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A Maitra

Publications and source records attributed to A Maitra.

At least 55 records · Page 3Linked to original sources
PubMed2000

Cytoplasmic inclusions in leukocytes. An unusual manifestation of cryoglobulinemia.

Cryoglobulins are circulating immunoglobulins characterized by reversible, cold-induced precipitation. A variety of laboratory abnormalities, including hypocomplementemia, elevated erythrocyte sedimentation rate, rheumatoid factor activity, pseudoleukocytosis, and pseudothrombocytosis, are associated with cryoglobulinemia. Extracellular, faintly basophilic, amorphous deposits of cryoglobulins occasionally have been described in blood smears. In the present study, smears prepared from blood collected at room temperature from 6 patients with cryoglobulinemia exhibited neutrophil and, occasionally, monocyte inclusions containing clear, light pink, or faintly basophilic amorphous material. The inclusions were absent in smears from blood collected and maintained at 37 degrees C. Ultrastructural examination revealed that the material within the leukocyte inclusions was consistent with phagocytosed immunoglobulins. The identification of characteristic cytoplasmic inclusions in leukocytes may be an important clue in the early recognition of cryoglobulinemia.

Aged↗
PubMed2000

Molecular changes in the bronchial epithelium of patients with small cell lung cancer.

To better understand the pathways involved in the pathogenesis of small cell lung carcinoma (SCLC), we compared the patterns of molecular changes present in these tumors and their accompanying bronchial epithelium with those present in the other two major types of lung cancer [squamous cell carcinoma (SQC) and adenocarcinoma (ADC)]. We obtained DNA from 68 microdissected invasive lung tumors (22 SCLCs, 21 ADCs, and, 25 SQCs) and 119 noncontiguous foci of histologically normal or hyperplastic epithelia from 10 tumors of each histological type. We determined loss of heterozygosity and microsatellite alterations at 12 chromosomal regions frequently deleted in lung cancers using 19 polymorphic microsatellite markers. Our major findings are as follows: (a) the mean index of allelic loss in SCLC (0.85) and SQC (0.71) tumors was higher than that in ADC (0.39) tumors; (b) although there was considerable overlap, each tumor type had a characteristic pattern of allelic loss; (c) most samples of bronchial epithelium accompanying SCLC (90%) had allelic loss at one or more loci compared with samples accompanying SQC (54%) or ADC (10%); (d) the mean index of allelic loss was much higher in bronchial epithelial samples from SCLC (0.27) than in those from SQC (0.08) or ADC (0.01); and (e) although the mean indices of microsatellite alterations in the tumor types were similar, the bronchial epithelial samples accompanying SCLC had a 10-fold higher mean index (0.063) than those accompanying SQC (0.006) or ADC (0.006). Our findings indicate that extensive genetic damage in the accompanying normal and hyperplastic bronchial epithelium is characteristic of SCLC tumors and suggest major differences in the pathogenesis of the three major lung cancer types.

Adenocarcinoma↗
PubMed2000

Molecular changes in second primary lung and breast cancers after therapy for Hodgkin's disease.

The risk of lung and breast cancer is significantly increased after therapy for Hodgkin's disease (HD), but there are few data that describe the molecular profiles of these tumors. We investigated the genetic abnormalities in second primary lung (n = 19) and breast cancers (n = 19) that follow therapy for HD ("post-HD cancers") and compared these with changes observed in corresponding tumor types (57 lung and 20 breast cancers) arising in the general population ("sporadic cancers"). DNA obtained from archival tissues was examined using PCR-based analyses for loss of heterozygosity and microsatellite alterations (MAs) at several chromosomal regions, TP53 and K-ras gene mutations, and frameshift mutations at minisatellite sequences at the coding regions of several genes (TGF-betaRII, IGFIIR, BAX, hMSH6, and hMSH3). The occurrence of loss of heterozygosity at all chromosomal regions taken together and frequencies at most individual areas were similar for the post-HD and sporadic cancers for both lung and breast sites. The overall frequency of MAs in the post-HD tumors was substantially greater (lung, 2.4-fold, P = 0.004; breast, 4.2-fold, P = 0.16) than that in the respective sporadic cancers. No differences in the pattern of TP53 and K-ras mutations were detected between post-HD and sporadic cancers. No mutations were detected at the minisatellite sequences examined. MAs, which reflect widespread genomic instability, occur at greatly increased frequency in post-HD lung and breast cancers. Although the mechanisms underlying the development of increased MAs are unknown, they have been associated with immunosuppression and radiation exposure. Future research should address the role that MAs, as well as other influences, may play in the development of neoplasias that occur after therapy for HD.

Adenocarcinoma↗
PubMed1999

Use of archival fine-needle aspirates for the allelotyping of tumors.

BACKGROUND: Loss of heterozygosity (LOH) analysis (allelotyping) based on polymorphic microsatellite DNA is one of the most powerful molecular tools currently available for studying carcinogenesis. However, allelotyping studies that require archival paraffin embedded tissues are often hampered by technical difficulties related to microdissection and poor DNA quality. METHODS: The authors compared allelotyping results from 12 paraffin embedded breast carcinoma cases with those from matching alcohol fixed fine-needle aspiration (FNA) cytology slides obtained for routine diagnostic purposes, using 30 polymorphic microsatellite markers at chromosomes 3p, 4p, 4q, 5q, 6p, 8p, 9p, 11q, 17p, and 17q. Cells from the alcohol fixed FNA slides were dissected and processed in three different ways, and DNA dilution experiments were performed to determine the minimum number of cells required for accurate allelotyping. RESULTS: LOH results were identical for paraffin embedded and alcohol fixed tumors for 97% of 114 polymerase chain reactions (PCR) when 1000-2000 cells were dissected from each FNA slide and DNA from 100 cells was used for each multiplex PCR. However, with lower cell numbers, the discordance rate increased and artifactual LOH was observed. Intratumor allelotype heterogeneity could not be documented. CONCLUSIONS: The use of alcohol fixed cytology preparations improves the ease of PCR-based allelotyping and greatly expands the range of archival materials available for study. The allelotyping is accurate and reproducible when DNA from >/=25 cells is used in the initial multiplex PCR. Cancer (Cancer Cytopathol)

Alleles↗
PubMed1999

Multiple clonal abnormalities in the bronchial epithelium of patients with lung cancer.

BACKGROUND: Several molecular changes, including loss of heterozygosity (i.e., deletion of one copy of allelic DNA sequences) and alterations in microsatellite DNA, have been detected early in the pathogenesis of lung cancer, even in histologically normal epithelium. In the bronchial epithelium of patients with lung cancer, we have determined the frequency, size, and patterns of molecularly abnormal clonal patches. METHODS: We studied formalin-fixed, paraffin-embedded samples from 16 surgically resected lung carcinomas (five squamous cell carcinomas, four small-cell carcinomas, six adenocarcinomas, and one large-cell carcinoma). From each carcinoma, we microdissected foci (each containing about 200 cells) of tumor tissue and equivalent samples of histologically normal and abnormal epithelium. Furthermore, multiple discontinuous foci of bronchial epithelium were analyzed from methanol-fixed samples from three additional patients with lung cancer (two with squamous cell carcinoma and one with adenocarcinoma). We used two-step polymerase chain reaction-based assays involving 12 microsatellite markers at seven chromosomal regions frequently deleted in lung cancer. RESULTS: Two hundred eighteen foci of nonmalignant bronchial epithelium (195 of histologically normal or slightly abnormal epithelium and 23 of dysplastic epithelium) were studied from the 19 surgically resected lobectomy specimens. Thirteen (68%) of the 19 specimens had at least one focus of bronchial epithelium with molecular changes. At least one molecular abnormality was detected in 32% of the 195 histologically normal or slightly abnormal foci and in 52% of the 23 dysplastic foci. Extrapolating from our two-dimensional analyses, we estimate that most clonal patches contain approximately 90 000 cells. Although, in a given individual, tumors appeared homogeneous with respect to molecular changes, the clonally altered patches of mildly abnormal epithelium were heterogeneous. CONCLUSIONS: Our findings indicate that multiple small clonal or subclonal patches containing molecular abnormalities are present in normal or slightly abnormal bronchial epithelium of patients with lung cancer.

Adenocarcinoma↗
PubMed1999

Multiple regions of chromosome 4 demonstrating allelic losses in breast carcinomas.

Allelotyping studies suggest that allelic losses at one or both arms of chromosome 4 are frequent in several tumor types, but information about breast cancer is scant. A recent comparative genomic hybridization analysis revealed frequent losses of chromosome 4 in breast carcinomas. In an effort to more precisely locate the putative tumor suppressor gene(s) on chromosome 4 involved in the pathogenesis of breast carcinomas, we performed loss of heterozygosity studies using 19 polymorphic microsatellite markers. After precise microdissection of archival surgical cases, we analyzed DNA obtained from 44 breast carcinomas for loss of heterozygosity. In addition, DNA from tumor cell lines derived from 14 of these 44 breast carcinomas were also analyzed. We observed deletions of chromosome 4 at multiple sites in both tumor cell lines and breast carcinomas. The deletions in cell lines and their corresponding tumors were extensive in nature, whereas they were more localized in noncultured breast carcinomas. The localized deletions in the noncultured breast carcinomas clearly defined four nonoverlapping regions of frequent deletions: 4q33-34 (76%); 4q25-26 (63%); 4p15.1-15.3 (57%); and 4p16.3 (50%). Our results suggest that there may be multiple putative tumor suppressor genes, located on both arms of chromosome 4, whose inactivation is important in the pathogenesis of breast cancer.

Alleles↗
PubMed1999

Loss of heterozygosity at 3p in benign lesions preceding invasive breast cancer.

BACKGROUND: Loss of heterozygosity (LOH) at chromosome 3p is one of the most common genetic abnormalities identified in human cancers and has occasionally been noted in benign proliferative lesions predisposing to breast cancer. If the frequency of LOH at 3p in benign proliferative lesions correlates with the subsequent development of breast cancer, it may be possible to develop powerful tools for molecular risk assessment based on this technology. MATERIALS AND METHODS: Archival paraffin-embedded tissues from benign breast biopsies in five women who have developed breast cancer and three women who have not developed breast cancer were microdissected and allelotyped at 3p using six microsatellite markers. RESULTS: No LOH was detected in the biopsies from women who have not developed breast cancer. For women developing breast cancer, the proportion of informative loci showing LOH in the benign proliferative lesions was 0.47 as compared to 0.57 for the associated breast cancers. There was no LOH detected in epithelial DNA from a fibroadenoma. Of 15 informative loci, 4 (27%) showed LOH in both the benign proliferative lesion and the associated cancer; however, the actual parental allele lost was different in three of these four cases. CONCLUSIONS: These results suggest that there are specific patterns of genetic instability common to preneoplastic lesions and the breast cancers that subsequently develop even when the paired lesions are not clonally related. LOH analysis of benign breast epithelium may provide a tool for molecular risk assessment and a surrogate endpoint for breast cancer chemoprevention trials.

Adult↗
PubMed1999

Low grade fibromyxoid sarcoma: fine-needle aspiration cytology with histologic, cytogenetic, immunohistochemical, and ultrastructural correlation.

BACKGROUND: Although the histologic features of the recently described low grade fibromyxoid sarcoma are well established, to the authors' knowledge there are no reports in the literature describing the cytologic features of this tumor by fine-needle aspiration. Recognition of this lesion is important because of its indolent but metastasizing nature. METHODS: The authors retrospectively reviewed their surgical pathology files for cases of low grade fibromyxoid sarcoma with a preoperative fine-needle aspiration biopsy (FNAB); three such cases were found. Immunohistochemical studies were performed in all three tumors, ultrastructural examination was performed in two tumors, and fresh tissue for cytogenetic analysis was obtained in one tumor. RESULTS: All FNABs showed similar features. The aspirates were relatively hypocellular with an abundant myxoid background; the neoplastic cells contained oval to spindle shaped nuclei with minimal pleomorphism. No capillaries or areas of fibrous tissue were identified. Cytogenetic study of one case revealed no chromosomal abnormalities. The histologic findings were characteristic for this lesion. By immunohistochemistry the tumor cells showed diffuse and strong reactivity for vimentin only; at the ultrastructural level the neoplastic spindle cells had characteristics of fibroblasts. CONCLUSIONS: The cytologic features of low grade fibromyxoid sarcoma are not specific enough for a definitive diagnosis based on FNAB alone; however, correlating the cytologic and clinical findings can narrow the range of diagnosis. The differential diagnosis includes other myxoid lesions, in particular superficial or intramuscular myxoma and myxofibrosarcoma. In addition, the immunohistochemical and ultrastructural findings support a fibroblastic origin for this neoplasm.

Adult↗
PubMed1999

The RNA component of telomerase as a marker of biologic potential and clinical outcome in childhood neuroblastic tumors.

BACKGROUND: Telomerase is a ribonucleoprotein enzyme associated with cellular immortality that may be useful in determining the biologic potential of a tumor. Neuroblastoma (NB), ganglioneuroblastoma (GNB), and ganglioneuroma (GN) are neuroblastic tumors (NTs) that exhibit a spectrum of histologic features and are often associated with unpredictable behavior and clinical outcome. METHODS: The authors investigated the expression of the RNA component of human telomerase (hTR) by in situ hybridization in 32 cases of NTs (including 24 NBs, 4 GNBs, and 4 GNs), using [35S]-UTP labeled single stranded sense and antisense RNA probes. Eight NBs were early stage, 12 NBs were advanced stage, and 4 NBs were Stage IVS, a widely metastatic variant associated with an excellent clinical prognosis. Four NBs had N-myc amplification. In addition, the authors compared a proliferation marker, MIB-1, with hTR expression in a subset of tumors. RESULTS: Thirty of 32 NTs expressed hTR, with expression varying from weak (1+) to intense (4+). Most advanced stage NBs (9 of 12) and only 2 of 8 early stage NBs had moderate to intense (2 to 4-) expression of hTR. The remaining early stage tumors (6 of 8) and 3 of 12 advanced stage NBs had absent or weak expression of hTR (0 to 1+). There was no disease progression in any of the patients with absent or weak expression of hTR. In contrast, 8 tumors (from 7 patients) with moderate to intense expression of hTR in the tumor sections had adverse clinical outcomes, including recurrence, persistent disease, or death. hTR expression in all the Stage IVS tumors was weak, despite the fact that the patients had widely metastatic disease at presentation. The mean hTR score of 3.1 for NBs associated with an adverse outcome (n = 8) was significantly different from the mean hTR score of 1.3 for NBs associated with a favorable outcome (n = 16), P < 0.001. hTR expression in the GNB/GNs was limited to the ganglion cells only; Schwann cells were negative for hTR expression. Stage IVS tumors, which are associated with an excellent outcome, had high MIB-1 but weak hTR expression, indicating that the latter may be a better discriminator of true biologic potential and that hTR levels do not always correlate with cell proliferation. CONCLUSIONS: Increased hTR expression may reflect the potential for aggressive behavior within the spectrum of NTs; conversely, down-regulation of hTR may be useful in identifying subsets with limited capacity for progression and a favorable prognosis.

Adolescent↗
PubMed1999

Allelic losses at chromosome 3p are seen in human papilloma virus 16 associated transitional cell carcinoma of the cervix.

OBJECTIVE: Transitional cell carcinomas (TCCs) of the cervix are rare neoplasms of the female genital tract. Although these tumors display urothelial differentiation, there is controversy regarding their histogenetic relationship to squamous cell carcinomas (SCC) of the cervix versus transitional cell carcinomas of the bladder. METHODS: We performed partial allelotyping of five TCCs of the cervix using 23 polymorphic markers located on chromosomes 3p and 9, which demonstrate frequent and early losses in cervical SCC and urothelial TCC, respectively. Multiplex polymerase chain reaction was used on DNA extracted from archival paraffin-embedded tissue using precise microdissection. Additionally, P53 gene mutation analysis was performed using single-strand confirmation polymorphism (SSCP) and the presence of human papilloma virus (HPV) sequences was analyzed using general and specific (types 16 and 18) primers. RESULTS: General HPV sequences were demonstrated in all cases, but the oncogenic strain HPV 16 was present in only three (60%) of the five tumors; no HPV 18 was detected in any sample. Three of five TCCs, all harboring HPV 16 sequences, demonstrated concurrent allelic losses at several 3p loci (specifically 3p12, 3p14.2 [the FHIT gene locus], 3p21.3, and 3p22-24.2). LOH at a single locus on 9q32-qter was demonstrated in one tumor; no other deletions were seen on chromosome 9. P53 gene mutations in exons 5-8 were absent by SSCP analysis. CONCLUSIONS: The infrequent involvement of chromosome 9 in TCCs of the cervix, along with the concurrent presence of 3p LOH and oncogenic HPV 16 in a subset of tumors, suggests a closer histogenetic relationship of this neoplasm to cervical SCCs rather than urothelial TCCs.

Carcinoma, Squamous Cell↗
PubMed1999

Survival in small cell lung carcinoma is independent of Bcl-2 expression.

Bcl-2 overexpression is a common event in small cell carcinomas (SCLC). The bcl-2 oncoprotein has a unique oncogenic role by inhibiting programmed cell death (apoptosis), resulting in tumorigenesis and chemoresistance. Forty-two cases of SCLC were stained immunohistochemically with bcl-2 monoclonal antibody (Biogenex, San Ramon, CA) after using an antigen retrieval step with citrate buffer. bcl-2 positivity was determined as detection of the oncoprotein in greater than 10% of noncrushed neoplastic cells. Twenty-five of 42 (60%) patients had extensive disease at presentation, 10 of 42 (24%) had limited disease, and 7 of 42 (16%) had disease localized to the lung. Twenty-four of 42 (57%) tumors were bcl-2 positive, and 18 of 42 (43%) tumors were bcl-2 negative. Follow-up in patients ranged from 7 days to 96 months (mean follow-up, 20 months). The median survival of patients with bcl-2-positive tumors was 11 months, as opposed to 13 months for bcl-2-negative tumors. There was no significant difference in median survival between bcl-2-positive and bcl-2-negative SCLC (log rank test, P = .2256). Using Cox's proportional hazards model, median survival in SCLC was determined to be independent of age at diagnosis, stage at presentation, therapeutic modality, and bcl-2 expression. bcl-2 expression does not significantly influence survival in SCLC.

Adult↗
PubMed1999

Molecular abnormalities associated with secretory carcinomas of the breast.

Secretory carcinomas (SCAs) represent a unique histological variant of invasive breast carcinomas, occurring predominantly in patients younger than 30 years of age. Data from limited series have shown SCAs to have a favorable prognosis in patients younger than 20 years of age, whereas the clinical course tends to parallel the more common in filtrating ductal carcinomas (IDCs) in patients older than 20 years. There are no reports on the molecular abnormalities associated with this unusual tumor. Microdissected archival formalin-fixed tissue from 10 SCAs collected from 2 institutions were used to determine the frequencies of allelic loss at 13 chromosomal regions with 19 microsatellite markers, using multiplex polymerase chain reaction (PCR)-based techniques. The results of loss of heterozygosity (LOH) and microsatellite alterations (MAs) analyses were compared with 20 cases of IDCs. P53 gene mutation analysis was also performed on the 10 SCAs using single-strand conformation polymorphism (SSCP) analysis, followed by sequencing of abnormal bands. LOH at multiple regions of chromosome 3p were the most common abnormality in both SCAs (55%) and IDCs (50%), followed by LOH at 17q21 (BRCA1 locus), 13q14 (retinoblastoma gene locus), and 8p21-23. No significant differences were seen in the frequencies of LOH at any chromosomal region except for 17p13 (p53 gene locus), where allelic losses were absent in SCAs, but evident in 46% of IDCs (P < .05). The 2 histological entities were similar in the fractional regional loss (FRL) index (0.26 v 0.24), fractional allelic loss (FAL) index (0.23 v 0.27), as well as in the frequency of MAs (0.015 v 0.005), P > .05. P53 gene missense mutation (G:C::A:T) was detected in 1 of 10(10%) SCAs. Based on the considerable similarities in the molecular abnormalities associated with both tumors, the formation of secondary lumina in both the in situ and the invasive components, as well as suggestions from limited series that the clinical behavior in adult patients parallels that of IDCs, SCA most likely reflects a secretory variant of IDCs.

Adult↗
PubMed1999

Partial nucleotide sequencing and molecular evolution of epidemic causing Dengue 2 strains.

To study the genetic variability and to detect evolutionary changes and movement of dengue 2 (DEN-2) strains, nucleotide sequencing of the envelope protein gene and the nonstructural protein 1 gene junction was performed for 9 isolates from the 1996 Delhi epidemic and 1 isolate from the 1967 Delhi epidemic. The epidemic strains had a divergence of 10%-11% from the 1967 strains, but were quite similar to DEN-2 isolates from Seychelles, Somalia, and Torres Strait. In addition, the sequence data were compared to the prototype DEN-2 strain, New Guinea C, and other published DEN-2 sequences from different parts of the world. The phylogenetic analysis by the Molecular Evolutionary Genetics Analysis program suggests that the 1996 Delhi isolates of DEN-2 were genotype IV. The 1967 isolate was similar to a 1957 isolate of DEN-2, P9-122, from India, and was classified as genotype V. This study indicates that earlier DEN-2 strains of genotype V have been replaced by genotype IV.

Base Sequence↗
PubMed1998

pH- and Thermo-sensitive Hydrogel Nanoparticles.

pH- and temperature-sensitive hydrogel nanoparticles of copolymers of vinylpyrrolidone (VP) and acrylic acid (AA) cross-linked with NN' methylene bis acrylamide (MBA) of sizes up to 50 nm diameter loaded with marker compound FITC-dextran (mol wt. 19.3 kD) were prepared in the aqueous core of reverse micellar droplets and were dispersed in aqueous buffer. These particles have high entrapment efficiency, and the lyophilized powder can be redissolved in buffer without any significant agglomeration. The release of FITC-dextran from these particles was found to be pH- and temperature-dependent. The release was slow in acid solution, but it increased considerably as the pH of the medium was increased. The release rate was also increased with the increase of temperature. Copyright 1998 Academic Press.

Journal Article↗
PubMed1998

Expression of the RNA component of telomerase in Wilms tumor and nephrogenic rest recapitulates renal embryogenesis.

Telomerase is a ribonucleoprotein enzyme associated with cellular immortality and has been detected in the vast majority of adult tumors. Wilms tumor is a histologically diverse embryonal malignancy of childhood, and the histological features of Wilms tumor and its precursor lesion, the nephrogenic rest, recapitulate the components of normal renal embryogenesis. Both the epithelial and the stromal components of Wilms tumor arise by differentiation of primitive mesodermal blastema. We compared expression of the RNA component of human telomerase (hTR) in normal developing kidneys, Wilms tumors, and nephrogenic rests and correlated expression of hTR with cell proliferation. Using a radioactive in situ hybridization method, we examined archival material from 17 Wilms tumors (including nine with nephrogenic rests), four therapeutically aborted embryos (37 to 56 days), three fetuses on whom autopsies had been performed, and one neonate for expression of hTR. Proliferative index was measured by immunohistochemical staining for MIB1. In the embryonic kidney, Wilms tumors, and nephrogenic rests, the patterns of hTR expression were similar: expression was usually maximal within the immature epithelial elements followed by the poorly differentiated blastema, but was weak or absent in the immature stroma. Mature tubules, glomeruli, and stroma were negative for hTR expression, as were differentiated heterologous elements present in post-therapy Wilms tumors. There was only a partial relationship between proliferative index and hTR expression. In the embryonic kidney, Wilms tumors, and nephrogenic rests, blastema had the highest proliferative index, whereas the indices were significantly lower in the immature epithelium and stroma. The proliferative index in mature and heterologous elements was low or zero. Thus, the pattern of hTR expression in Wilms tumor and its precursor lesion recapitulates embryogenesis precisely and may represent that aspect of the persistent fetal phenotype which predisposes to the development of malignancy.

Child, Preschool↗
PubMed1998

Telomerase enzyme activity and RNA expression during the multistage pathogenesis of breast carcinoma.

Telomerase, an RNA-containing enzyme, is associated with cellular immortality and malignancy. We investigated the role of telomerase during the multistage pathogenesis of breast cancer. We used the semiquantitative, PCR-based telomeric repeat amplification protocol assay for enzyme activity (42 specimens from 42 patients) and a radioactive in situ assay for expression of its RNA component (human telomerase RNA; hTR) for the identification of telomerase-positive cells in archival resection samples (n = 67 from 39 patients). Low telomerase activity was detected in 1 (14%) of 7 samples of benign breast disease, in 4 (67%) of 6 fibroadenomas, in 11 (92%) of 12 carcinoma in situ (CIS) lesions, and in 16 (94%) of 17 invasive breast cancers. There was a progressive increase in the mean telomerase levels with progressive increase in severity of histopathological change (P < 0.05). Almost all of 67 resection samples expressed hTR, irrespective of histology. Expression was low to moderate in some samples of normal epithelium and nonproliferative fibrocystic changes. hTR expression was limited to epithelial cells; expression in stromal cells, including those in fibroadenomas, was negative. Increased hTR expression was observed in some foci of apocrine metaplasia and atypical hyperplasia. Increased hTR expression was also observed in all CIS and invasive lesions, although considerable heterogeneity was noted. Focal up-regulation was frequently noted in CIS lesions in the vicinity of invasive tumors. Thus, up-regulation of hTR may be a predictive marker for invasive tumor development.

Breast↗