- Email: [email protected]
In This Issue
Human Pathology (2008) 39
www.elsevier.com/locate/humpath
In This Issue Toker cells of the breast. Morphological and immunohistochemical characterization of 40 cases Tommaso et al Page 1295 Toker cells are usually located in the nipple epidermis and in other intraepidermal sites. They are larger than keratinocytes, with oval-shaped nuclei and 1 or 2 small nucleoli. They are usually concentrated in the basal layer or arranged into glandular structures growing up to the spinous layer. Although most Toker cells have bland cytologic features, a small percentage have cytological atypia. Tommaso and co-workers examined normal and atypical Toker cells in the breast epidermis using the immunohistochemical profile of these cells and attempted to separate them from Paget’s disease cells. Toker cells were usually positive for estrogen and progesterone receptors and negative for CD138 and TP53. In contrast, Paget’s disease cells were often negative for estrogen and progesterone receptor proteins but positive for CD138, TP53, and HER2/NEU. Both cell types were positive for cytokeratin and epithelial membrane antigen. The authors recommend using antibodies to CD138 and TP53 to help distinguish atypical Toker cells from Paget’s disease cells.
Case 1
Case 7
Case 11
Case 12
Case 13
Case 16
Genetic alterations in colorectal cancers with demethylation of insulin-like growth factor II Ohta et al Page 1301 Loss of imprinting is an epigenetic alteration in some malignancies that involves the loss of parental origin-specific expression of imprinted genes. Loss of imprinting of insulin-like growth factor II has been observed in colorectal, ovarian, lung, and liver tumors. With loss of imprinting there is usually an increase in the insulin-like growth factor II levels in normal and tumor tissues. Ohta and co-workers examined loss of insulin-like growth factor II genomic imprinting status by evaluating the demethylation of the insulin-like growth factor II differentially methylated region. They also examined the genetic mutation of KRAS, BRAF, and PIK3CA, expression of CTNNB1 and TP53; and microsatellite instability in the same cases. Colorectal cancers with normal insulin-like growth factor II imprinting were located more in the distal colon, while more cases with loss of genomic imprinting tended to be in the proximal colon. PIK3CA gene mutation was more common in tumors with normal imprinting. Multivariate analysis showed significant relationships among proximal tumor location, PIK3CA genetic mutation, and insulin-like growth factor II genomic imprinting status. The authors conclude that colorectal cancers with demethylation of the insulin-like growth factor II gene are distinct from normal imprinting tumors clinically and in molecular genetic features.
0046-8177/$ – see front matter doi:10.1016/S0046-8177(08)00343-2
IgA-dominant postinfectious glomerulonephritis: a report of 13 cases with common ultrastructural features Haas et al Page 1309 Postinfectious glomerulonephritis is an immune complex mediated form of glomerulonephritis that is usually associated with group A streptococcal infections. In poststreptococcal glomerulonephritis the glomerular immune complex deposits are composed mainly of IgG and complement. A recent report in Human Pathology showed that some cases of acute postinfectious glomerulonephritis were characterized by glomerular deposits of IgA as the dominant immunoglobulin. These cases occurred after development of methicillin-sensitive Staphylococcus aureus or after Staphylococcus epidermidis infections in patients with underlying diabetic nephropathy. Haas and co-workers examined a series of patients with IgA dominant postinfectious glomerulonephritis and described demographic, clinical, and renal biopsy findings. Each case was characterized by subepithelial humps at various stages of resolution. Based on their findings, the authors concluded that IgA dominant postinfectious glomerulonephritis resembles post streptococcal glomerulonephritis in histological spectrum and ultrastructural features, was often associated with staphylococcal infection, and occurred in diabetic as well as non-diabetic patients. They also found that the disease may resolve if renal failure at presentation was not severe.
www.elsevier.com/locate/humpath
In This Issue Toker cells of the breast. Morphological and immunohistochemical characterization of 40 cases Tommaso et al Page 1295 Toker cells are usually located in the nipple epidermis and in other intraepidermal sites. They are larger than keratinocytes, with oval-shaped nuclei and 1 or 2 small nucleoli. They are usually concentrated in the basal layer or arranged into glandular structures growing up to the spinous layer. Although most Toker cells have bland cytologic features, a small percentage have cytological atypia. Tommaso and co-workers examined normal and atypical Toker cells in the breast epidermis using the immunohistochemical profile of these cells and attempted to separate them from Paget’s disease cells. Toker cells were usually positive for estrogen and progesterone receptors and negative for CD138 and TP53. In contrast, Paget’s disease cells were often negative for estrogen and progesterone receptor proteins but positive for CD138, TP53, and HER2/NEU. Both cell types were positive for cytokeratin and epithelial membrane antigen. The authors recommend using antibodies to CD138 and TP53 to help distinguish atypical Toker cells from Paget’s disease cells.
Case 1
Case 7
Case 11
Case 12
Case 13
Case 16
Genetic alterations in colorectal cancers with demethylation of insulin-like growth factor II Ohta et al Page 1301 Loss of imprinting is an epigenetic alteration in some malignancies that involves the loss of parental origin-specific expression of imprinted genes. Loss of imprinting of insulin-like growth factor II has been observed in colorectal, ovarian, lung, and liver tumors. With loss of imprinting there is usually an increase in the insulin-like growth factor II levels in normal and tumor tissues. Ohta and co-workers examined loss of insulin-like growth factor II genomic imprinting status by evaluating the demethylation of the insulin-like growth factor II differentially methylated region. They also examined the genetic mutation of KRAS, BRAF, and PIK3CA, expression of CTNNB1 and TP53; and microsatellite instability in the same cases. Colorectal cancers with normal insulin-like growth factor II imprinting were located more in the distal colon, while more cases with loss of genomic imprinting tended to be in the proximal colon. PIK3CA gene mutation was more common in tumors with normal imprinting. Multivariate analysis showed significant relationships among proximal tumor location, PIK3CA genetic mutation, and insulin-like growth factor II genomic imprinting status. The authors conclude that colorectal cancers with demethylation of the insulin-like growth factor II gene are distinct from normal imprinting tumors clinically and in molecular genetic features.
0046-8177/$ – see front matter doi:10.1016/S0046-8177(08)00343-2
IgA-dominant postinfectious glomerulonephritis: a report of 13 cases with common ultrastructural features Haas et al Page 1309 Postinfectious glomerulonephritis is an immune complex mediated form of glomerulonephritis that is usually associated with group A streptococcal infections. In poststreptococcal glomerulonephritis the glomerular immune complex deposits are composed mainly of IgG and complement. A recent report in Human Pathology showed that some cases of acute postinfectious glomerulonephritis were characterized by glomerular deposits of IgA as the dominant immunoglobulin. These cases occurred after development of methicillin-sensitive Staphylococcus aureus or after Staphylococcus epidermidis infections in patients with underlying diabetic nephropathy. Haas and co-workers examined a series of patients with IgA dominant postinfectious glomerulonephritis and described demographic, clinical, and renal biopsy findings. Each case was characterized by subepithelial humps at various stages of resolution. Based on their findings, the authors concluded that IgA dominant postinfectious glomerulonephritis resembles post streptococcal glomerulonephritis in histological spectrum and ultrastructural features, was often associated with staphylococcal infection, and occurred in diabetic as well as non-diabetic patients. They also found that the disease may resolve if renal failure at presentation was not severe.