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R A Soslow

Publications and source records attributed to R A Soslow.

At least 37 records · Page 2Linked to original sources

B-lineage lymphoblastic lymphoma is a clinicopathologic entity distinct from other histologically similar aggressive lymphomas with blastic morphology.

BACKGROUND: The authors present clinical, histopathologic, and immunophenotypic data regarding B-lineage lymphoblastic lymphoma (B-LBL), a rare entity that has not been extensively studied. To emphasize some of its unique clinical characteristics, the authors compare B-LBL with a group of histologically similar, very aggressive lymphomas, T-lineage lymphoblastic lymphoma (T-LBL) and the blastoid variant of mantle cell lymphoma (BVMCL); all were evaluated concurrently. METHODS: Clinical data were obtained on 29 patients with very aggressive lymphomas (12 B-LBLs, 10 T-LBLs, and 7 BVMCLs) from whom paraffin-embedded material was available. The diagnoses were confirmed on review of the hematoxylin and eosin-stained slides and the immunophenotype data. RESULTS: The mean age of patients with B-LBL was 39 years. Patients presented with both lymph node and extranodal disease, although involvement of the mediastinum and bone marrow was infrequent. Four were Stage I, 3 were Stage II, 2 were Stage III, and 3 were Stage IV. B-LBL patients were treated primarily with cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP), and one patient underwent allogeneic bone marrow transplantation. The mean follow-up time was 30 months. Seven of 11 had no evidence of disease at 48 months, whereas 4 patients were dead of disease at 5.6 months. The overall median survival was 24 months. The clinical characteristics of B-LBL patients differed significantly from those of T-LBL patients; there was more frequent bone marrow and mediastinal involvement in T-LBL cases (P = 0.03 and 0.04, respectively). T-LBL patients were also less likely to achieve a complete remission than B-LBL patients (P = 0.02). The mean age of BVMCL patients significantly exceeded that of B-LBL patients (P = 0.03). CONCLUSIONS: The authors believe that the distinction of B-LBL from its histologic mimics, T-LBL and BVMCL, has important clinical implications. Patients with B-LBL present differently from those with the other very aggressive lymphomas studied, and they achieve complete remissions more often than T-LBL patients.

Adolescent↗

Cyclooxygenase-2 expression is up-regulated in human pancreatic cancer.

A large body of evidence suggests that cyclooxygenase-2 (COX-2) is important in gastrointestinal cancer. The purpose of this study was to determine whether COX-2 was expressed in adenocarcinoma of the human pancreas. Quantitative reverse transcription-PCR, immunoblotting, and immunohistochemistry were used to assess the expression of COX-2 in pancreatic tissue. Levels of COX-2 mRNA were increased by >60-fold in pancreatic cancer compared to adjacent nontumorous tissue. COX-2 protein was present in 9 of 10 cases of adenocarcinoma of the pancreas but was undetectable in nontumorous pancreatic tissue. Immunohistochemical analysis showed that COX-2 was expressed in malignant epithelial cells. In cultured human pancreatic cancer cells, levels of COX-2 mRNA and protein were induced by treatment with tumor-promoting phorbol esters. Taken together, these results suggest that COX-2 may be a target for the prevention or treatment of pancreatic cancer.

Adenocarcinoma↗

Cyclooxygenase-2 expression is up-regulated in squamous cell carcinoma of the head and neck.

The purpose of this study was to determine whether cyclooxygenase-2 (COX-2) was overexpressed in squamous cell carcinoma of the head and neck (HNSCC). Quantitative reverse transcription-PCR, immunoblotting, and immunohistochemistry were used to assess the expression of COX-2 in head and neck tissue. Mean levels of COX-2 mRNA were increased by nearly 150-fold in HNSCC (n = 24) compared with normal oral mucosa from healthy volunteers (n = 17). Additionally, there was about a 50-fold increase in amounts of COX-2 mRNA in normal-appearing epithelium adjacent to HNSCC (n = 10) compared with normal oral mucosa from healthy volunteers. Immunoblotting demonstrated that COX-2 protein was present in six of six cases of HNSCC but was undetectable in normal oral mucosa from healthy subjects. Immunohistochemical analysis showed that COX-2 was expressed in both HNSCC and adjacent normal-appearing epithelium. Taken together, these results suggest that COX-2 may be a target for the prevention or treatment of HNSCC.

Carcinoma, Squamous Cell↗

Acidic fibroblast growth factor is progressively increased in the development of oesophageal glandular dysplasia and adenocarcinoma.

AIMS: To determine by immunohistochemistry and amplification of cDNA the relationship between fibroblast growth factor (FGF) expression and progressive changes in Barrett's oesophagus associated with oesophageal adenocarcinoma (OA). The FGFs are potent mitogens that possess angiogenic properties and the capability to regulate growth and differentiation of various cell types. They have also been implicated in the development and progression of numerous solid tumours, including some carcinomas of the aerodigestive tract, such as nasopharyngeal carcinoma and pancreatic adenocarcinoma. MATERIAL AND RESULTS: We studied the expression of the two prototypic FGFs, acidic FGF (FGF-1) and basic FGF (FGF-2), in OA and OA precursor lesions, including intestinal metaplasia (IM), low-grade dysplasia (LGD) and high-grade dysplasia (HGD). Fresh tissue from 10 OAs and four associated HGDs was available for the determination of FGF-1 and FGF-2 mRNA expression accomplished by the PCR amplification of cDNA. Using immunohistochemistry, we studied the expression of the FGF-1 and FGF-2 proteins in archival, paraffin-embedded tissue that was available from 17 oesophageal resection specimens that included OAs and OA precursor lesions. As compared to gastric fundic mucosal controls, OAs and HGDs showed significantly enhanced expression of FGF-1 mRNA and protein. IMs and LGDs showed significantly lesser degrees of FGF-1 immunoreactivity that were not increased over controls. In contrast, both the overall percentage of FGF-2-reactive OAs and the overall FGF-2 protein expression, assessed using an immunoreactivity score, are comparable to FGF-2 expression in controls. CONCLUSIONS: It appears that FGF-2 is ubiquitously expressed in OA and in normal oesophageal and gastric mucosa while significant FGF-1 expression is essentially restricted to HGD and OA. Our data also suggest that FGF-1 is sequentially upregulated in the progression from metaplasia to dysplasia and adenocarcinoma.

Adenocarcinoma↗

Suppression of apoptosis does not foster neoplastic growth in Barrett's esophagus.

Esophageal adenocarcinoma often arises in association with metaplastic and dysplastic mucosa in Barrett's esophagus. Derangements in cell cycle control and apoptosis regulation might be responsible for the progression from metaplasia to dysplasia and adenocarcinoma We tested this hypothesis by performing cell cycle analysis, in situ detection of apoptosis, and evaluation for the immunohistochemical expression of proteins involved in proliferation (Ki-67), the control of apoptosis (bcl-2, bcl-x and bax), and cell cycle regulation (retinoblastoma and cyclin D1). We studied 17 randomly selected paraffin-embedded esophagectomy specimens that contained intestinal metaplasia without dysplasia, low-grade dysplasia, high-grade dysplasia, and esophageal adenocarcinoma Compared with gastric controls and intestinal metaplasia without dysplasia, high-grade dysplasia and esophageal adenocarcinoma demonstrated greater numbers of cells in S phase and G2 phase. Comparison of the proliferation index and the apoptotic rate in intestinal metaplasia without dysplasia, low-grade dysplasia, high-grade dysplasia, and esophageal adenocarcinoma showed a statistically significant trend that linked an increasing proliferation index and apoptotic rate with increasing histologic severity (P = .006 and P = .0002, respectively). A statistically significant linear association was found between bcl-x expression, bax expression, and the bcl-2-to-bax expression ratio versus increasing histologic severity (P = .0004, P = .007, and P = .03, respectively). These data support the hypothesis that neoplastic transformation of intestinal metaplastic epithelium in the esophagus might result from sequential changes in the expression of proteins involved in the control of apoptosis and the cell cycle. Furthermore, suppression of apoptosis does not seem to foster neoplastic growth in Barrett's esophagus. These observations will lead to a better understanding of the pathogenesis of esophageal adenocarcinoma and might contribute to enhancing the diagnostic accuracy when presented with dysplastic lesions.

Adenocarcinoma↗

mdm-2 expression correlates with wild-type p53 status in esophageal adenocarcinoma.

Several immunohistochemical studies showed that p53 protein is expressed in 50 to 80% of esophageal adenocarcinomas (EAs). Mutations of this tumor suppressor gene are present in 40 to 70% of EAs, so it is possible that p53 expression might occur as a result of mechanisms other than gene mutation. The human homologue of the murine double minute-2 gene (mdm-2) is a known regulator of p53 activity, and its expression results in stabilization of the wild-type p53 protein and loss of its tumor suppressor function. In this study, we evaluated the frequency of mdm-2 amplification and expression in EA and investigated the relationship between mdm-2 expression and p53 mutation. Thirty-three resection specimens of EAs and associated Barrett's esophagus were evaluated by immunohistochemical methods for p53 and mdm-2 expression. Sixteen of these cases were also evaluated for p53 mutations with use of polymerase chain reaction, single-strand conformational polymorphism, and DNA sequencing and for mdm-2 amplification with a differential polymerase chain reaction-based amplification analysis. Overexpression of p53 was present in 23 EAs (70%), and 18 EAs (55%) overexpressed mdm-2. p53 mutation was observed in 7 (43%) of 16 cases, whereas mdm-2 gene amplification was not detected in any. To summarize, we found substantial discordance of p53 immunohistochemical features and mutation in EA. Significant expression of mdm-2 occurred only in cases with wild-type p53, whereas all of the cases with p53 mutation showed little if any expression of mdm-2. Also, mdm-2 expression in cases with p53 overexpression but without p53 mutation exceeded mdm-2 expression in cases with p53 overexpression and p53 gene mutation. In cases without p53 mutation, overexpression of mdm-2 occurred in 50% of cases and might be responsible for stabilization of p53 protein and possible loss of tumor suppressor function.

Adenocarcinoma↗

Familial papillary serous carcinoma of the cervix, peritoneum, and ovary: a report of the first case.

OBJECTIVE: We report an occult primary papillary serous carcinoma of the endocervix that was encountered in a woman whose mother and identical twin sister died of papillary serous carcinomas (PSCs) of the peritoneum and ovary, respectively. METHODS: The medical records and the histologic material belonging to the patient, her sister, and her mother were reviewed. RESULTS: The cervical PSC was histologically similar to the peritoneal and ovarian carcinomas. The patient has recurred with peritoneal carcinomatosis 24 months following surgery and postoperative radiotherapy and chemotherapy. CONCLUSIONS: Primary papillary serous carcinoma of the cervix is a very rare adenocarcinoma variant; there have been approximately 30 such cases reported, and, to our knowledge, this is the first documented case of familial peritoneal/ovarian/uterine papillary serous carcinoma. The prophylaxis achieved through bilateral oophorectomy in individuals with a family history of ovarian cancer does not address the risk of PSCs arising in the uterus, cervix, or peritoneum.

Adult↗

Atypical cells in radiation dermatitis express factor XIIIa.

Dendritic cells that express factor XIIIa are present in the normal dermis and are increased in a variety of pathologic conditions. Atypical dermal cells are often seen in biopsy specimens of skin that has been previously irradiated. We sought to determine whether the atypical dermal cells in chronic radiation dermatitis express factor XIIIa. We employed standard immunohistochemical techniques with antibodies to factor XIIIa and CD34 to study 16 biopsy samples showing changes of radiation dermatitis. All cases showed diffuse positive cytoplasmic staining of atypical dermal cells with antibody to factor XIIIa. Of 16 cases, 10 showed focal staining of dermal cells with antibody to CD34, but this antibody did not react with most of the atypical dermal cells. We conclude that the majority of atypical dermal cells in radiation dermatitis are derived from dermal dendritic cells which express factor XIIIa.

Adult↗

Distinctive p53 and mdm2 immunohistochemical expression profiles suggest different pathogenetic pathways in poorly differentiated endometrial carcinoma.

Endometrial serous carcinoma (ESC) and FIGO (International Federation of Gynecology and Obstetrics) grade 3 endometrioid adenocarcinoma (EC) are high-grade endometrial tumors that have different clinical and morphologic attributes. Alteration of p53 tumor suppressor protein function has been implicated in the pathogenesis of both tumors, although the mechanisms may differ. We sought to investigate this difference by comparing immunohistochemical expression of p53 and mdm2. p53 immunoreactivity often correlates with gene mutation, whereas increased mdm2 expression is linked to complex formation with wild-type p53 resulting in its inactivation. Twenty cases of ESC and 21 cases of EC were evaluated and an immunoreactivity score (IRS) was assigned using both the percentage of cells stained and the intensity of staining. The overall IRSs were significantly different in ESCs versus ECs for both p53 and mdm2 (p < 0.001 and p < 0.01, respectively). Strong mean immunoreactivity for p53 was detected in 15 (75%) ESCs as compared to only weak mean immunoreactivity in 17 (81%) ECs. Conversely, for mdm2 expression, 17 (81%) ECs had moderate mean immunoreactivity whereas 9 (45%) ESCs showed only weak mean immunoreactivity. mdm2 expression more closely correlated with p53 expression in ECs than in ESCs. In ECs, mdm2 was detected in 16 of 17 (94%) p53-positive tumors but in only 1 of 3 (33%) p53-negative tumors (p < 0.025). In ESCs, mdm2 was detected in 9 of 15 (60%) p53-positive tumors but in none of the 5 p53-negative tumors (p < 0.10). Overall, our results demonstrate an inverse relationship between the expression of p53 and mdm2 in ESC versus high-grade EC. Specifically, strong p53 immunoreactivity is associated with weak mdm2 expression-in ESC and weak p53 expression is associated with moderate mdm2 expression in EC. These results suggest different pathogenetic pathways resulting in loss of normal p53 function in these two tumors: by p53 gene mutation (strong p53 overexpression) in ESCs, or by mdm2 complex formation and inactivation of p53 in high-grade ECs.

Adult↗

The CD44v6-negative phenotype in high-grade uterine carcinomas correlates with serous histologic subtype.

Uterine serous carcinomas (USCs) and poorly differentiated (International Federation of Gynecology and Obstetrics Grade 3) endometrioid adenocarcinomas (ECs) are two histologic subtypes of high-grade uterine carcinoma that differ in clinical presentation, patterns of dissemination, and biologic aggressiveness. To investigate the mechanisms responsible for this heterogeneity, we studied CD44 and CD44v6 expression in a series of 20 USCs and 21 poorly differentiated ECs. CD44 is a protein involved in cell adhesion and lymphocyte homing, and one of its isoforms, CD44v6, might be related to capillary-lymphatic space invasion and metastasis. Eight (40%) of 20 USCs expressed CD44, compared with 18 (86%) of 21 ECs (P < .005). None of the USCs were reactive with antibodies against CD44v6, whereas 45% of the ECs were immunoreactive (P < .001). CD44v6 expression was observed in the myoinvasive ECs but was not seen in foci of capillary-lymphatic space invasion in either the ECs or the USCs. In summary, the USCs were significantly more likely to demonstrate a CD44- and CD44v6-negative phenotype than were the poorly differentiated ECs.

Adult↗

Cytopathologic features of hepatic epithelioid hemangioendothelioma.

We present the cytological features of hepatic epithelioid hemangioendothelioma (EH), which is considered to be a vascular proliferation of intermediate malignant potential. The case report concerns a 52-yr-old previously healthy man discovered to have multiple hepatic masses upon evaluation for abnormal liver function tests. Fine-needle aspiration demonstrated a neoplasm composed of interanastomosing epithelioid cells that contained intracytoplasmic lumens. Histologic sections, immunohistochemistry, and ultrastructural evaluation were confirmatory. Although hepatic EH is a rare tumor, its characteristic cytological, histological, and ultrastructural features permit a straightforward diagnosis. It is important to distinguish this entity from adenocarcinoma and angiosarcoma because long-term disease-free survival is possible, especially in the setting of orthotopic liver transplantation.

Biopsy, Needle↗

Expression of acidic fibroblast growth factor in Barrett's esophagus and associated esophageal adenocarcinoma.

OBJECTIVE: Adenocarcinoma of the esophagus is generally attributed to the neoplastic transformation of intestinal metaplastic lesions (Barrett's esophagus). On the basis of our preliminary data that showed significant acidic fibroblast growth factor mRNA and protein expression in adenocarcinoma of the esophagus, we studied expression of fibroblast growth factor in esophageal adenocarcinoma and its precursor lesions, intestinal metaplasia, low-grade dysplasia, and high-grade dysplasia. Fibroblast growth factor belongs to a family of polypeptides that are involved in differentiation and cellular proliferation. METHODS: We examined 30 esophagectomy specimens that were resected for adenocarcinoma (n = 27) and high-grade dysplasia (n = 3). After confirmation of the diagnosis by routine light microscopy, the index lesions (invasive carcinomas) and adjoining Barrett's mucosa were evaluated with a monoclonal antibody against human acidic fibroblast growth factor. The results are expressed with the use of an immunoreactive score that allows distinction between weak, moderate, and strong immunoreactivity. RESULTS: Adenocarcinoma demonstrated a moderate-to-strong mean immunoreactive score of 8. In contrast, high-grade dysplasia demonstrated a weak-to-moderate mean score of 4.5, which was significantly different (p < 0.05). Intestinal metaplasia and low-grade dysplasia displayed even weaker expression of fibroblast growth factor, with a negligible immunoreactive score less than 1 (p < 0.005). Seventy-five percent of evaluable cases demonstrated an increasing degree of fibroblast growth factor expression in the spectrum of lesions ranging from metaplasia to dysplasia and carcinoma. CONCLUSIONS: These data indicate that in patients with adenocarcinoma arising in association with Barrett's esophagus, fibroblast growth factor is generally sequentially accumulated in the progression from metaplasia to neoplasia. This progression may affect future investigation into the role of fibroblast growth factors in tumorigenesis and, possibly, the application of fibroblast growth factor immunohistochemistry to diagnosis.

Adenocarcinoma↗

MIC2, TdT, bcl-2, and CD34 expression in paraffin-embedded high-grade lymphoma/acute lymphoblastic leukemia distinguishes between distinct clinicopathologic entities.

We propose that 12E7 (CD99) expression, along with TdT, bcl-2, and CD34 reactivity in lymphoblastic lymphoma (LyL)/acute lymphoblastic leukemia (ALL), distinguishes this group of neoplasms from small noncleaved cell lymphomas (SNCLs) in both pediatric and adult patients, thereby narrowing the differential diagnosis of high-grade non-Hodgkin's lymphomas and acute lymphoblastic leukemias in paraffin sections. 12E7 (CD99) is one of a group of available antibodies that recognizes the product of the mic-2 gene, which was originally identified in ALL. Despite this, most clinicopathological research has focused on the reactivity of 12E7 in a subset of the small round cell tumors of childhood. Although TdT is widely used in the subtyping of blastic leukemias, its use in the distinction of high-grade lymphomas in paraffin sections has been limited. We collected 24 cases of LyL/ALL (13 B-cell and 11 T-cell) and 15 cases of SNCL from 1984 through 1993. We confirmed the diagnoses using morphology and analysis of immunologic data. We performed immunohistochemistry with the 12E7 antibody, TdT, bcl-2, and CD34 on formalin-fixed, paraffin-embedded material. The patients' ages ranged from 4 to 81 years; nine of the study patients were children. Sixteen of the 24 LyL/ALLs stained with 12E7. In contrast, none of the 15 cases of SNCL reacted with this antibody (chi-square P < .0001). A larger percentage of T-cell LyL/ALLs reacted with 12E7 than did B-cell LyL/ALLs (82% v 54%). Sixteen of 20 LyL/ALLs reacted with the anti-TdT antibody, as compared with none of 11 SNCLs (chi-square P < .0001). Six LyL/ALLs were CD34 positive (of 23), and none of the SNCLs were CD34 positive (0 of 12) (chi-square P = .0519). Bcl-2-positive cases were found among both LyL/ ALLs and SNCLs, although they were more prevalent among LyL/ ALLs (92% v 25%; chi-square P < .0001). When one considers the differential diagnosis of a high-grade lymphoma/acute lymphoblastic leukemia, positive reactions with 12E7, TdT, bcl-2, and CD34 support the diagnosis of LyL/ALL over SNCL. Moreover, we present data that suggests that evaluating for TdT in formalin-fixed paraffin-embedded tissue is a more sensitive test than using either 12E7, bcl-2 or CD34 alone.

Adult↗

Evaluation of classic architectural criteria in non-mycosis fungoides cutaneous lymphomas.

Ninety-seven cases of non-mycosis fungoides (non-MF) cutaneous lymphoma were evaluated employing published criteria for the categorization of B- and T-cell cutaneous malignancies. Included in the study were 77 primary and secondary cutaneous B-cell lymphomas, in which the diagnosis was supported by immunohistochemical studies identifying lineage. These cases were randomized with 20 cases of non-MF and T-cell lymphoma. Hematoxylin and eosin (H & E)-stained slides from each case were reviewed by at least two dermatopathologists, who were unaware of the previous diagnoses, and a judgment regarding histologic pattern was rendered. The histologic criteria employed emphasized architectural features. For B-cell patterns, these included the presence of dense perivascular, periappendageal and/or nodular collections of lymphocytes, centering in the deep dermis, and separation from the epidermis by a grenz zone. Employed criteria for cutaneous T-cell pattern included location restricted primarily to the upper dermis, interstitial pattern, the presence of epidermotropism, and the lack of a grenz zone. Three B-cell lymphomas were judged to have indeterminate patterns. Four of 74 (5.4%) of the remaining B-cell lymphomas were incorrectly categorized as T-cell lymphomas by architectural criteria. The most striking findings included epidermotropism in rare B-cell lymphomas. Three of the four miscategorized cases were large-cell lymphomas. A preference for B-cell pattern was also confirmed in non-MF T-cell lymphomas. We conclude that most B-cell lymphomas in the skin demonstrate a recognizable B-cell pattern, but rarely a pattern more reminiscent of T-cell lymphoma may be seen. This may occur more often with B-large-cell lymphomas. In addition, this study supports previous work indicating that many non-MF T-cell lymphomas show prominent architectural features typically ascribed to B-cell lymphomas. In summary, our findings support the impression that the vast majority of non-MF lymphomas show a B-cell pattern regardless of their lineage. As such, caution is indicated with regard to pattern interpretation.

Adult↗

Immunophenotypic analysis of ovarian and testicular Müllerian papillary serous tumors.

Intratesticular Müllerian papillary serous tumors lacking stromal invasion are uncommon neoplasms whose immunophenotypic properties have not been studied extensively. We present such information here and compare it with information from a group of ovarian papillary serous tumors of low malignant potential ("borderline serous tumors") that are morphologically identical. We compared the histologic features of our index case of intratesticular Müllerian papillary serous tumor with those of nine ovarian papillary serous tumors. We then evaluated both the index case and the ovarian tumors with antibodies against carcinoembryonic antigen, LeuM1, CA125, estrogen receptors, progesterone receptors, cytokeratin 7, and cytokeratin 20, by use of established immunohistochemical techniques. The testicular and ovarian tumors were morphologically indistinguishable. The intratesticular Müllerian papillary serous tumor expressed LeuM1, CA125, estrogen receptors, progesterone receptors, cytokeratin 7, and weak cytokeratin 20; carcinoembryonic antigen was not expressed. All of the ovarian papillary serous tumors expressed CA125, estrogen receptors, and cytokeratin 7. Eight of nine expressed progesterone receptors. Five of nine stained with LeuM1. Two of nine were focally weakly positive with cytokeratin 20. LeuM1 expression helps distinguish testicular papillary serous tumors from mesothelial proliferations, which might seem morphologically similar. The immunophenotype of intratesticular and female genital papillary serous tumors is similar; this similarity extends to expression of estrogen and progesterone receptors, which is rare in neoplasms in men, especially among testicular neoplasms.

Aged↗

BCL-1 (PRAD-1/cyclin D-1) overexpression distinguishes the blastoid variant of mantle cell lymphoma from B-lineage lymphoblastic lymphoma.

The blastoid variant of mantle cell lymphoma (MCL-BV) can occur de novo or can represent a morphologic transformation of MCL associated with aggressive clinical disease. Its cytologic appearance is very similar to that of lymphoblastic lymphoma (LBL) because of its characteristic nuclear features and high proliferative rate. To assess the usefulness of antibodies to cyclin D-1 (BCL-1/ PRAD-1), CD99 (12E7), CD34, and TdT in distinguishing between MCL-BV and LBL in formalin-fixed, paraffin-embedded tissue, we studied from the Stanford data base 10 cases originally diagnosed as B-lineage LBL, 5 MCL-BVs, 2 cases thought likely to represent MCL-BV, and 2 blastic lymphomas whose morphology and immunophenotype were indeterminate. Six (60%) of 10 LBLs stained with CD99, as opposed to none of 7 MCL-BVs. Four (40%) of 10 LBLs reacted with CD34, as compared with none of 7 MCL-BVs. Eight (89%) of nine LBLs were positive for TdT, but all of the four MCL-BVs tested were negative. In contrast, the anti-cyclin D-1 antibody stained the nuclei of all of the MCL-BVs and none of the LBLs tested. On the basis of our evaluation, the probable MCL-BV cases were considered to be definite MCL-BV. Of the indeterminate cases, one was considered to be LBL, whereas we felt that the other represented MCL-BV. We conclude that staining formalin-fixed, paraffin-embedded, high-grade lymphomas with anti-cyclin D-1 antibody is useful in confirming the diagnosis of MCL-BV, whereas positive reactions with CD99, CD34, and particularly TdT are more characteristic of LBL.

12E7 Antigen↗

True histiocytic lymphoma following therapy for lymphoblastic neoplasms.

True histiocytic lymphomas (THLs) are rare tumors in which the malignant cells show morphologic and immunophenotypic evidence of histiocytic differentiation. We describe THLs that arose after therapy for one case of T-lineage lymphoblastic lymphoma (LyL) and two cases of acute lymphoblastic leukemia (ALL) (both CD10+, one pre-B phenotype). The lymphoblastic neoplasms were not unusual in any way, and responded well to standard therapy. The THLs arose 10 to 20 months after complete remission was achieved for the lymphoblastic neoplasms, at which time there was still no clinical or pathologic evidence of the lymphoblastic neoplasms. All three THLs exhibited clinical and morphologic features of malignancy. Neoplastic cells in the THLs had abundant eosinophilic vacuolated cytoplasm and pleomorphic nuclei, and expressed histiocytic antigens in the absence of lymphocyte-specific lineage markers. Because THLs are rare neoplasms, their occurrence after otherwise successful therapy for lymphoblastic neoplasms in these three cases may constitute a distinct clinicopathologic entity.

Adult↗

Atypical polypoid adenomyofibroma (APA) versus well-differentiated endometrial carcinoma with prominent stromal matrix: an immunohistochemical study.

It can be extremely difficult in some cases to distinguish atypical polypoid adenomyomas (APAs) from invasive adenocarcinoma in an endometrial curettage or biopsy specimen. In order to determine if immunophenotypic features can be exploited to differentiate between these two entities in problematic cases, a series of APAs and myoinvasive well-differentiated endometrial carcinomas (WDCAs) were studied with a panel of standard immunohistochemical markers. All 23 APAs had stromal smooth muscle actin (SMA) reactivity, 12 of 23 had variable degrees of stromal desmin reactivity, and nine of 22 had CD34-positive stromal cells. All epithelial components of the APAs were cytokeratin (AE1 and CAM5.2) positive, whereas 22 of 23 were positive for estrogen receptor (ER) and progesterone receptor (PR). Among the 10 myoinvasive WDCAs, all contained at least some SMA-positive stromal cells, seven of 10 desmin-positive stromal cells, and four of eight CD34-positive stromal cells. All carcinomas studied demonstrated CAM5.2 and PR-positive epithelia; nine of 10 were ER positive. We conclude that the immunophenotype of APAs does not differ significantly from well-differentiated endometrial adenocarcinoma and that immunophenotyping is of little value in distinguishing APA from carcinoma. Because the stroma in APAs histologically and immunophenotypically more closely resembles a hybrid myofibromatous stroma, we prefer to refer to these lesions with the modified designation "atypical polypoid adenomyofibroma," although "APA" may be retained for clinical use.

Adenocarcinoma↗