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Giovannella Palmieri

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    MS08 - Management of Thymic Carcinoma (ID 71)

    • Event: WCLC 2019
    • Type: Mini Symposium
    • Track: Thymoma/Other Thoracic Malignancies
    • Presentations: 5
    • Now Available
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      MS08.01 - Adjuvant Radiotherapy for Resected Thymic Carcinoma (Now Available) (ID 3481)

      14:00 - 15:30  |  Presenting Author(s): Anthony Brade

      • Abstract
      • Presentation
      • Slides

      Abstract

      Thymic carcinoma is a rare malignancy with peak incidence in the 4th-6th decade. In contrast to thymoma, it is commonly associated with higher rates of both lymph node and distant metastatic spread and also with shorter disease free survival. For localized or locally advanced disease, surgical resection, with the intention of complete disease extirpation, remains the standard of care. Due to its rarity however, definitive clinical trial data regarding optimal and appropriate addition of adjuvant therapy is lacking. Thus decision making for post-operative patients is guided by data from large institutional, national or international retrospective series or databases (evidence level IV or V).

      Recommendations for adjuvant therapy for thymic carcinoma are influenced principally by stage and adequacy of resection (R0 vs R1 vs R2). Thymic carcinoma is classically staged us the Masaoka-Koga (MK) system but, based on recommendation to the AJCC by the IASLC Staging Prognostic Factors Committee and the International Thymic Malignancy Interest Group (ITMIG), using a database of more than 10 000 patients (Detterbeck et al 2014), a TNM-based system has now been incorporated into the 8th Edition of the AJCC/UICC TNM Classification of Malignant Tumours. However, since much of the published data regarding thymic malignancies is based on the Masaoka-Koga system, at present this remains commonly used for clinical decision-making but, as data continues to accumulate, will likely be superseded by the TNM system over time.

      Post-operative radiotherapy is routinely recommended for patients with MK stage III (TNM Stage I – T1bN0, Stage II, IIIA/B) thymic carcinoma following R0 resection. Similarly, adjuvant radiation is recommended following R1 resection, regardless of stage, with adjuvant chemoradiation recommended following R2 resection.

      Adjuvant radiotherapy is not recommended for MK I or IIA (TNM Stage 1 T1aN0 with no extension to mediastinal fat) disease.

      Controversy exists regarding the utility of adjuvant radiotherapy in the management of MK IIB (TNM Stage I – T1aN0 with extension to mediastinal fat) disease but can be considered for this group of patients.

      The optimal adjuvant radiotherapy dose remains undefined for thymic carcinoma patients but typical doses reported in the literature for patients in the above recommended groups range from 45-50 Gy in 1.8-2 Gy per fraction daily. Following R1 resection, 50-54 Gy in 1.8-2 Gy per fraction is typically recommended. Following R2 resection, 60-70 Gy (with or without concurrent chemotherapy) is considered standard.

      Nodal involvement is much more frequent in patients with thymic carcinoma compared with thymoma. Resected, unexpectedly N+ patients are typically recommended to receive adjuvant RT to 45-60 Gy if complete resection was obtained or 60-70 Gy (with or without concurrent chemotherapy) if residual nodal disease is suspected/documented. Under the TNM staging system, N1 nodes are defined as those in the anterior mediastinal compartment (IASLC levels 1, 3a, 6 and/or supradiaphragmatic/inferior phrenics/pericardial) and N2 nodes are defined as deep intrathoracic or cervical nodes (IASLC levels 2, 4, 5, 7, 10 and/or internal mammary nodes). Whether inclusion of N1 or N2 nodal compartments in adjuvant RT target volumes is of benefit for N0 or completely resected N1 or N2 patients remains unknown but may be prudent to consider during radiotherapy planning based on clinical factors.

      Radiotherapy should conform to modern standards with CT-based simulation with photon-based 3D conformal or beam-modulated treatment delivery, motion management and image guidance to reduce margins and dose to organs at risk. The utility of adjuvant proton-based RT for patients with resected thymic malignancy remains the focus of ongoing study but may offer some dosimetric advantages with respect to OAR dose (e.g. lung or heart).

      Selected References:

      N. Girard et al., Thymic epithelial tumours: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Annals of Oncology 26 (Supplement 5): v40–v55, 2015

      Imbimbo et al., Treatment guidelines: Best practices for the management of thymic epithelial tumors: A position paper by the Italian collaborative group for ThYmic MalignanciEs (TYME)
      Cancer Treatment Reviews 71 (2018) 76–87

      Detterbeck et al. The IASLC/ITMIG Thymic Epithelial Tumors Staging Project: proposal for an evidence-based stage classification system for the forthcoming (8th) edition of the TNM classification of malignant tumors. J Thorac Oncol 2014; 9(Suppl 2): S65–S72.

      Shepherd et al. Thymic Carcinoma Management Patterns among International Thymic Malignancy Interest Group (ITMIG) Physicians with Consensus from the Thymic Carcinoma Working Group. J Thorac Oncol 2017;12:745-51

      Weksler et al., Impact of Positive Nodal Metastases in Patients with Thymic Carcinoma and Thymic Neuroendocrine Tumors. J Thorac Oncol. 2015;10: 1642–1647

      Willmann and Rimner. The expanding role of radiation therapy for thymic malignancies. J Thorac Dis 2018;10(Suppl 21):S2555-S2564.

      Vogel J, Lin L, Litzky LA, et al. Predicted rate of secondary malignancies following adjuvant proton versus photon radiation therapy for thymoma. Int J Radiat Oncol Biol Phys. 2017;99:427–433

      Vogel J, Lin L, Simone CB, et al. Risk of major cardiac events following adjuvant proton versus photon radiation therapy for patients with thymic malignancies. Acta Oncol. 2017;56: 1060–1064.

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      MS08.02 - Induction Therapy for Locally Advanced Thymic Carcinoma (Now Available) (ID 3482)

      14:00 - 15:30  |  Presenting Author(s): Robert Korst

      • Abstract
      • Presentation
      • Slides

      Abstract

      Thymic carcinoma (TC) is a rare mediastinal malignancy that occurs in approximately 10% of all patients with thymic epithelial tumors. There are several different histologic subtypes of TC with squamous cell carcinoma predominating. TC is an aggressive lesion, and frequently presents in more advanced stages and metastasizes to other organs compared to thymoma. This biologic behavior is reflected in the survival rates associated with TC, which are significantly shorter than that of thymoma. Clinical trials conducted exclusively in TC patients have been scarce with only a handful of studies reported in the literature, all focused on advanced, nonsurgical patients.

      Locally advanced, nonmetastatic disease is a common presentation of TC. In the largest retrospective series reported to date, locally advanced disease was the most common stage at presentation, accounting for 45% of patients in whom pathologic stage was recorded1. The importance of complete resection for patients with locally advanced TC cannot be overemphasized. Virtually all reported series of exclusively TC patients that undergo surgical resection have determined that the ability to perform a complete resection is an independent favorable prognostic factor. Despite this, the rate of complete resection in the large, aforementioned series for locally advanced TC was only 64%.

      Given that thymic epithelial tumors (thymoma and TC) are sensitive to both chemotherapy and radiotherapy, an approach that has been favored for patients with locally advanced disease is to administer one or both of these agents preoperatively (neoadjuvant therapy). This strategy is thought to increase the chances of performing a complete resection for marginally resectable or unresectable tumors. Although no clinical trials have been reported exclusively for TC patients using the neoadjuvant strategy, two retrospective reports in TC patients utilizing neoadjuvant chemotherapy or chemoradiation demonstrated complete resection rates of 86% and 69% in marginally resectable or unresectable locally advanced disease2,3. In a phase II clinical trial of neoadjuvant chemoradiotherapy for locally advanced thymic tumors, the complete resection rate for the seven patients that had thymic carcinoma was 71%4. Despite these data, the ability of neoadjuvant therapy to definitively enhance the resectability of locally advanced TC has not been demonstrated due to the absence of randomization and a control group in these studies.

      Some published data have also suggested that TC may respond better to neoadjuvant therapies when compared to the thymoma histotypes. In the previously described phase II trial of neoadjuvant chemoradiotherapy, the patients with TC not only had a better radiographic response to treatment, they were more likely to have a near complete pathologic response (<10% viable tumor) than the patients with thymoma (57% versus 8%)4. Similarly, in a retrospective pathologic analysis of 49 patients with unresectable thymic tumors that underwent neoadjuvant therapy followed by surgical resection at a single institution, the median percent viable tumor in the surgical specimen was significantly less in the TC specimens compared to thymoma (20% versus 91%)5. These two studies also suggest that TC may respond better to chemoradiotherapy than chemotherapy alone.

      Whether targeted or immune therapies can be used successfully in the neoadjuvant setting for TC remains to be determined. Active targeted agents against this disease have remained elusive and immunotherapy may be associated with autoimmune toxicities that may preclude their use in this approach6.

      In summary, the use of induction therapy for locally advanced TC is based on the premise that this approach may enhance resectability of these aggressive tumors, which is an overwhelmingly positive prognostic indicator. However, no published data has conclusively determined that this strategy is effective in enhancing resectability due to a lack of controlled studies. TC may respond better to induction therapy when compared to thymoma, and chemoradiotherapy may induce more radiographic and pathologic responses than chemotherapy alone, but these data are preliminary.

      References.

      Ahmad U, Yao X, Detterbeck F, et al. Thymic carcinoma outcomes and prognosis: Results of an international analysis. J Thorac Cardiovasc Surg 2015;149:95-101.

      Kawasaki H, Taira N, Ichi T, et al. Weekly chemotherapy with cisplatin, vincristine, doxorubicin and etoposide followed by surgery for thymic carcinoma. Eur J Surg Oncol 2014;40:1151-1155.

      Shintani Y, Masayoshi I, Tomohiro K, et al. Multimodality treatment for advanced thymic carcinoma: outcomes of induction therapy followed by surgical resection in 16 cases at a single institution. Gen Thorac Cardiovasc Surg 2015;63:159-63.

      Korst RJ, Bezjak A, Blackmon S, et al. Neoadjuvant chemoradiotherapy for locally advanced thymic tumors: A phase II, multi-institutional clinical trial. J Thorac Cardiovasc Surg 2014;147:36-46.

      Johnson GB, Aubry MC, Yi ES, et al. Radiologic response to neoadjuvant treatment predicts histologic response in thymic epithelial tumors. J Thorac Oncol 2016;12:354-67.

      Giaccone G, Kim C, Thompson J, et al. Pembrolizumab in patients with thymic carcinoma: a single-arm, single-centre, phase 2 study. Lancet Oncol 2018;19:347-355.

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      MS08.03 - Optimal Management of Metastatic Thymic Carcinoma (Now Available) (ID 3483)

      14:00 - 15:30  |  Presenting Author(s): Guiseppe Giaccone

      • Abstract
      • Presentation
      • Slides

      Abstract

      Thymic carcinoma represents approximately 10-15% of all thymic epithelial tumors, it is more aggressive than thymomas and also somewhat less sensitive to chemotherapy. More often than thymomas, thymic carcinomas are not resectable and therefore the use of systemic therapies and radiation are more often required than in thymomas. In general the sensitivity of thymic carcinomas to chemotherapy is lower than with thymomas, with response rates usually less than 50% in metastatic disease, and somewhat higher in locally advanced disease.

      In presence of borderline operable cases, neoadjuvant chemotherapy is indicated, in order to make the tumor more easily operable. Because thymic carcinomas often infiltrate surrounding tissues, radical resection are sometimes not achievable. The use of postoperative radiation is indicated even if margins are clear. Several chemotherapy regimens have been used, and the more commonly employed remain platinum combinations, with or without an anthracycline (mainly doxorubicin). More recently data the combination carboplatin-paclitaxel has been added to the potential chemotherapy regimens and it is often preferred becasue of its milder toxicity profile. When radiation is planned, the use of doxorubicin is contraindicated, becasue of the enhanced toxicity. The role of debulking surgery, reoperation and metastasectomy is much more controversial in thymic carcinomas than in thymomas, given the more aggressive behaviour. However, the histological diagnosis sometimes is not paralleled by an aggressive phenotype and individual treatment decisions should always be considered.

      Unfortunately thymic carcinoma have the tendency to metastatize wildly to virtually all organs, and brain metastases are all but rare. Complete staging procedures, including brain MRI are therefore indicated in patients with thymic carcinoma. In patients with metastatic disease, chemotherapy is indicated as first line therapy, and the CAP regimen (cisplatin, doxorubicin, cyclophosphamide) or carboplatin-paclitaxel, are the preferred regimens, with response rates in the range of 30-50%. Unfortunately, chemotherapy at this stage is not curative and most patients will require further systemic therapies after failure of chemotherapy. There have been a number of studies in recent years, which have established activity of a few agents, such as sunitinib and pembrolizumab in thymic carcinomas. Both of them are now listed in the NCCN guidelines and have a response rate of about 25%. Pembrolizumab however has a much longer duration of response, albeit the frequency of severe autoimmune disorders is higher than in other diseases in which immune checkpoint inhibitors are used. Further chemotherapy also has some activity, such and the combination gemcitabine-capecitabine and other single agents, with responses in the 20-30% range.

      The biology of thymic carcinoma does not appear to provide clues to specific treatments, although mutations in epigenetic genes have been found in a significant number of patients. No easily targetable mutations or genetic abnormalities have so far been found. The most common mutation is in the p53 gene, in about 30% of cases, which is not targetable and is associated with a poorer survival.

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      MS08.04 - Novel Biomarkers for Thymic Carcinoma (Now Available) (ID 3484)

      14:00 - 15:30  |  Presenting Author(s): Mirella Marino  |  Author(s): Beatrice Casini, Enzo Gallo, Enrico Melis, Fabiana Letizia Cecere, Valentina Laquintana, Virna Cerasoli, Francesco Facciolo, Edoardo Pescarmona, Francesco Fazi

      • Abstract
      • Presentation
      • Slides

      Abstract

      Thymic carcinoma (TC), the rarer among Thymic Epithelial Tumors (TET), occur with an incidence rate of 0.2-0.5/million/yr. Difficulties in the evaluation of molecular aspects derive from the extreme rarity of these tumors. The Squamous cell carcinoma (SQCC) is the most frequently analyzed, however the other rarer histotypes could differ both in molecular pathogenesis and in clinical behaviour. The Cancer Genome Atlas Thymoma study (TCGA-THYM) in a series of ten TC cases including four SQCC, four undifferentiated carcinoma and both one large cell neuroendocrine carcinoma as well as one TC, NOS, identified a few genes rarely mutated, including KIT, HRAS, NRAS and TP53, reflecting the low mutational burden of these tumors (1). In the last years, only a limited number of TC has been investigated by other groups and only a limited number of relevant alterations has been identified. In addition to genomic events, however, epigenetic factors could contribute to TET carcinogenesis. Wang et al. in 2014 performed targeted sequencing of 197 cancer-associated genes in 78 advanced-stage TET patients, including 47 TC and 31 thymoma (THYM) cases. They reported that TC showed a higher incidence of somatic non-synonymous mutations than THYM. Moreover, they found that mutations of epigenetic regulatory genes involved in chromatin modification pathways are common in TC in comparison to THYM (2).

      In the last years we have been interested in the characterization of genomic and epigenetic findings related to TET development. In our earlier microRNA (miR) study, we reported, among other findings, preliminary data on mature microRNAs differentially expressed in TC vs THYM, as revealed by microarray-based unsupervised clustering analysis. Among the differentially expressed miRs, 3 were validated by RT-qPCR (miR128, miR142-5p and miR-181c-5p) (3). By a different approach, we analyzed by Next Generation Sequencing (NGS) thirteen TC cases and one Atypical Type A thymoma case. The tissues derived from Formalin-fixed, paraffin embedded (FFPE) material including biopsies/surgical specimens of tumors and a single case of matched peritumoral thymus. The percentage of neoplastic cells was not < 70-80% of total cells. The DNA was extracted using the QIAcube and QIAamp DNA FFPE Tissue Kit (Qiagen, Valencia, CA) from microdissected 5 μm FFPE tissue sections. The NGS platform Ion S5 (Thermofisher) and the Ion AmpliSeq™Cancer Hotspot Panel v2 were used. This panel is designed to amplify 207 amplicons covering over 2,800 COSMIC mutations from 50 oncogenes and tumor suppressor genes. Libraries from Ion AmpliSeq Cancer Hotspot Panel v2 were prepared and sequenced by Ion Chef and S5 system. Data analysis was conducted by using the dedicated Ion Reporter Software. Among other genomic variants (polymorphysms and mutations were found in four cases), in one out of these four TC cases a KIT mutation (c.1900C>T; p.R634W, exon 13), already reported in TC, was identified. Moreover, a further KIT mutation ( c.1718C>T p.P573L, exon11) was found in a second case. In addition, a missense TP53 mutation ( c.824G>T; p.C275F), occurring in exon 8, was observed in a single case of TC, NOS. The patient harbouring a TC with this TP53 mutation had a R0 robotic-assisted thymectomy of a pT2 Thymic carcinoma (according to the 8th TNM edition), and after adjuvant chemotherapy and radiotherapy is alive and in complete remission with a follow-up of 22 months . The recent case of Atypical Type A thymoma showed a NOTCH1 c.4732_4734delGTG p.V1578del in exon 26 of uncertain significance.

      Basing on the relatively few cases reported in the literature, analyzed by different techniques for their genomic alterations, it appears that the mutation status of TC is highly heterogeneous. In the cases examined so far by NGS we didn’t find recurrent genetic aberrations, but a variety of alterations. Each case, with the panel available, revealed either polymorphisms or, in few cases, mutations in cancer-associated genes, both oncogenic and oncosuppressor. Among the genes involved, both the KIT reported variants could be considered relevant for targeted therapy. Moreover, the tumor suppressor gene TP53 is already known for its importance and frequency of mutations particularly in TC. Moreira et al reported recurrent TP53 mutations with unfavorable prognostic value (4). The TP53 mutation found in one of our cases (previously reported in cases of SQCC of upper respiratory tract, in lung, head & neck and esophageal carcinoma) affects, among others, the DNA damage repair, the cell cycle and the apoptosis pathways. In human thymus, the Notch pathway, activated in thymic EC, is crucial to T cell differentiation; moreover the Notch signaling is also involved in hematological and in solid tumors. The NOTCH1 c.4732_4734delGTG p.V1578del in exon 26 we reported in a Atypical case A thymoma was already described in lymphoid tissues. The clinical and prognostic value of the genomic alterations we observed needs to be definied.

      1) Radovich M, et al., The integrated genomic landscape of thymic epithelial tumors - Cancer Cell, 2018 Feb 12;33(2):244-258

      2) Wang Y, et al., Mutations of epigenetic regulatory genes are common in thymic carcinomas - Sci Rep. 2014 Dec 8;4:7336

      3) Ganci F, et al., MicroRNAs Expression Profiling of Thymic Epithelial Tumors - Lung Cancer 2014, 85 (2) 197–204

      4) Moreira AL, et al, Massively parallel sequencing identifies recurrent mutations in TP53 in thymic carcinoma associated with poor prognosis - J Thorac Oncol. 2015 Feb;10(2):373-80

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      MS08.05 - Basic Pathological Features (Now Available) (ID 3485)

      14:00 - 15:30  |  Presenting Author(s): Cesar Moran

      • Abstract
      • Presentation
      • Slides

      Abstract

      IASLC WCLC 2019

      MS08 – Management of Thymic Carcinoma

      Cesar A. Moran, MD

      Professor of Pathology

      M D Anderson Cancer Center

      Houston, TC

      USA

      Pathologic Features

      The basic pathological features of thymic carcinomas are essentially those seeing in other tumors elsewhere and require the presence of conventional features such mitotic activity, cellular and nuclear atypia, and necrosis among others. However, the diagnosis of thymic carcinoma contrary to the diagnosis of carcinomas in other anatomical areas requires a more strict radiological correlation, as thymic carcinoma can show similar histological features as other tumors such lung or head and neck area. Therefore, the clinical information of an anterior mediastinal mass in the absence of tumor elsewhere becomes an important diagnostic tool in the assessment of thymic carcinoma.

      The histopathological features of thymic carcinomas are vast and highly heterogeneous. It is possible that such heterogeneity may be due the different cell types that may be encountered in the normal thymus. However, in general terms, thymic carcinomas can be separated into neuroendocrine and non-neuroendocrine carcinomas, and further sub-divided into: 1) low grade and 2) high grade carcinomas (see table 1). Among the neuroendocrine carcinomas, similar spectrum as in other organ systems has been recognized, including: low grade, intermediate grade, and high grade neuroendocrine carcinoma. Some of these tumors may have special association with particular syndromes. Aside from the neuroendocrine carcinomas, the vast majority of thymic carcinomas are of the squamous type, which can show diversity in their growth pattern from well-differentiated keratinizing to the high-grade lymphoepithelioma-like carcinoma and anaplastic/pleomorphic carcinoma. In addition, the tumors may show different cell types and growth patterns that may include: papillary, micropapillary, clear cell, sarcomatoid carcinomas, and micronodular among others. In addition, it is important to highlight the occurrence of salivary gland type carcinomas in the thymus, examples of that include: mucoepidermoid carcinoma, adenoid cystic carcinoma and epithelial-myoepithelial carcinoma. More interesting is the fact that a small subset of thymic carcinomas will belong to the adenocarcinoma type, with similar features as those adenocarcinomas in other organ systems – mainly a malignant glandular proliferation. These tumors may also show variability in their growth pattern and may show a solid glandular proliferation or a predominantly mucinous component. Needless to say, these thymic adenocarcinomas can mimic metastatic disease from other organ systems such as lung or colon. Therefore, a close clinical correlation is also highly suggested before determining site of origin. It is due to this heterogeneity that the diagnosis of primary thymic carcinoma requires more strict clinical-radiological-pathological criteria, as there are no pathognomonic features that can define a thymic carcinoma, mainly in cases in which there is only a small mediastinoscopic biopsy for evaluation.

      From the immunohistochemical point of view, thymic carcinomas commonly express keratin, keratin 5/6, p63, p40, CD5. In addition, it is also well known that some neuroendocrine markers such as synaptophysin may be seen positive in otherwise conventional thymic carcinomas. On the other hand, thymic adenocarcinomas may express different immunohistochemical phenotype that may include: keratin 7, keratin 20, CDX-2, and CEA. In cases of neuroendocrine carcinomas the use of neuroendocrine markers including chromogranin, synaptophysin, and CD56 may prove useful. However, the grade of differentiation still can be done on morphological grounds. More recently, it has been identified a poorly differentiated carcinoma the so-called NUT carcinoma that by histology most likely represents a poorly differentiated squamous carcinoma but that shows positive staining using the immunohistochemical stain for NUT and also may show more specific cytogenetic and chromosomal abnormalities. Such diagnosis should be suspected in poorly differentiated carcinomas.

      Regarding the prognosis of thymic carcinoma, it has been identified that the presence of lymph node metastasis, regardless of the location of the lymph node, plays an important role in the clinical outcome of these patients. Therefore, thymic carcinomas are best suited for a TNM staging, contrary to the use of the TNM for thymomas.

      TABLE 1

      Histological Variants of Thymic Carcinoma

      Low grade High grade Neuroendocrine

      Mucoepidermoid carcinoma lymphoepithelioma-like Low grade (carcinoid)

      Basaloid carcinoma P.D. squamous cell Ca Intermediate (atypical carcinoid)

      Epithelial-myoepithelial Ca Anaplastic Ca High-grade (Small cell Ca)

      Well-diff. Squamous cell Ca Sarcomatoid Ca

      Rhabdoid Ca

      Hepatoid Ca

      Micronodular Ca

      Papillary/micropapillary Ca

      Clear Cell Ca

      NUT carcinoma

      Adenocarcinoma

      REFERENCES

      1.Shimosato Y, Kameya T, Nagai K, Suemasu K. Squamous cell carcinoma of the thymus. Analysis of 8 cases. Am J Surg Pathol 1977; 1:109-121.

      2.Snover DC, Levine GD, Rosai J. Thymic carcinoma. Five distinctive histological variants. Am J Surg Pathol 1982; 6:451-470.

      3.Suster S, Moran CA. Thymic carcinoma. Spectrum of differentiation and histologic types. Pathology 1998; 30:111-112.

      4.Moran CA, Suster S. Thymic carcinoma. Current concepts and histological features. Hematol Oncol Clin N Am 2008; 22:393-407.

      5. Suster S, Rosai J. Thymic carcinoma. A clinicopathologic study of 60 cases. Cancer 1991; 67:1025-1032.

      6.Weissferdt A, Moran CA. Thymic carcinoma, part I. A clinicopathologic and immunohistochemical study of 65 cases. Am J Clin Pathol 2012; 138: 103-114.

      7.Weissferdt A, Moran CA. Thymic carcinoma, part 2. A clinicopathologic correlation of 33 cases with a proposed staging system. Am J Clin Pathol 2012; 138:115-121.

      8.Kalhor N, Moran CA. Primary thymic adenocarcinomas: a clinicopathological and immunohistochemical study of 16 cases with emphasis on the morphological spectrum of differentiation. Hum Pathol 2018; 74:73-82.

      9.Moran CA, Suster S. Neuroendocrine carcinomas (Carcinoid Tumor) of the thymus. A clinicopathologic analysis of 80 cases. Am J Clin Pathol 2000; 114:100-110.

      10. Kalhor N, Moran CA. Mediastinal Pathology, Springer 2019, Chapter 8, pp 237-286.

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