Metastasis to the breast from medullary carcinoma of the thyroid is extremely rare. We report a case of metastatic medullary carcinoma of the thyroid which presented as multiple breast masses with ipsilateral axillary lymphadenopathy in a 48-year-old woman. Six years ago, she underwent total thyroidectomy and neck dissection because of palpable neck masses, with a diagnosis of medullary thyroid carcinoma. Histological features of breast masses showed single- file or linear-cord arrangements, with plasmacytoid appearance, and the initial diagnosis was invasive lobular carcinoma. She underwent modified radical mastectomy. The tumor cells were diffusely positive for E-cadherin, calcitonin and thyroid transcription factor-1 (TTF-1) and were metastatic medullary carcinoma of thyroid. In the patients with a history of medullary carcinoma of the thyroid, a careful examination is necessary for a breast mass composed of solid and cord-like clusters of small round to ovoid cells with plasmacytoid appearance. Immunohistochemical staining for E-cadherin, calcitonin and TTF-1 could be helpful for differential diagnosis.
Breast* ; Cadherins ; Calcitonin ; Carcinoma, Lobular* ; Carcinoma, Medullary* ; Diagnosis ; Diagnosis, Differential ; Female ; Humans ; Lymphatic Diseases ; Mastectomy, Modified Radical ; Middle Aged ; Neck ; Neck Dissection ; Neoplasm Metastasis ; Thyroid Gland* ; Thyroid Neoplasms ; Thyroidectomy

BACKGROUND: Carcinoma of the ampulla of Vater is rare and its pathogenesis is unclear. The role of epigenetic changes in the APC or CDH1, in the Wnt pathway, has not been reported in ampullary carcinomas. METHODS: We performed immunohistochemistry on 73 sporadic ampullary carcinomas to identify Wnt-related molecules (APC, beta-catenin, E-cadherin, c-erbB2, cyclin D1) and examined mutations in the CTNNB1, loss of heterozygosity of 5q21, and the methylation status of the CpG island of APC and CDH1. RESULTS: Thirteen tumors (17.8%) showed abnormal nuclear localization of beta-catenin; this was more prominent in the intestinal type than in the pancreaticobiliary type (p=0.01). The loss of APC correlated with the loss of beta-catenin or c-erb B2 (p<0.01). The prognosis was worse in the group with APC loss than when APC was maintained (p<0.05). There was no mutation identified in CTNNB1. Six (24%) out of 25 informative cases had 5q21 allelic loss. CpG island methylation in APC and CDH1 was detected in 33 (45.2%) and 29 (31.5%) cases, respectively. CONCLUSIONS: The absence of mutations in CTNNB1 and the epigenetic alteration of APC and CDH1, might be characteristic changes in the Wnt/beta-catenin signaling pathway during the carcinogenesis of ampullary carcinomas.
Ampulla of Vater* ; beta Catenin ; Cadherins ; Carcinogenesis ; CpG Islands ; Cyclins ; Epigenomics* ; Immunohistochemistry ; Loss of Heterozygosity ; Methylation ; Prognosis ; Wnt Signaling Pathway

The authors present the fine needle aspiration cytology (FNAC) cytologic findings of a case of extranodal marginal zone B cell lymphoma (MZBCL), which featured abundant plasma cells and eosinophilic histiocytes arising in both parotid glands. A 49-year-old female presented with palpable masses in both parotid glands. She had been suffering from systemic lupus erythematosus and rheumatoid arthritis. The lesions were evaluated by FNAC and smears showed a small number of clusters of oncocytic cells with abundant eosinophilic granular cytoplasm and small nuclei, intermixed with small to medium-sized lymphoid cells containing round to lobulated nuclei, which suggested Warthin's tumor. Some of lymphoid cells had a plasmacytoid appearance, and some scattered large cells contained a large amount of eosinophilic cytoplasm. Bilateral superficial parotidectomy was performed and a histopathologic study indicated MZBCL with abundant plasma cells, intermixed with eosinophilic histiocytes. The presence of oncocytic cells and a mixture of lymphoid and plasma cells indicates Warthin's tumor, but the cytologic features of a relatively monotonous small to medium-sized lymphoid infiltrate suggest the possibility of MZBCL in the clinical setting of an FNAC study performed on a patient suffering from a connective tissue disease.
Arthritis, Rheumatoid ; Biopsy, Fine-Needle* ; Connective Tissue Diseases ; Cytoplasm ; Eosinophils* ; Female ; Histiocytes* ; Humans ; Lupus Erythematosus, Systemic ; Lymphocytes ; Lymphoma, B-Cell, Marginal Zone* ; Middle Aged ; Parotid Gland* ; Plasma Cells* ; Plasma*

We present a case of recurrent follicular lymphoma with an extensive plasma cell component involving infra-auricular lymph nodes in a 64 year-old woman. Immunohistochemical staining showed a strongly positive reaction of the follicles with CD20, bcl-2, bcl-6, CD10 and CD21 on the first biopsy specimen. The intrafollicular and interfollicular plasma cells showed monoclonality for IgG heavy chain and lambda light chain. The histological and immunohistochemical findings in the recurrent tumor were identical with those of the original. Discussion is focused on the importance of the differential diagnosis between reactive lymphoid hyperplasia and other lymphomas having plasmacytic differentiation.
Biopsy ; Diagnosis, Differential ; Female ; Granuloma, Plasma Cell ; Humans ; Immunoglobulin G ; Lymph Nodes ; Lymphoma ; Lymphoma, Follicular* ; Middle Aged ; Plasma Cells* ; Plasma* ; Pseudolymphoma ; Stomach

BACKGROUND: Tyrosine kinase receptor (TKR) is an important protein for normal-development, growth and tumorigenesis in human tissues. The purpose of this study was to evaluate the effect of TKR in the progression of breast cancer. METHODS: The expressions of EphA2, c-met and c-erbB-2 were examined, by using immunohistochemical methods and RT-PCR, in samples of breast tissue that included 111 samples of normal epithelium, 34 samples of ductal carcinoma in situ (DCIS), and 109 samples of invasive ductal carcinomas (IDC). The results were compared with the prognostic parameters of breast cancer including the tumor grade, growth pattern, lymph node metastasis and the expressions of ER, PR, p53 and Ki-67. RESULTS: The protein expressions of the three TKRs were higher in DCIS and IDC than in normal epithelium. The protein expression of EphA2 was correlated with a tumor grade, a labeling index of Ki-67, and the protein expression of c-met. Overexpression of c-erbB-2 was correlated with lymph node metastasis. The mRNA levels of the three TKRs were correlated with each other in normal tissue and IDC. The level of c-met mRNA was higher in the low grade tumors. CONCLUSIONS: The three TKRs may play roles in the tumorigenesis of human breast cancer. The overexpressions of EphA2 and c-erbB-2 may be a poor prognostic parameter in breast cancers.
Breast Neoplasms ; Breast* ; Carcinogenesis ; Carcinoma, Ductal ; Carcinoma, Intraductal, Noninfiltrating ; Epithelium ; Humans* ; Lymph Nodes ; Neoplasm Metastasis ; Protein-Tyrosine Kinases* ; Receptor Protein-Tyrosine Kinases* ; RNA, Messenger ; Tyrosine*

Liposclerosing myxofibrous tumor (LSMFT) is a benign fibro-osseous lesion that is characterized by a complex mixture of histologic elements, including its fibrous dysplasia-like features and its lipoma, myxofibroma, xanthoma and pseudo-Paget's bone patterns. However, this lesion is considered by some researchers as a variant of fibrous dysplasia or as the non-specific end result of degenerative change, while it is considered by others as a definite clinicopathologic entity. Here, we report on a case of LSMFT occurring in tibia, which is a very uncommon location for this tumor, and we review the related literatures. The case presented here shares features with those described for LSMFT, except for the location of this tumor. We believe that more studies on a larger scale that compare LSMFT with other benign bone lesions, including fibrous dysplasia, are required to clarify the origin and behavior of this lesion.
Fibroma ; Lipoma ; Tibia* ; Xanthomatosis

BACKGROUND: Mannose-binding lectin (MBL) is a serum protein of innate immunity. Its genetic mutations lead to deficiency of serum MBL and recurrent pyogenic infection in childhood. However, little is known about the frequency of its gene mutations or serum levels in Korean population and patients with cancers. METHODS: We studied the mutational genotypes of MBL exon 1 codon 52, 54, and 57 or serum MBL levels from 102 normal adults and 228 cases of breast, stomach, colon, uterine cervical, and lung cancers by allele-specific PCR and enzyme-linked immunosorbent assay. RESULTS: MBL gene mutations were found in 32 of 102 normal adults (31.4%), and were restricted only to exon 1 codon 54 showing homozygous (n=5, 4.9%) or heterozygous mutations (n=27, 26.5%). Mean and median serum MBL in the patients with cancers were increased (2,647+/-1,742 and 2,915 ng/mL, mean+/-S.D. and median) than those of normal adults (1,906+/-1,359 and 1,758 ng/mL). Serum MBL level was significantly increased in the patients with stomach, uterine cervical, colon, and lung cancers. CONCLUSION: Our results indicate that the frequency and pattern of MBL gene mutations and its serum level is very similar among northeastern Asian populations. In addition, MBL might be involved in an immunologic response against common cancers, although further studies are needed.
Adult ; Asian Continental Ancestry Group ; Breast ; Codon ; Colon ; Enzyme-Linked Immunosorbent Assay ; Exons ; Genotype ; Humans ; Immunity, Innate ; Lung Neoplasms ; Mannose ; Mannose-Binding Lectin* ; Polymerase Chain Reaction ; Stomach

BACKGROUND: The colorectal adenoma-carcinoma sequence represents a well-known para-digm for the sequential development of cancer driven by the accumulation of genomic defects. Although the colorectal adenoma-carcinoma sequence has been well investigated, the studies about tumors of different dignity co-existent in the same patient are rare. K-ras mutation is an early genetic change in colon cancer. The genes involved in the cell cycle such as cyclin D1, p16, and p53 are important in the tumorigenesis of the colon. The aims of this study were to determine K-ras gene mutation and expression of K-ras, p16, cyclin D1 and p53 in synchronous lesions of the colon adenoma-carcinoma sequences and their possible relationship with K-ras mutation. METHODS: The materials included 45 colonic adenocarcinomas which were accompanied by adenoma (22 low grade and 26 high grade). By using polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP), we detected K-ras mutation of codon 12. An aberrant K-ras, p16, cyclin D1 and p53 expressions were stained using an immunohistochemical method. RESULTS: K-ras mutation was 52.4% (11/21) of high grade adenomas. K-ras expression was 65.4% (17/26) of high grade adenomas. p16 and cyclin D1 expressions were 50% (11/22) and 90.9% (20/22) of low grade adenomas, respectively. p53 expression was 75.6% (34/45) of adenocarcinomas. There were statistical correlations among K-ras, p16 and cyclin D1. CONCLUSIONS: These results indicate that the ras gene mutation is an early event and the overexpressions of p16, cyclin D1 and p53 are associated with K-ras mutation and expression in adenoma-carcinoma sequences.
Adenocarcinoma ; Adenoma ; Carcinogenesis ; Cell Cycle ; Codon ; Colon* ; Colonic Neoplasms ; Colorectal Neoplasms ; Cyclin D1* ; Cyclins* ; Genes, ras* ; Humans

BACKGROUND: Infection of Epstein Barr virus (EBV) into B cells drives the infected cells into the cell cycle and frequently results in lymphoblastoid cells. Mitomycin C inhibits DNA synthesis of epithelial cells as well as lymphoid cells by cross-linking with DNA. Many of the cancer cells have various pathways for escaping the responsiveness to the negative growth-regulatory effects of mitomycin C and gaining the immortalized property. The auther performed a cell culture of an EBV infected Jijoye lymphoma cell line, and compared the cell cycle and cancer related genes between the mitomycin treated- and non-treated group. METHODS: DNA and RNA were extracted from the Jijoye cells; and EBV nuclear antigen (EBNA)-1, 2 and latent membrane protein (LMP) of EBV and p53 and p21 mRNA analyse was performed. RESULTS: Mitomycin C blocked G2/M phase, however, mitomycin did not affect the expression of EBNA-1, 2 and LMP. Mitomycin C also increased the p21 mRNA expression without p53 mRNA increase. CONCLUSIONS: Mitomycin C induces B cell apoptosis by blocking the G2/M phase and by increasing p21 mRNA independent to p53, which reveals the presence of an alternative pathway of p21 induction by mitomycin C in EBV positive lymphoma cells
Apoptosis ; B-Lymphocytes ; Burkitt Lymphoma* ; Cell Culture Techniques ; Cell Cycle ; Cell Line* ; DNA ; Epithelial Cells ; Herpesvirus 4, Human ; Lymphocytes ; Lymphoma ; Membrane Proteins ; Mitomycin* ; RNA ; RNA, Messenger ; United Nations

PURPOSE: Hepatocellular carcinoma (HCC) patients are asymptomatic and the tumor remains in an unresectable state until the tumor progresses. Recently much efforts for elucidation of the early hepatocarcinogenesis have been made, and for this purpose it is very crucial to investigate the genetic abnormalities. We evaluated microsatellite alterations of five markers from chromosome 9, 13, 16 and investigated the relationships with the clinicopathological parameters in HCC. METHODS: The microsatellite alteration analysis was performed using polymerase chain reaction with five polymorphic microsatellite markers (D9S171, D9S1747, D13S156, D16S419, D16S3106) in 40 surgically resected HCCs and their respective non-tumorous counterparts. RESULTS: D9S171, D9S1747, D13S156, D16S419, D16S3106 abnormalities were detected in 20.0%, 14.3%, 50.0%, 32.4% and 22.6%, respectively. Loss of heterozygosity (LOH) of D9S171 correlated well with higher tumor histologic grade and LOH of D13S156, D16S419 and D16S3106 correlated well with increased tumor size. Microsatellite instability (MSI) was found in two markers, D13S156, D16S419. CONCLUSION: As a result, we concluded that alterations in microsatellites of various chromosomes may contribute to the hepatocarcinogenesis and tumor progression. Especially LOH of chromosome 13 and 16 are considered to correlate with tumor progression.
Carcinoma, Hepatocellular* ; Chromosomes, Human, Pair 13 ; Chromosomes, Human, Pair 9 ; Humans ; Loss of Heterozygosity ; Microsatellite Instability ; Microsatellite Repeats* ; Polymerase Chain Reaction