Pleomorphic Giant Cell Carcinoma Research Articles

Clinicopathological features and differential diagnosis of gastric pleomorphic giant cell carcinoma.

The aim of this study was to investigate the clinicopathological features and differential diagnosis of gastric pleomorphic giant cell carcinoma. Histopathology, immunohistochemistry, and human epidermal growth factor receptor 2 (HER2) gene testing were conducted for seven cases of gastric pleomorphic giant cell carcinoma. In histomorphological terms, all seven cases involved pleomorphic giant cell carcinoma, accounting for more than 10% of the entire tumor, with pleomorphic spindle cells and giant cells mixed with various histomorphological structures of adenocarcinoma with high, intermediate, and low differentiation. There was large heterogeneity in the HER2 protein expression and HER2 gene amplification in the gastric pleomorphic giant cell carcinoma, and both levels of HER2 were focal in three cases, accounting for 42.9% (3/7). The mismatch repair gene proteins MLH1, MSH2, PMS2, and MSH6 were positive. Routine immunohistochemical markers, i.e., pan-cytokeratin, epithelial membrane antigen, villin, caudal-type homeobox 2, E-cadherin, and p53, were positive in the gastric pleomorphic giant cell carcinoma, while vimentin, calponin, smooth muscle actin, nestin, S-100, cluster of differentiation (CD) 99, desmin, and CD34 were focally expressed in both the spindle and the giant cells, with Ki-67-positive cells accounting for 70-80%. Gastric pleomorphic giant cell carcinoma presents multiple histomorphological features and is easily confused with various tumors. Clarifying the histopathological features of this type of tumor is important for differential diagnosis and precise treatment.

Pleomorphic giant cell carcinoma of the prostate: clinicopathologic analysis and oncological outcomes

We report on the clinicopathologic features of 27 pleomorphic giant cell carcinoma (PGCC) cases of the prostate identified in 20 patients with an age range of 51 to 84 years (68 ± 9; median 71 years). Charlson comorbidity index ranged from 3 to 12. Serum PSA ranged from 4.30 to 662 ng/mL (median 13 ng/mL). On histologic examination, bizarre giant cells with pleomorphic nuclei characterized pleomorphic giant cell carcinoma of the prostate. PGCC component was present in 5% to 100%, with half of the patients presenting with ≥ 20%. Half of the patients initially presented with T4 and 26% with T3 disease. All patients were considered Gleason scores of 9 to 10 (ISUP grade 5). A combination of hormone therapy with chemotherapy with or without radiation therapy was applied in 68% of patients. On follow-up, 14 patients (52%) were alive with disease (1–69 months) or dead of disease (1–38 months). Patients diagnosed earlier with lower TNM stage had longer survival than those diagnosed at a later T-stage or with metastatic disease (p = 0.02). The percentage of PGCC was not related to survival in the current study. Molecular alterations in 3 samples showed a microsatellite-stable disease with low tumor mutation burden and variable PTEN, PTCH1, KDM6A, ARv7, and PIK3CA loss/alteration, TP53 mutation, TMPRSS2-ERG fusion, and MYC, PIK3CB, RICTOR, or IRS2 amplification. Our findings suggest that PGCC is a rare and aggressive subtype of prostate carcinoma whose recognition may steer clinicians to adopt more aggressive treatments and investigate new therapeutic strategies.

Pleomorphic (giant cell) carcinoma revisited: A historical perspective and conceptual reappraisal.

The term pleomorphic "giant cell" carcinoma was coined by Sommers and Meissner in 1954 for a pancreatic carcinoma variant showing a "sarcoma-like transformation" and characterized by an admixture of undifferentiated cells with striking variation in size and shape. Based on the predominant cell type, four patterns were recognized: spindle cell (sarcomatoid), pleomorphic "giant cell", osteoclastic giant cell-rich, and anaplastic round cell. These four basic patterns frequently coexisted within same tumor, albeit to a significantly variable extent. Follow-up series further characterized the entity, expanded its topographic distribution to include almost all organ systems, and illustrated its morphological and phenotypic homology among different organs. Although resemblance of the neoplastic cells to rhabdomyoblasts was already pointed out by Stout in 1958, the term "rhabdoid" (introduced in 1978 for specific kidney tumors) was not used for carcinomas until 1993. Review of the old and recent literature indicates pleomorphic "giant cell" carcinoma is not an entity but a morphological pattern in the spectrum of undifferentiated (anaplastic) and sarcomatoid carcinoma that can originate in any organ, either in a pure form or as a dedifferentiated carcinoma component. These tumors fall into two major categories: a monomorphic (variable admixture of small or larger "gemistocyte-like" rhabdoid cells and epithelioid cells) and a pleomorphic (bizarre large polygonal, spindled, or multinucleated malignant cells) subtype. The few available genetic studies suggest close association of the monomorphic type with SWI/SNF pathway defects, while bizarre-looking pleomorphic tumors usually harbor complex and heterogeneous genetic alterations. Most tumors dominated by the pleomorphic "giant cell" pattern are extremely aggressive, resulting in death, soon after diagnosis, irrespective of treatment modalities. This review gives an historical account on the evolution of the pleomorphic "giant cell" carcinoma concept with special reference to their relationship to SWI/SNF complex alterations.

Pleomorphic Giant Cell Carcinoma of Urinary Bladder with Brain Metastases Despite Initial Response to Cisplatin and Gemcitabine: A Case Report

A 59-year-old male presented with haematuria and was diagnosed with pleomorphic giant cell carcinoma of the urinary bladder, a very rare variant of urothelial carcinoma. The tumour was staged at pT2N3M1 and the primary tumour was removed by transurethral resection, and nodal metastases were treated with the standard systemic cisplatin and gemcitabine for urothelial cell carcinoma of the bladder. This treatment rendered the tumour clinically undetectable. Despite this treatment the patient developed brain metastases which were not found until the patient presented with neurological symptoms. This is the first recorded case of brain metastases from pleomorphic giant cell carcinoma of the urinary bladder recorded in the literature. CT imaging of the brain should be considered in the follow-up in patients with this tumour.

Gene fusion characterisation of rare aggressive prostate cancer variants-adenosquamous carcinoma, pleomorphic giant-cell carcinoma, and sarcomatoid carcinoma: an analysis of 19 cases.

To evaluate the molecular underpinnings of the rare aggressive prostate cancer variants adenosquamous carcinoma, pleomorphic giant-cell carcinoma, and sarcomatoid carcinoma. We retrieved 19 tumours with one or more variant(s), and performed ERG immunohistochemistry, a next-generation sequencing assay targeting recurrent gene fusions, and fluorescence in-situ hybridisation (FISH) for ERG and BRAF. Divergent differentiation included: sarcomatoid carcinoma (n=10), adenosquamous carcinoma (n=7), and pleomorphic giant-cell carcinoma (n=7). Five patients had more than one variant. Four had variants only in metastases. ERG rearrangement was detected in nine (47%, seven via sequencing, showing TMPRSS2-ERG fusions and one GRHL2-ERG fusion, and two via FISH, showing rearrangement via deletion). ERG was immunohistochemically positive in the adenocarcinoma in eight of nine (89%) patients, but was immunohistochemically positive in the variant in only five of nine patients (56%, typically decreased). One patient had a false-positive ERG immunohistochemical result in the sarcomatoid component despite a negative FISH result. Two (11%) harboured BRAF fusions (FAM131A-BRAF and SND1-BRAF). ERG fusions are present in these rare prostate cancer variants with a frequency close to that in conventional prostate cancer (9/19, 47%). ERG immunohistochemistry usually detects rearrangement in the adenocarcinoma, but is less sensitive for the variant histology, with weak to negative staining. Adenosquamous and sarcomatoid variants can, particularly, occur together. Molecular assessment may be an additional tool in selected cases to confirm the prostatic origin of unusual tumours. The presence of two BRAF rearrangements suggests that this gene fusion may be enriched in this setting, as RAF kinase fusions have been previously reported in 1-2% of prostate cancers.

Pleomorphic Spindle and Giant Cell Carcinoma of Lung With Widespread Metastases: An Autopsy Case Report

Pleomorphic Spindle and Giant Cell Carcinoma of Lung With Widespread Metastases: An Autopsy Case Report

A new WHO classification of prostate tumors

The paper reviews the 2016 WHO classification of prostate tumors, notes the alterations made, and describes approaches to the diagnosis of cancer types and grades. It also gives original photomicrographs from the authors' collection. The main alterations were as follows: - The types of prostate adenocarcinoma were added by pleomorphic giant-cell carcinoma; oncocytic (8290/3) and lymphoepithelial (8082/3) carcinomas were excluded. - Grade III prostatic intraepithelial neoplasia (PIN) was substituted for high grade PIN (8148/2). - Intraductal carcinoma (8500/2) was added. - Basal cell adenoma (8147/0) was excluded. - Carcinoids were referred to as low-grade neuroendocrine tumors according to the current terminology; large cell neuroendocrine cancer (8013/3) was added. - Paraganglioma (8613/3) and neuroblastoma (9500/3) were excluded. Stromal tumors were grouped with mesenchymal neoplasms. -Malignant fibrous histiocytoma, malignant peripheral nerve sheath tumor, chondroma, and hemangiopericytoma were excluded. - Synovial sarcoma (9040/3), inflammatory myofibroblastic tumor (8825/1), osteosarcoma (9180/3), undifferentiated pleomorphic sarcoma (8802/3), solitary fibrous tumor (8815/1), and malignant solitary fibrous tumor (8815/3) were added. The section of lymphoproliferative diseases was extended. The tumors of unknown origin included paraganglioma and neuroblastoma from a group of neuroendocrine tumors. The TNM staging was completely consistent with the 2010 AJCC version.

Pleomorphic giant cell carcinoma of the urinary bladder: an extreme form of tumour de-differentiation.

Vesical pleomorphic giant cell carcinoma (PGCC) is a variant of urothelial carcinoma (UC) characterized by highly pleomorphic tumour with giant cells. Fewer than 10 cases have been reported, and our aim was to determine the clinical and pathological features of a series of tumours from a specialized uropathology laboratory. Thirteen cases of PGCC of the bladder were identified. There were nine males and four females, ranging in age from 53 to 92years (mean 72years). Associated conventional high-grade UC was seen in eight cases, while three cases also had micropapillary UC and one plasmacytoid UC. UC insitu (CIS) was present in five cases and occasional bizarre cells were seen in both UC and CIS. The proportion of PGCC present varied from 40% to 100% of tumour. Immunostaining performed on 10cases showed uniform positivity for CK 8/18 and AE1/AE3, while most tumours were positive for CK7, CK20, uroplakin III and GATA binding protein 3 (GATA3). β-human chorionic gonadotrophin (β-hCG) was negative. Of 10 patients with follow-up, five died within 1year and four are alive with tumour. The association of PGCC with UC and an overlap in immunoexpression suggests that PGCC represents an extreme form of UC de-differentiation.

Pleomorphic Giant Cell Carcinoma of Pancreatic Tail Diagnosed By Endoscopic Ultrasound

Introduction: Pleomorphic giant cell carcinoma of the pancreas is a very rare malignant tumor with aggressive behavior and poor prognosis. Here we present a case of pleomorphic giant cell carcinoma of pancreas diagnosed by endoscopic ultrasound-guided fine needle aspiration (EUS-FNA). Case Report: A 67-year-old white male patient presented to outpatient clinic with mild left upper quadrant abdominal pain for 1 year, which was progressively worsening recently. He reports 8 pounds weight loss over 1 month. Patient denies nausea, vomiting, or change in bowel habits. Past medical history was significant for hypertension and obstructive sleep apnea. He doesn’t smoke or drink alcohol. No significant family history of malignancies. Vital signs were stable. Body mass index was 51 kg/m2. Abdominal exam revealed mild epigastric tenderness with no palpable masses. The patient had CT scan of the abdomen which revealed bulging in the distal pancreatic body (Figure 1). CA19-9 and CEA were 136.9 units/mL and 0.6 ng/mL, respectively. MRI/MRCP of the abdomen revealed a pancreatic tail mass suspicious for malignancy. CT-guided fine needle aspiration and biopsy revealed atypical cells with no confirmed malignancy. The patient underwent endoscopic ultrasound which showed large, hypoechoic, heterogeneous mass with well-demarcated border at the tail of the pancreas measuring 48.6 x 30.6 mm (Figure 2A). The mass was encasing the splenic vein with no invasion to the splenic artery. EUS-FNA was performed for the pancreatic tail mass in the presence of cytopathologist who confirmed the adequacy of the samples (Figure 2B). Pathology study of the samples revealed numerous pleomorphic malignant tumor cells consistent with pleomorphic giant cell (anaplastic) carcinoma of the pancreas.Figure 1: CT scan reveals mass in the pancreatic tail.Figure 2: (A) Endoscopic ultrasound reveals large, hypoechoic, mass at the tail of the pancreas. (B) EUS-guided fine needle aspiration of the mass.Conclusion: Pleomorphic giant cell carcinoma of the pancreas is a rare type of pancreatic malignancies. EUS-FNA can help in the diagnosis of this rare neoplasm.

Long-term survivor of a resected undifferentiated pancreatic carcinoma with osteoclast-like giant cells who underwent a second curative resection: A case report and review of the literature

An undifferentiated carcinoma with osteoclast-like giant cell tumors (UC-OGC) is a rare type of tumor, which predominantly occurs in the pancreas. Due to the rarity of UC-OGC, sufficient clinical data are not available and its prognosis following surgical resection remains unclear. In the current report the case of a 37-year-old female is presented, in whom an UC-OGC of the pancreas was removed and following this, a second carcinoma of the remnant pancreas was removed during a second surgical procedure. At the patient’s initial admission, the preoperative images demonstrated a well-demarcated mass with a marked cystic component at the pancreatic head. The patient underwent a pylorus-preserving pancreaticoduodenectomy. The final pathological diagnosis was UC-OGC of the pancreas and the tumor was considered to have been curatively resected based on the histopathological findings. Four years after the initial surgery, a small mass was detected in the remnant pancreas and a partial resection of the remnant pancreas was subsequently performed. Histopathologically, the tumor consisted of a poorly differentiated tubular adenocarcinoma. A retrospective pathological analysis showed a segment of a poorly differentiated tubular adenocarcinoma in the initial resected specimen. Therefore, the final diagnosis was considered to be an intra-pancreatic recurrence of UC-OGC. The patient survived 66 months following the initial surgery and 18 months since the second resection. A meta-analysis was performed in the current study by comparing UC-OGC patients who survived more than two years following surgical resection (long-term survivors) with those who succumbed less than one year following surgical resection (short-term survivors). The characteristics of the short-term survivors were patients of an older age, males, and those exhibiting smaller tumors, positive lymph node metastasis, and concomitant components of ductal adenocarcinoma, as well as pleomorphic giant cell carcinoma. The concomitant component of mucinous cystic neoplasm was not considered to be a prognostic factor. To the best of our knowledge, the patient in the current report is the first five-year survivor following a curative second resection.

Undifferentiated Pancreatic Carcinoma with Osteoclast-Like Giant Cells: a Case Report

Undifferentiated pancreatic carcinoma with osteoclast-like giant cells (UPC-OGCs) is a rare neoplasm with frequency of 0.2 % of reported pancreatic carcinomas [1]. Tumors with osteoclast-like giant cells have rarely been reported in a variety of extra-skeletal sites. On the alimentary tract, the pancreas is the most concerned [2, 3]. A number of terms have been used to describe variants of undifferentiated pancreatic carcinoma, especially pleomorphic carcinoma, pleomorphic giant cell carcinoma, sarcomatoid carcinoma, spindle cell carcinoma, anaplastic carcinoma, undifferentiated carcinoma, and osteoclastic or pleomorphic giant cell tumors [4]. Histologically, the tumor combines two main cell populations, a malignant mononuclear cells population and the scattered nonneoplastic osteoclast-like giant cells [3, 5]. Since the first description by Rosai in 1968 [6], there have been only a few cases reported in the world literature. Our aim is to describe a new case of undifferentiated carcinoma of the pancreas with osteoclast-like giant cells which was early diagnosed, with a review of literature.

Pleomorphic giant cell carcinoma of the urinary bladder

Pleomorphic giant cell carcinoma is a rare aggressive variant of urothelial carcinoma characterized by the presence of highly pleomorphic bizarre tumor giant cells similar to giant cell carcinoma of the lung. Although mentioned in the 2004 WHO classification as a type of urothelial carcinoma with giant cells, characteristics of pleomorphic giant cell carcinoma were described in the literature only in 2009 when Lopez Beltran et al . reported a series of 8 cases. It occurs more commonly in older males (ages ranging 55–88 years) with patients presenting with hematuria, dysuria or frequency. The pleomorphic giant cell component in the reported series varied from 20% to 100% of the tumor. This tumour has expansile masses of pleomorphic epithelioid tumor with bizarre anaplastic multinucleated and mononu-cleated tumor giant cells. Extensive necrosis is common. Tumor cells have abundant cytoplasm, and have frequent typical or atypical mitotic figures. Tumour cells are positive for CK7, CAM 5.2, AE1/AE3 and EMA. Some cases are positive for P63, thrombomodulin and Uroplakin111. This tumour must be differentiated from metastatic malignancy to the bladder including pleomorphic giant cell carcinoma of the prostate. This tumor has a very poor prognosis. Patients often have advanced stage cancer at presentation.

Polyomavirus (BK)-associated pleomorphic giant cell carcinoma of the urinary bladder: a case report

This report describes the morphological features of a pleomorphic giant cell carcinoma with focal trophoblastic differentiation of the urinary bladder in a male, 12 years post living related donor renal transplant. The voided urine cytology demonstrated rare decoy cells admixed with markedly atypical urothelial cell clusters, papillae and giant cells. Cystoprostatectomy demonstrated a nodular mass involving the trigone and right lateral-posterior wall, adjacent to the ureteral orifice. Hematoxylin-eosin stained sections showed two synchronous malignancies: (a) pleomorphic giant cell carcinoma with focal trophoblastic differentiation of the urinary bladder, metastatic to the omentum and (b) prostatic adenocarcinoma, Gleason score 3+4=7, involving the right prostate lobe. Strong diffuse expression of polyomavirus large T antigen was demonstrated in the primary and metastatic pleomorphic giant cell carcinoma, supporting a possible role for polyomavirus (BK) in the oncogenetic pathway. The prostatic adenocarcinoma was negative for polyomavirus large T antigen. Our findings of p63, CK7 and CK903 expression in pleomorphic giant cell carcinoma suggest that the tumor is of urothelial derivation. This is the first report describing the morphological features of urinary bladder pleomorphic giant cell carcinoma with trophoblastic differentiation, positive for polyomavirus large T antigen, arising in the background of BKV reactivation.

Recently described and unusual variants of urothelial carcinoma of the urinary bladder

Urothelial carcinoma (UC) of the urinary bladder has a great propensity to undergo divergent differentiation. The resulting subtypes are morphologically unique and have significant prognostic and therapeutic differences. While squamous and glandular subtypes are the most common, a number of other well characterised morphological subtypes were described in the 2004 World Health Organization Classification. More recently additional variants of UC have been described, while others have been more fully characterised. In this review we report the details of recently described and selected unusual variants of UC. Specifically, the pathological and clinical details are discussed, relating to large nested and nested variant of UC, large cell undifferentiated carcinoma, lymphoepithelioma-like carcinoma, osteoclast rich undifferentiated carcinoma, pleomorphic giant cell carcinoma, UC with syncytiotrophoblastic giant cells, lipid cell variant of UC, micropapillary UC, UC with abundant myxoid stroma and plasmacytoid UC.

Histological variants of prostatic carcinoma and their significance

The vast majority of prostatic cancers are acinar adenocarcinomas. Histological variants of prostatic carcinoma have been variably defined. One approach is to consider two groups of variants. The first group comprises histological variants of acinar adenocarcinoma and the second group non-acinar carcinoma variants or types. Variants of usual acinar adenocarcinoma defined in 2004 by the World Health Organization (WHO) include atrophic, pseudohyperplastic, foamy, colloid, signet ring, oncocytic and lymphoepithelioma-like carcinomas. The second group of non-acinar carcinoma histological variants or types of prostatic carcinoma accounts for about 5-10% of carcinomas that originate in the prostate. These include sarcomatoid carcinoma, ductal adenocarcinoma, urothelial carcinoma, squamous and adenosquamous carcinoma, basal cell carcinoma, and neuroendocrine tumours, specifically small-cell carcinoma. Recently characterized variants not present in the 2004 WHO classification, including microcystic adenocarcinoma, prostatic intraepithelial neoplasia-like adenocarcinoma, large-cell neuroendocrine carcinoma, and pleomorphic giant cell carcinoma, are also described. The aims of this review are to present the essential histomorphological diagnostic attributes of these variants, and to emphasize the clinical signficance of the variants, when different from usual acinar adenocarcinoma, including clinical presentation and outcome.

Pleomorphic Giant Cell Carcinoma of the Pancreas with Hepatic Metastases—Initially Presenting as a Benign Serous Cystadenoma: A Case Report and Review of the Literature

Introduction. Pleomorphic giant cell pancreatic cancer is a very rare and aggressive pancreatic neoplasm. A case of pleomorphic giant cell pancreatic cancer presenting as a cystic lesion and in association with a serous cystadenoma presents a unique case which has not been described before. Case Presentation. A 44-year-old alcoholic man presented with abdominal pain, vomiting, and weight loss. Initially, imaging suspected a pancreatic pseudocyst measuring 4.2 cm. Endoscopic ultrasound- (EUS-) guided fine-needle aspiration revealed a serous cystadenoma. With conservative intervention only (fluid resuscitation, analgesia, and antiemetics) the patient improved and was discharged under close observation. Follow-up scan at four months revealed minimal change. Three months later, he was admitted acutely. Repeat scans demonstrated mild cyst enlargement with new liver lesions. Laparoscopic biopsy revealed pleomorphic giant cell carcinoma with the organ of origin the pancreas. Conclusion. This unusual case highlights the challenges in managing pancreatic cystic lesions and emphasizes the importance of considering less common forms of pancreatic cystic masses when the findings are atypical for the presentation. Surgical excision in these cases over conservative steps may be the most appropriate management.

Pleomorphic giant cell carcinoma of the urinary bladder

In this report, we present the clinicopathologic features of 8 cases of the pleomorphic giant cell variant of urothelial carcinoma. This is a rare variant of bladder cancer recognized by the current World Health Organization classification of urologic tumors. The pleomorphic giant cell component varied from 20% to 100% of the tumor specimen; in 2 cases, the pleomorphic giant cell component composed greater than 50% of the tumor with 1 case showing pure pleomorphic giant cell carcinoma. The architectural pattern of the tumor varied from infiltrating pleomorphic tumor with bizarre giant cells to solid expansile nests with discohesive growth pattern; a hypocellular desmoplastic stromal response was present in 2 cases (25%) with single cells in sclerotic stroma. At histology, giant, bizarre, anaplastic cells with frequent typical or atypical mitotic figures were present in all cases. Seven mixed cases had concurrent conventional high-grade urothelial carcinoma; 2 cases presented features of micropapillary or lymphoepithelioma-like urothelial carcinoma. Variable size intracytoplasmic vacuoles were present in 2 cases. All patients had advanced-stage cancer (>/=pT3), and 6 (75%) had lymph node metastases. Immunohistochemical staining demonstrated that both pleomorphic giant cell and associated conventional urothelial carcinoma were positive for cytokeratins 7, CAM 5.2 and AE1/AE3, and epithelial membrane antigen; P63, thrombomodulin, and uroplakin III were positive in 6, 3, and 2 cases, respectively. Follow-up information was available in all cases (range, 6-74 months; mean, 20 months). Five of the patients died of disease from 6 to 17 months, and 2 patients were alive with metastases at 11 and 19 months. One patient had no evidence of disease at 74 months. In summary, pleomorphic giant cell is an aggressive variant of urothelial carcinoma associated with poor prognosis that presents at an advanced clinical stage. In limited samples, it may be misdiagnosed as secondary carcinoma or sarcoma, a pitfall of paramount importance for its clinical management.

Giant‐cell containing neoplasms of the pancreas: An aspiration cytology study

Giant-cell containing neoplasms of the pancreas are rare with few reports documenting their cytologic appearance. Giant-cell containing neoplasms of the pancreas have been divided into two subtypes corresponding to the osteoclastic giant-cell tumor of the pancreas and the pleomorphic giant-cell carcinoma of the pancreas. Despite the better prognosis reported in some series for osteoclastic giant-cell tumors, the most recent edition of the World Health Organization classification lumps the two entities into a single category designated as undifferentiated carcinoma with osteoclast-like giant cells. Smears obtained from osteoclastic giant-cell tumors show numerous giant-cells with clustered overlapping, bland appearing nuclei containing prominent nucleoli consistent with an osteoclast-type multinucleated giant-cell. These neoplasms contain a second population of mononuclear cells showing more marked nuclear atypia. Pleomorphic giant-cell carcinomas are characterized by anaplastic giant-cells displaying marked nuclear pleomorphism. The mononuclear component is also pleomorphic with markedly atypical epithelioid and spindle shaped cells. In three reported cases, a tumor contained a mixture of the two cell patterns. Thus, undifferentiated carcinoma with osteoclast-like giant cells and pleomorphic giant cell carcinoma may represent a morphologic spectrum with pure osteoclast-like giant-cell tumors at one end and pleomorphic giant-cell carcinoma at the other. Fine-needle aspiration specimens from pure osteoclast-like giant-cell tumors will contain a population of bland multinucleated osteoclastic-like giant-cells that differ markedly from the anaplastic giant-cells of pleomorphic giant-cell carcinoma. The difference in the appearance of the giant-cells aids in distinction of the two neoplasms. When in pure form, the two neoplasms may follow different clinical courses.

Abnormal Nuclear Structures (Micronuclei, Nucleoplasmic Bridges, and Nuclear Buds) in a Pleomorphic Giant Cell Carcinoma of the Stomach

A rare case of pleomorphic giant cell carcinoma of the stomach in a 70-year-old man is reported. Characteristic microscopic findings included a general lack of architectural cohesiveness, aggregates of mononucleated or multinucleated giant cells, extensive areas of coagulative necrosis, and numerous mitoses. Immunohistochemically, tumor cells displayed cytoplasmic immunoreactivity for cytokeratin AE1/AE3 as well as overexpression of p53 and Ki-67. Electron microscopy revealed paranuclear tonofilaments bundles in giant cells confirming their epithelial nature. Furthermore, giant cells contained two or more nuclei with heterogeneous size, nucleoplasmic bridges, nuclear buds, and micronuclei. Similar abnormal nuclear structures have been closely related to breakage-fusion-bridge type of mitotic disturbances in tumor cell lines, and have not been previously reported in a human tumor.

Esophageal pleomorphic giant cell carcinoma combined with small cell carcinoma

Herein is presented the case of an esophageal pleomorphic giant cell carcinoma combined with small cell carcinoma (SCC). The patient, a 77-year-old man, initially presented with dysphagia and hoarseness, and endoscopy indicated a large esophageal tumor. Despite chemoradiation therapy, the patient died from widespread local extension of the tumor and distant metastases approximately 8 months after onset of the symptoms. Histologically, the primary tumor was composed of pleomorphic tumor components, SCC components, and a tiny focus of squamous cell carcinoma. The pleomorphic tumor cells, consisting of solid sheets of poorly cohesive epithelioid cells and numerous multinucleated giant cells with abundant eosinophilic cytoplasm, were immunohistochemically positive for vimentin and desmin, with scattered positivity for epithelial membrane antigen (EMA) and neuron-specific enolase (NSE), but negative for myoglobin. These findings were histopathologically compatible with pleomorphic giant cell carcinoma occurring at other sites such as the lung. SCC cells, morphologically similar to their pulmonary counterpart, were positive for EMA and some neuroendocrine markers such as chromogranin A and NSE, and occasionally positive for vimentin and desmin. Esophageal pleomorphic giant cell carcinoma can occur in close association with SCC, and should be included in the differential diagnosis of esophageal tumors showing pleomorphism.