Nerve Growth Factor Receptor Immunoreactivity in Breast Cancer Patients

Aragona, Marcello; Panetta, Stefania; Silipigni, Anna Maria; Romeo, D; Pastura, Giuseppe; Mesiti, M.; Cascinu, Stefano; Torre, Francesco La

doi:10.1081/cnv-100106144

Cited by 20 publications

(25 citation statements)

References 15 publications

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“…Similarly to the previous reports, 13,14 we found that p75 NTR is consistently expressed in the myoepithelial cells of the human mammary gland. We also showed that p75 NTR always highlighted the myoepithelial cells in the benign breast lesions (slerosing adenosis, ductal hyperplasia, intraductal papilloma) and carcinoma in situ and was absent in the majority of the invasive carcinomas.…”

Section: Discussionsupporting

confidence: 90%

“…The data support the notion that p75 NTR can be used to evaluate difficult sclerosing lesions or to distinguish between in situ and invasive disease. All metaplastic carcinomas included in our study as well as a small portion of invasive ductal carcinomas, showed expression of p75 NTR Similarly, Aragona et al, 14 who used the same monoclonal antibody on frozen sections, have found that 15% of the breast cancers included in their study are positive for p75 NTR However, using a polyclonal antibody on paraffin sections, Sakamoto et al 15 have reported that 73% of the breast carcinomas express p75 NTR in more than 15% of cancer cells. Those discrepancies might be explained with the use of different antibodies and different tissue preparation techniques.…”

Section: Discussionsupporting

confidence: 79%

“…p75 NTR has been previously detected in the nerves 13,14,[11][12][13][14][15][16][17][18][19][20][21][22][23] and vessels. 13,14 Although we did not observe significant p75 NTR expression in the fibroblast in normal breast stroma and in the stroma around the carcinoma, we found strong p75 NTR expression in the fibroblasts of the expanding intralobular stroma (fibroadenomatoid change). In addition to the myoepithelial positivity, further immunohistochemical staining performed on six fibroadenomas revealed similar strong stromal p75 NTR expression.…”

Section: Discussionmentioning

confidence: 92%

“…Those discrepancies might be explained with the use of different antibodies and different tissue preparation techniques. In addition, Aragona et al 14 have shown that p75 NTR expression is associated with estrogen receptor positivity and more differentiated histologic grade. This result is unexpected since the tumors that express myoepithelial/basal markers usually lack estrogen receptors and are poorly differentiated.…”

Section: Discussionmentioning

confidence: 98%

“…p75 NTR is expressed in neural as well as in non-neural tissues including breast myoepithelial cells. 13,14 However, its diagnostic utility as a marker of breast myoepithelial cells has not been evaluated. Here we examine p75 NTR expression in benign and malignant breast lesions and compare its expression pattern with those of well-established myoepithelial markers such as p63 and myosin heavy chain.…”

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confidence: 99%

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Diagnostic utility of p75 neurotrophin receptor (p75NTR) as a marker of breast myoepithelial cells

et al. 2005

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We evaluated the low affinity neurotrophin receptor (p75 NTR ) as a marker of breast myoepithelial cells. Immunohistochemical staining for p75 NTR was performed on paraffin sections of 122 malignant breast lesions, 28 benign lesions and the adjacent normal breast tissue. The staining pattern was compared to those of myosin heavy chain and p63. p75 NTR immunostain was consistently positive and compatible with p63 and myosin immunoreactivity in the myoepithelial cells of the normal mammary gland, benign breast lesions (six usual ductal hyperplasias, six specimens with sclerosing adenosis, eight intraductal papillomas, six fibroadenomas), and carcinoma in situ (18 ductal carcinomas in situ, two noninvasive papillary carcinomas, two lobular carcinomas in situ). The luminal cells were negative for p75 NTR , but rare positive cells were noticed in the solid areas of some of the usual ductal hyperplasias. Four of 64 invasive ductal carcinomas (6%) and all metaplastic carcinomas (n ¼ 3, 100%) showed a variable degree of p75 NTR positivity. No p75 NTR expression was found in the malignant cells in all in situ carcinomas, invasive lobular carcinomas (n ¼ 11), tubular carcinomas (n ¼ 10), invasive papillary carcinomas (n ¼ 6), mucinous carcinomas (n ¼ 4), and medullary carcinomas (n ¼ 2). No myosin imunoreactivity was seen in the luminal/tumor cells, but p63 pattern of staining in the luminal/tumor cells was quite similar to that of p75 NTR . Although significant p75 NTR immunoreactivity was noticed in the vessels, nerves, and stromal component of fibroadenomas, no difficulties in the evaluation of the immunostain of myoepithelial cells were encountered. Our study shows that p75 NTR is a useful marker for breast myoepithelial cells and can be used to rule out invasive disease as well as to evaluate difficult for diagnosis sclerosing lesions. Our data suggest a role of neurotrophins in the development of fibroepithelial breast tumors and some of the breast carcinomas. Modern Pathology (2005) 18, 1535-1541.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 99%

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Diagnostic utility of p75 neurotrophin receptor (p75NTR) as a marker of breast myoepithelial cells

et al. 2005

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Profiling genomic copy number changes in retinoblastoma beyond loss of RB1

Bowles

Corson

Bayani

et al. 2006

Genes Chromosomes & Cancer

113

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Loss of both RB1 alleles is rate limiting for development of retinoblastoma (RB), but genomic copy number gain or loss may impact oncogene(s) and tumor suppressor genes, facilitating tumor progression. We used quantitative multiplex polymerase chain reaction to profile "hot spot" genomic copy number changes for gain at 1q32.1, 6p22, and MYCN, and loss at 16q22 in 87 primary RB and 7 cell lines. Loss at 16q22 (48%) negatively associated with MYCN gain (18%) (Fisher's exact P = 0.031), gain at 1q32.1 (62%) positively associated with 6p "hot spot" gain (43%) (P = 0.033), and there was a trend for positive association between 1q and MYCN gain (P = 0.095). Cell lines had a higher frequency of MYCN amplification than primary tumors (29% versus 3%; P = 0.043). Novel high-level amplification of 1q32.1 in one primary tumor, confirmed by fluorescence in situ hybridization, strongly supports the presence of oncogene(s) in this region, possibly the mitotic kinesin, KIF14. Gene-specific quantitative multiplex polymerase chain reaction of candidate oncogenes at 1q32.1 (KIF14), 6p22 (E2F3 and DEK), and tumor suppressor genes at 16q22 (CDH11) and 17q21 (NGFR) showed the most common gene gains in RB to be KIF14 in cell lines (80%) and E2F3 in primary tumors (70%). The patterns of gain/loss were qualitatively different in 25 RB compared with 12 primary hepatocellular carcinoma and 12 breast cancer cell lines. Gene specific analysis of one bone marrow metastasis of RB, prechemotherapy and postchemotherapy, showed the typical genomic changes of RB pretreatment, which normalized after chemotherapy.

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