An-Hi Lee

Granulomatous gastritis: A clinicopathologic analysis of 18 biopsy cases

Granulomas in gastric biopsy specimens are extremely rare, and in Western countries, more than half are associated with Crohn’s disease. To evaluate the incidence and their etiology in a gastric carcinoma (and Helicobater pylori infection)-prevalent area, gastric mucosal biopsies were reviewed and their clinicopathologic findings were analyzed. The clinicopathologic diagnoses of the 18 patients with granulomatous gastritis were as follows: chronic gastritis with (n = 14) and without (n = 1) H. pylori infection; gastric adenocarcinomas (n = 2); and Crohn’s disease (n = 1). Almost all cases of granulomatous gastritis in this study showed small erosions or ulcers on the endoscopic examinations. H. pylori were found to be one of the most common causes of granulomatous gastritis after excluding all other causes for the granulomas in this study. The granulomas were more frequently found in the antrum, superficially located, and were related to damage within a pit in which the H. pylori were commonly observed. These findings suggest that H. pylori can be causal in the pathogenesis of granulomatous gastritis.

Composite glandular-endocrine cell carcinomas of the stomach: clinicopathologic and methylation study.

Four cases of very rare composite glandular‐endocrine cell carcinoma of the stomach are presented with methylation findings. All but one of the tumors arose in the antrum and two of them were at the early stage. Each composite carcinoma was accompanied by atrophic and metaplastic gastritis in the adjacent mucosa. Three cases showed lymph nodes metastasis, and one of them showed both glandular and neuroendocrine tumor components within the metastatic nodes. Mucin stains were positive in the adenocarcinoma areas while only the neuroendocrine markers were positive in neuroendocrine tumor components. Of all seven markers tested for, p16INK4A methylation was observed in both components of one composite carcinoma and hMLH1 was methylated in the neuroendocrine tumor component within the same tumor. An additional six gastric large cell neuroendocrine carcinomas showed no methylation. Follow up of patients indicated short survival in patients with poorly differentiated neuroendocrine carcinoma components and advanced stages of tumors, while patients with well‐differentiated neuroendocrine tumor components and early stages showed long disease‐free survival. Our results suggest that hypermethylation of tumor suppressor genes is rare in gastric composite and neuroendocrine carcinomas, and prognosis of gastric composite carcinomas appears to be related to the histopathology of neuroendocrine components and tumor stage.

HER-2/neu Oncogene Amplification by Chromogenic in situ Hybridization in 130 Breast Cancers Using Tissue Microarray and Clinical Follow-up Studies

Determining of HER-2/neu oncogene amplification has become clinically important for managing breast cancer. Fluorescent in situ hybridization (FISH) and immunohistochemistry (IHC) are currently regarded as the standard methods. Chromogenic in situ hybridization (CISH) was investigated as a new modification with an accurate, sensitive technique. From 1998 to 2002, using CISH and IHC, the amplification and protein expression of the HER-2/neu oncogene were examined using paraffin sections in 130 breast carcinomas and to determine the prognostic role of HER-2/neu for outcome after a follow-up of 24-64 months. Amplifications by CISH and overexpression by IHC were observed in 28 (22%) and 27 cases (20.8%), respectively. Of the 104 patients, 20 patients (19.2%) with amplification had a shorter disease-free interval (34.9 months vs. 38.0 months in controls) (p=0.372). 15 patients (14.4%) had a disease recurrence, but there is no significant difference between 3 patients amplifying the oncogene and 12 patients without oncogene (20.6 months vs. 19.6 months) (p=0.862). 6 patients (5.8%) of these died. CISH is a useful alternative, particularly for confirming the IHC results. There is no relationship between the early recurrence and the HER-2/neu positive group, but lymph node status was statistically significant.

Huge tophaceous pseudogout associated with tenosynovial chondromatosis arising from flexor digitorum tendon sheaths of the foot: a case report

Synovial chondromatosis (SC) is a benign proliferative process of synovial tissue creating multiple cartilaginous nodules in joints. It most commonly occurs in the large joints of the knee, hip, and shoulder, uncommonly in the small joints of the hand and foot, and only rarely in the tenosynovial membrane of tendon sheath, termed tenosynovial chondromatosis (TC). Unlike SC, TC predisposes to the foot or hand. The rarity and unfamiliarity of imagers with TC, as well as the variability of its histologic features often lead to an erroneous diagnosis of extraskeletal chondroma or even chondrosarcoma as in the present case. Calcium pyrophosphate dehydrate (CPPD) crystals are usually deposited in the articular cartilage or periarticular structures such as synovium and capsule, and rarely in other soft tissue structures including bursa, tendon, subcutaneous tissue, and dura mater. CPPD crystals may also be deposited in extraskeletal chondroma and SC. We present an exceptionally rare case of huge tophaceous pseudogout associated with TC that is considered to arise from the flexor digitorum longus tendon sheaths of the foot, initially mistaken for a chondrosarcoma.

Infarct associated sarcoma: A possible pathogenesis based on histological observation of repair tissue origin in two cases

Although the absolute majority of bone sarcomas are primary in origin, transformed sarcomas occasionally arise from benign bone tumors or even nonneoplastic bone diseases [1,2]. Indeed, it has been proven that sarcomas develop from chronic infarct of the long bone, the incidence of which has been reported to be 1% of all bone sarcomas [3,4]. To date about 60 cases of infarct associated sarcomas (IAS) have been fi led in the world literature. The pathogenesis of IAS is not established although the reparative tissue adjacent to an infarct has been assumed as source of sarcomatous transformation [1,5 – 8]. To our knowledge no actual histological evidence to support the assumption has been published. Recently, we observed a defi nite transition zone to exist in the space between ancient infarct and transformed sarcoma in our two cases. The transition zone consisted of granulation tissues that included interlacing spindle cell fascicle, capillary proliferation with foamy macrophage and chronic infl ammatory cells and also cellular atypism of varying degrees. Furthermore, in the distal (sarcoma-side) transition zone atypical spindle cells were observed to imperceptibly merge into highgrade spindle cell sarcoma. We describe our histological observation of a transition zone between infarct and sarcoma, which might be an origin of sarcomatous transformation in bone infarct. A 58-year-old Korean male was referred to us because of severe, painful swelling of his left knee. Earlier, the pain was negligible lasting for four years but became aggravated during the recent six month period. He was bedridden due to intervening schizophrenic disorder and diabetes mellitus for years. No history of alcohol or steroid abuse, dysbaric working conditions, hemoglobinopathies, pancreatitis, Gaucher ’ s disease, or hereditary bone dysplasia was elicited. Pertinent laboratory data was within normal limits except mild anemia. Conventional radiography showed classic signs of multiple, ancient, bone infarcts involving both the right and left distal femora and proximal tibiae (Figure 1A). The infarct in the left proximal tibia was attended by bizarre expansive bone destruction with cortical rupture. Magnetic resonance (MR) imaging demonstrated bizarre signal intensity changes that matched well with radiographic fi ndings of infarcts and malignant transformation (Figure 1B). Scan microscopy showed a bone infarct (I) and sarcoma (OS) with a typical transitional zone (TZ) in-between (Figure 2A). Low-power microscopy revealed TZ to commence at the distal part of disintegrated infarct in where interlacing spindle cells were defi nitely bland on high power view (Figure 2B). The islands of infarct in the transformed part presented trabecular and marrow necrosis with irregular calcifi cations while the infarcts proper were completely free of malignant change. Medium-power view showed TZ to contain interlacing spindle-cell fascicles and capillary proliferation with foamy macrophage, chronic infl ammatory cells as well as atypical cells of varied populations. Atypical cells were sparse in number, if any, at the center of TZ (Figure 2C) and gradually increased in number and grade of cellular atypism as the sarcoma region was approached (Figure 2D). In the distal TZ atypical spindle cells imperceptibly Acta Oncologica, 2010; 49: 868–872

Type and Incidence of Soft Tissue Sarcomas in Korea: 2001-2007

Malignant melanoma involving the ovary is uncommon. Most of the reported ovarian malignant melanomas are metastatic, and only 44 cases are primary. Teratoid elements must be identified in the ovary for the diagnosis of primary malignant melanoma because ovaries normally do not contain melaninproducing cells. However, it is challenging to assess the primary site of ovarian malignant melanoma because it is almost always found in an advanced state, replacing entire ovarian structures, and this makes it difficult to determine whether the lesion is a primary ovarian melanoma. Mature cystic teratoma is the most common benign germ cell tumor of the ovary, and it constitutes 15-25% of ovarian tumors overall. A wide variety of malignant tumors may arise within a mature cystic teratoma, including squamous cell carcinoma (75%), adenocarcinoma (7%), undifferentiated carcinoma, basal cell carcinoma, and various sarcomas (7%). Malignant melanoma arising from mature cystic teratoma has also been reported, but it is very rare. Here, we report on an uncommon case of primary malignant melanoma arising from a mature ovarian cystic teratoma with multiple metastatic lesions.

Chromomycosis presenting as soft-tissue mass: report of a case with MRI features

Chromomycosis is primarily a skin disease that superficially presents as slowly growing, verrucous lesions, often warty or cauliflower-like in appearance. It may occasionally create a flat, plaque-like lesion in the skin but deep-seated tumorous presentation has not previously been reported. As the lesion is limited to the cutaneous and superficial subcutaneous tissues, hitherto reported cases have been described from the view point of dermatology and, so, without MRI study. We report a patient with pathologically proven chromomycosis that produced a subcutaneous mass in the dorsum of the hand with an emphasis on MRI features.

Thymic carcinoma initially presented with geographic destruction of scapula in a child

As the conventional histopathologic examination of thymic carcinoma (TC) is nonspecific, immunohistochemical studies along with correlative radiographic investigations are needed for its correct diagnosis. TC commonly occurs in the late 5th to early 6th decades of life but is extremely rare in childhood. It may be incidentally detected from chest radiographs taken as routine or for other reasons. However, most patients present with symptoms such as chest pain, cough, shortness of breath, dysphagia and hoarseness, which are directly attributable to the mediastinal mass. Although TC frequently invades the neighboring organs, pleura and pericardium and metastasizes to the lymph nodes, liver and lung at the time of the first diagnosis, initial or late metastasis to the bone has been seldom reported in adults. Indeed, the English literature revealed no earlier report on initial bony metastasis in a child to date. We report a case of TC in a 12-year-old boy who initially presented with scapular osteolysis masquerading as a primary bone tumor to emphasize the usefulness of combined imaging for staging and histologic studies, particularly for such an unexpected case.