Cytokeratin positivity in myxopapillary ependymoma – a potential diagnostic pitfall

<p>Abstract</p> <p>Background</p> <p>Myxopapillary ependymomas (MPE) occur in the filum terminale of the spinal cord, but also present in extra-spinal locations such as subcutaneous tissue and brain. They are slow growing grade I gliomas. Areas of solid growth pattern with aggregates of cells with "epithelioid morphology" seen in MPE can mimic metastatic carcinoma. The presence of occasional cells with clear cytoplasm and morphology can resemble Chordoma. Diagnosis can be missed due to these morphological similarities, which could affect patient management and hence, long term survival.</p> <p>Case presentation</p> <p>We describe two cases of MPE with cytokeratin (AE1 AE3, CAM 5.2, Cytokeratin 7 and cytokeratin 20) expression.</p> <p>Conclusion</p> <p>MPE can be positive for Cytokeratins (CAM 5.2, AE1 AE3, CK7) and focally for EMA, which could be misdiagnosed as metastatic carcinoma. In cases demonstrating epithelioid and clear cell morphology, the diagnosis of MPE should be made in conjunction with histology, proper immunohistochemical profile which includes co-expression of GFAP, S-100 protein and epithelial markers, radiologic findings and site. It is important to be aware of the cytokeratin profile in MPE to avoid erroneous diagnosis with other tumour entities.</p

Lymphoproliferative Lesions in the Setting of HIV Infection: A Five-Year Retrospective Case Series and Review

A wide variety of noninfectious lesions have been identified in association with HIV infection. Many hematolymphoid lesions are possible in this patient group, both reactive and neoplastic. Epidemiologic data suggests that lymphoid malignancies are among the most common neoplasms in patients with HIV. We present a selective case series assembled over a 5-year period from the relatively low HIV-prevalence Hamilton Regional Laboratory Medicine Program (HRLMP), a tertiary care referral centre in Southern Ontario. This series serves to demonstrate the wide variety of lymphoid lesions that may be encountered in patients with HIV. In addition to outlining the pathologic work-up necessary in these cases, we discuss characteristics that distinguish the HIV-associated lesions from the pathobiologically similar non-HIV-associated lymphoid lesions

Primary anaplastic large cell lymphoma of the breast arising in reconstruction mammoplasty capsule of saline filled breast implant after radical mastectomy for breast cancer: an unusual case presentation

<p>Abstract</p> <p>Background</p> <p>Primary non-Hodgkin lymphoma (NHL) of the breast represents 0.04–0.5% of malignant lesions of the breast and accounts for 1.7–2.2% of extra-nodal NHL. Most primary cases are of B-cell phenotype and only rare cases are of T-cell phenotype. Anaplastic large cell lymphoma (ALCL) is a rare T-cell lymphoma typically seen in children and young adults with the breast being one of the least common locations. There are a total of eleven cases of primary ALCL of the breast described in the literature. Eight of these cases occurred in proximity to breast implants, four in relation to silicone breast implant and three in relation to saline filled breast implant with three out of the eight implant related cases having previous history of breast cancer treated surgically. Adjuvant postoperative chemotherapy is given in only one case. Secondary hematological malignancies after breast cancer chemotherapy have been reported in literature. However in contrast to acute myeloid leukemia (AML), the association between lymphoma and administration of chemotherapy has never been clearly demonstrated.</p> <p>Case Presentation</p> <p>In this report we present a case of primary ALCL of the breast arising in reconstruction mamoplasty capsule of saline filled breast implant after radical mastectomy for infiltrating ductal carcinoma followed by postoperative chemotherapy twelve years ago.</p> <p>Conclusion</p> <p>Primary ALK negative ALCL arising at the site of saline filled breast implant is rare. It is still unclear whether chemotherapy and breast implantation increases risk of secondary hematological malignancies significantly. However, it is important to be aware of these complications and need for careful pathologic examination of tissue removed for implant related complications to make the correct diagnosis for further patient management and treatment. It is important to be aware of this entity at this site as it can be easily misdiagnosed on histologic grounds and to exclude sarcomatoid carcinoma, malignant melanoma and pleomorphic sarcoma by an appropriate panel of immunostains to arrive at the correct diagnosis of ALCL.</p

Synchronously diagnosed lymph nodal collision tumor of malignant melanoma and chonic lymphocytic leukemia/small lymphocytic lymphoma: case report

Synchronous composite tumors have been described but are uncommon. Moreover, simultaneous occurrence of synchronous tumors in the same tissue or organ is even less common. We report a case of chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma and malignant melanoma (MM) occurring synchronously in the same lymph node. Several cases of an association between cutaneous malignancies and lymphoproliferative disorders have been reported. Some of which included CLL and MM, occurring in the same patient often CLL after MM. The risk of having CLL after MM has been reported to be increased. Various genetic and environmental etiologies have been postulated, but have as yet not been proven. To our knowledge this is the first time that synchronous occurrence of these two malignant processes in the same tissue is described. In this case it is important that the melanoma was recognized in the excised lymph node, as this finding had much more critical treatment and long term survival consequences

Composite Multifocal Basal Cell carcinoma and Precursor B Acute Lymphoblastic Leukemia: Case report

Synchronous composite tumors though described are uncommon. Moreover, simultaneous occurrence of synchronous tumors involving the same tissue or organ at multiple sites is even less common. We report a case of acute lymphoblastic leukemia (ALL) and basal cell carcinoma (BCC) occurring simultaneously in multiple skin sites. Several cases showing an association between cutaneous malignancies and lymphoproliferative disorders have been reported. Some of these cases included ALL and BCC and occurred often in the pediatric population with the BCC arising as a post-ALL therapy sequela. Other rare genetic causes may be considered. To our knowledge this is the first time that the synchronous occurrence of these two malignant processes in the same tissue involving multiple sites in an elderly patient is described

Morphological alterations and the effect on tumour supressor gene expression induced by high dose rate intraluminal brachytherapy in oesophageal carcinoma

1. To review the radiation changes in total oesophagectomy specimens from 10 patients with Squamous cell carcinoma [SCC], given preoperative High Dose Rate Intraluminal Brachytherapy [HDRILBT] of 20 Gy in two fractions of 10 Gy each weekly. 2. To evaluate the effect of HDR ILBT on p-glycoprotein, the MDR-1 gene product in oesophageal SCC. 3. To examine the effect of HDR ILBT in the expression of p53, bcl-2 and apoptosis in oesophageal cancer. METHODS Ten consecutive patients with a preoperative diagnosis of moderate to poorly differentiated SCC of the oesophagus were investigated in this study. 1. The post-brachytherapy oesophagectomy specimens were sampled at the resection margins, edge of irradiated length, 1 cm from edge of visible tumour proximally and distally, centre of the tumour and lymph nodes. Both pre and post HDR ILBT specimens were: 2. examined for the expression of p-glycoprotein, the MDR-1 gene product using antibody to p-glycoprotein (clone JSB-1, using the modified sandwich technique). 3. examined for the expression of p53, bcl-2 and apoptosis using immunohistochemical markers. RESULTS 1. Radiation changes in the form of fibrosis was limited to the submucosa at the resection margins, circular muscle layer at the edge of irradiated length and full thickness at 1 cm from the edge of visible tumour and centre of the tumour. Surface epithelium did not show any changes at the resection margins but showed basal cell hyperplasia at the edge of the irradiated length, and ulceration at 1 cm from the edge of visible tumour and centre of the tumour. Endarteritis obliterans in the blood vessels were seen only 1 cm from the edge of visible tumour and at the centre of tumour. Necrosis, intense keratin formation and giant cell reaction were observed at the centre of the tumour. When compared to the pre-radiotherapy biopsies, the amount of keratin in the post-radiotherapy specimens was extensive. 2. p-glycoprotein was not expressed in either the pre-brachytherapy or postbrachytherapy tumour tissue specimens. 3. In one patient there was no expression of p53 in either pre or post-brachytherapy specimens. In 8 patients, p53 staining was strongly positive (3+), with approximately 50% or more cells showing a diffuse pattern in the pre-brachytherapy biopsies. The tumour areas of the postbrachytherapy specimens of these patients showed strong 3+ positivity with p53 (10-50% positive cell count), with the pattern being focal and peripheral in the tumour islands. The centre of the tumour islands showed necrosis and/or keratinization. In one patient, the prebrachytherapy biopsy showed expression of p53, whilst the post-brachytherapy specimen was negative, bcl-2 expression was equivocal in both pre and post-brachytherapy. Apoptosis was not demonstrated in either the pre or post-brachytherapy tissue sections in the presence of positive control. CONCLUSION 1. HDRILBT may induce keratin gene in the irradiated cells to differentiate towards better differentiated cells. Preopa?,tive HDR ILBT may have a role in improving the prognosis of early oe sophageal cancer treated with a combination of radiotherapy and surgery. 2. p-glycoprotein expression is of no value in predicting the responsiveness of the tumour to radiotherapy in SCC of the oesophagus. 3. Brachytherapy does not cause cell death by apoptosis but by necrosis and maturation of the cells into better differentiated cells which is caused by OH" free radical and induction of the keratin gene respectively. It is possible that brachytherapy may cause destruction of cells producing wild type p53, while mutant p53 in cells located at the tumour periphery escapes the effect of brachytherapy. This maybe responsible for the high incidence of local recurrence and distant metastasis in oesophageal cancer treated with radiotherapy. Brachytherapy does not affect bcl-2 expression in oesophageal cancer