp Cell Res, 264:29-41, 2001 20. Nakamura T, Ishizaka Y, Nagao M, et al: Expression of the ret protooncogene product in human normal and neoplastic tissues of neural crest origin. J Pathol, 172:255-260, 1994 21. Asai N, Jijiwa M, Enomoto A, et al: RET receptor signaling: Dysfunction in thyroid cancer and Hirschsprung’s disease. Pathol Int, 56:164-172, 2006 22. Agrawal, N, Jiao Y, Sausen M, et al: Exomic sequencing of medullary thyroid cancer reveals dominant and mutually exclusive oncogenic mutations in RET and RAS. J Clin Endocrinol Metab 98:E364-E369, 2013
DOI: 10.1200/JCO.2013.49.3213; published online ahead of print at www.jco.org on March 24, 2014
■ ■ ■
e76
© 2014 by American Society of Clinical Oncology
JOURNAL OF CLINICAL ONCOLOGY
Information downloaded from jco.ascopubs.org and provided by at CAMBRIDGE UNIV MEDICAL LIBRARY on September Copyright © 2015 American Society Clinical Oncology. All rights reserved. 12, 2015 from of 131.111.164.128
33
䡠
NUMBER
17
䡠
JUNE
10
2015
JOURNAL OF CLINICAL ONCOLOGY
Follicular Dendritic Cell Sarcoma Presenting As a Thyroid Mass Case Report A 44-year-old white woman with a history of Hashimoto’s thyroiditis presented to her primary care physician for routine evaluation. A palpable right-sided thyroid nodule was noted. Ultrasound demonstrated heterogeneous enlargement of the thyroid with two 1 cm thyroid nodules (one hypoechoic, one isoechoic) in the lower pole of the right thyroid lobe. A 6-month follow-up ultrasound revealed a hypoechoic nodule measuring 2.7 ⫻ 1.7 ⫻ 2.2 cm (Fig 1A, gold arrow) with peripheral nodularity (Fig 1A, white arrowheads) and Doppler flow (Fig 1B)—all features of malignancy. Fine-needle aspiration suggested anaplastic thyroid carcinoma.
A
B
Fig 1. e74
© 2014 by American Society of Clinical Oncology
D I A G N O S I S
I N
O N C O L O G Y
The patient underwent a total thyroidectomy, central compartment dissection, and parathyroid reimplantation. Pathology revealed a 2.5 cm extranodal follicular dendritic cell sarcoma (FDCS) (Figs 2A and 2B, inset) in a background of a lymphocytic infiltrate. The tumor was described as high grade due to significant cytological atypia and nuclear pleomorphism. One intrathyroidal parathyroid gland was involved by tumor, as were three of 11 lymph nodes in the central compartment (Fig 2C). Surgical margins of the tumor were negative. Immunostains for CD21 (Fig 2D), CD23 (Fig 2E), vimentin, clusterin (Fig 2F), fascin, podoplanin, and CXCL13 were positive. No features of Castleman’s disease were seen within the tumor specimen or lymph nodes removed. Epstein-Barr virus (EBV) in situ hybridization was negative, as was calcitonin. Adjuvantly, our patient received parotidsparing intensity-modulated radiation therapy (IMRT) to the bilateral neck and tumor bed with 54 Gy. She did not receive adjuvant chemotherapy due to the lack of benefit in reported series.1 Because of the rarity of the tumor, lack of benefit with known systemic agents, and absence of genomic characterization in the literature, we analyzed the genomic profile of the tumor utilizing the Foundation One genomic analysis developed by the Broad Institute (Cambridge, MA). The assay uses next-generation sequencing to evaluate the status of 236 cancer-related genes. Discussion FDCS has been defined by the World Health Organization as a low-grade sarcoma with follicular dendritic cell differentiation.2 The disease was first described by Monda et al in 1986.3 Pathology is characterized by spindle to ovoid cells in fascicular, whorled, or storiform patterns with occasional multinucleated giant cells. Here we report only the third case of extranodal FDCS involving the thyroid.4,5 Interestingly, all three cases (including ours) of FDCS involving the thyroid were in the background of Hashimoto’s thyroiditis (ie, lymphocytic thyroiditis). The etiology is unknown but some studies have identified FDCS in association with hyaline vascular Castleman’s disease to suggest that Castleman’s may be a precursor.6,7 Because of a possible association with EBV and Castleman’s disease,8,9 EBV in situ hybridization testing has been previously performed in FDCS.10-12 Only one of twenty seven cases had positive EBV in situ hybridization and this case did have evidence of Castleman’s disease. Immunohistochemistry of FDCS typically identifies one or more of the following markers: CD21, CD23, CD35, podoplanin,13 and CXCL-13.14 In the two largest published series (51 and 54 patients), FDCS has a median age of 41 and 53 years with no gender predilection.1,15 It usually presents as cervical or axillary lymphadenopathy; however, up to one third may present with extranodal disease.1 Extranodal presentation is usually in the head, neck, and abdominal regions.15 Due to its rarity, FDCS is often initially misdiagnosed. Duan et al12 reported that of the 36 cases they reviewed, 21 (58%) were initially misdiagnosed. An adequate biopsy specimen is crucial to making the correct diagnosis. Our patient’s initial biopsy showed large atypical cells suggestive of a poorly differentiated carcinoma. In the setting of a thyroid mass the Journal of Clinical Oncology, Vol 33, No 17 (June 10), 2015: pp e74-e76
Information downloaded from jco.ascopubs.org and provided by at CAMBRIDGE UNIV MEDICAL LIBRARY on September Copyright © 2015 American Society Clinical Oncology. All rights reserved. 12, 2015 from of 131.111.164.128
Diagnosis in Oncology
A
B
C
500 µm
D
500 µm
E
500 µm
F
500 µm
500 µm
500 µm
Fig 2.
diagnosis of anaplastic thyroid carcinoma was considered. Some features that would help the clinician differentiate FDCS from poorly differentiated carcinomas is negative immunohistochemistry (IHC) for cytokeratin and epithelial membrane antigen, lack of irregular infiltrative tumor islands, lack of crowded nuclei, and the presence of excess cytoplasm and multinucleated giant cells. Tumors that have been confused with FDCS (especially extranodal FDCS) include: melanoma, soft tissue sarcoma, squamous cell carcinoma, meningioma, and inflammatory pseudotumor. Outcomes of this malignancy were analyzed in 54 patients with FDCS using a SEER database.15 While patients with localized disease had a median overall survival that was not reached, the median overall survival for those who presented with distant disease was 48 months. The largest review of extranodal FDCS by Duan et al12 included 39 cases with pharyngeal presentations. They reported recurrence, metastasis, and mortality rates of 23%, 21%, and 3%, respectively (27month median follow-up). The results were consistent with this malignancy being a low-grade sarcoma, as classically described. In contrast, a series of 17 patients (10 extranodal, 7 nodal) described by Chan et al10 reported recurrence, metastasis, and mortality rates of 43%, 24%, and 17%, respectively (36-month median follow-up). Case series have suggested predictors of poorer outcomes including intraabdominal presentation, high mitotic count (ⱖ 5 per 10 HPF), coagulative necrosis, and cytologic atypia.10,11 The mainstay of treatment for this disease is complete surgical resection, if feasible. Adjuvant radiation has not been shown to improve survival.15 We decided to use localized radiation therapy for our patient because of the cytological atypia suggesting a worse prognosis, along with the 20% to 40% local recurrence rate reported in previous studies cited above. The benefit of chemotherapy in this malignancy remains in question namely because of the small number of cases and lack of uniform indications for use. Reports have described chemowww.jco.org
therapy used for bulky tumors,1 incomplete surgical resections,6,11 and misdiagnosis. Cyclophosphamide, doxorubicin, vincristine, and prednisone (ie, lymphoma-based treatment) is the most commonly reported regimen that has been used with this neoplasm.1,16 There is also reported experience with sarcoma-based regimens (ie, gemcitabine, ifosfamide, etoposide).1,16 Little is known of molecular drivers of FDCS, particularly extranodal FDCS of the thyroid. Using polymerase chain reaction on a FDCS tumor of the thyroid in a patient with a history of Hashimoto’s thyroiditis, Yu and Yang5 revealed clonality of immunoglobulin (Ig) H and Ig in both the tumor and adjacent inflamed thyroid suggesting that FDCS arose in the setting of chronic inflammation. In another study, Sun et al17 evaluated eight FDCS cases for epidermal growth factor receptor (EGFR) expression using IHC. Results revealed seven out of eight tumors expressed EGFR in a variable fashion suggesting that agents that inhibit the EGFR pathway may be useful for subsets of this patient population. In order to detect potential mutations in the DNA for our patient’s tumor, we utilized the Foundation One assay to sequence all exons of 236 cancer-related genes. This analysis revealed mutations in the genes the following three genes: PTEN, RET, and TP53. Both mutations in phosphatase and tensin homolog (PTEN), E40* and K267fs*9, are nonsense mutations, resulting in a truncated and nonfunctional protein, and have previously been described in endometrial, colorectal, and breast cancers.18 PTEN is a tumor suppressor that negatively regulates the P13K/Akt/mTOR pathway, and loss of PTEN leads to uncontrolled cell growth and suppression of apoptosis.19 The rearranged during transfection (RET) mutation (M1109T) is a missense mutation that has not been described previously. RET encodes a receptor tyrosine kinase involved in transmitting growth and differentiation signals in tissues derived from the neural crest.20 Constitutive activation of RET leads to increased cell proliferation, decreased © 2014 by American Society of Clinical Oncology
Information downloaded from jco.ascopubs.org and provided by at CAMBRIDGE UNIV MEDICAL LIBRARY on September Copyright © 2015 American Society Clinical Oncology. All rights reserved. 12, 2015 from of 131.111.164.128
e75
Starr et al
apoptosis, increased cell migration, and altered cell adhesion.21 RET mutations have been well characterized as a driver mutation in medullary thyroid cancer; however, the functional significance of the reported mutation in our patient sample remains unknown.22 Tumor protein (TP) 53, the most common mutation noted in malignancies, was reported to be a missense mutation (I254V) that is well described as a loss of function mutation in other malignancies. No mutation of EGFR was identified in this tumor, despite a previous study17 suggesting overexpression of EGFR with IHC staining. Whether we can use the genetic information to guide therapy in this patient remains unknown as the functional significance of these mutations in this sample remains unclear. With that being said, should the patient develop a recurrence, treatment options that inhibit the PI3K/AKT/mTOR and RET pathways should be at least considered given the limited active agents available for this malignancy. In conclusion, we describe a case of high-grade extranodal FDCS of the thyroid arising in the inflammatory background of Hashimoto’s thyroiditis. To our knowledge, this is the first report to characterize DNA mutations in this disease. The clinical significance of these mutations remains unknown.
Jason S. Starr, Steven Attia, Richard W. Joseph, David Menke, John Casler, and Robert C. Smallridge Mayo Clinic, Jacksonville, FL
ACKNOWLEDGMENT
This work was supported by the Mayo Clinic Center for Individualized Medicine and a generous gift from Alfred D. and Audrey M. Petersen. AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST
The author(s) indicated no potential conflicts of interest. REFERENCES 1. Fonseca R, Yamakawa M, Nakamura S, et al: Follicular dendritic cell sarcoma and interdigitating reticulum cell sarcoma: A review. Am J Hematol, 59:161-167, 1998 2. S. Swerdlow, Campo E, Harris NL, et al: WHO Classification of Tumours of Hematopoeitic and Lymphoid Tissue (ed 4), 2008 3. Monda L, Warnke R, Rosai J: A primary lymph node malignancy with features suggestive of dendritic reticulum cell differentiation: A report of 4 cases. Am J Pathol, 122:562-572, 1986
4. Galati LT, Barnes EL, Myers EN: Dendritic cell sarcoma of the thyroid. Head Neck, 21:273-275, 1999 5. Yu L, Yang SJ: Primary follicular dendritic cell sarcoma of the thyroid gland coexisting with Hashimoto’s thyroiditis. Int J Surg Pathol, 19:502-505, 2011 6. Chan JK, Tsang WY, Ng CS: Follicular dendritic cell tumor and vascular neoplasm complicating hyaline-vascular Castleman’s disease. Am J Surg Pathol 18:517-525, 1994 7. Chan AC, Chan KW, Chan JK, et al: Development of follicular dendritic cell sarcoma in hyaline-vascular Castleman’s disease of the nasopharynx: Tracing its evolution by sequential biopsies. Histopathology 38:510-518, 2001 8. Gomes, H, Huyett, Laver N, et al: A unique presentation of Epstein-Barr virus-associated Castleman’s disease. Am J Otolaryngol 3:262-264, 2013 9. Chen, CH, Liu HC, Hung TT, et al: Possible roles of Epstein-Barr virus in Castleman disease. J Cardiothorac Surg 4:31, 2009 10. Chan JK, Fletcher CD, Nayler SJ, et al: Follicular dendritic cell sarcoma: Clinicopathologic analysis of 17 cases suggesting a malignant potential higher than currently recognized. Cancer 79:294-313, 1997 11. Perez-Ordonez B, Erlandson RA, Rosai J: Follicular dendritic cell tumor: Report of 13 additional cases of a distinctive entity. Am J Surg Pathol, 20:944955, 1996 12. Duan GJ, Wu F, Zhu J, et al: Extranodal follicular dendritic cell sarcoma of the pharyngeal region: A potential diagnostic pitfall, with literature review. Am J Clin Pathol, 133:49-58, 2010 13. Yu H, Gibson JA, Pinkus GS, et al: Podoplanin (D2-40) is a novel marker for follicular dendritic cell tumors. Am J Clin Pathol, 128:776-782, 2007 14. Vermi W, Lonardi S, Bosisio D, et al: Identification of CXCL13 as a new marker for follicular dendritic cell sarcoma. J Pathol, 216:356-364, 2008 15. Perkins SM, Shinohara ET: Interdigitating and follicular dendritic cell sarcomas: A SEER analysis. Am J Clin Oncol 36:395-398, 2013 16. Soriano AO, Thompson MA, Admirand JH, et al: Follicular dendritic cell sarcoma: A report of 14 cases and a review of the literature. Am J Hematol, 82:725-728, 2007 17. Sun X, Chang KC, Abruzzo LV, et al: Epidermal growth factor receptor expression in follicular dendritic cells: A shared feature of follicular dendritic cell sarcoma and Castleman’s disease. Hum Pathol, 34:835-840, 2003 18. My Cancer Genome. 2013. www.mycancergenome.com 19. Simpson L, Parsons R: PTEN: Life as a tumor suppressor. Exp Cell Res, 264:29-41, 2001 20. Nakamura T, Ishizaka Y, Nagao M, et al: Expression of the ret protooncogene product in human normal and neoplastic tissues of neural crest origin. J Pathol, 172:255-260, 1994 21. Asai N, Jijiwa M, Enomoto A, et al: RET receptor signaling: Dysfunction in thyroid cancer and Hirschsprung’s disease. Pathol Int, 56:164-172, 2006 22. Agrawal, N, Jiao Y, Sausen M, et al: Exomic sequencing of medullary thyroid cancer reveals dominant and mutually exclusive oncogenic mutations in RET and RAS. J Clin Endocrinol Metab 98:E364-E369, 2013
DOI: 10.1200/JCO.2013.49.3213; published online ahead of print at www.jco.org on March 24, 2014
■ ■ ■
e76
© 2014 by American Society of Clinical Oncology
JOURNAL OF CLINICAL ONCOLOGY
Information downloaded from jco.ascopubs.org and provided by at CAMBRIDGE UNIV MEDICAL LIBRARY on September Copyright © 2015 American Society Clinical Oncology. All rights reserved. 12, 2015 from of 131.111.164.128
