PMID- 23056620
OWN - NLM
STAT- MEDLINE
DCOM- 20130531
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 7
IP  - 10
DP  - 2012
TI  - Apocrine-eccrine carcinomas: molecular and immunohistochemical analyses.
PG  - e47290
LID - 10.1371/journal.pone.0047290 [doi]
LID - e47290
AB  - Apocrine-eccrine carcinomas are rare and associated with poor prognosis. 
      Currently there is no uniform treatment guideline. Chemotherapeutic drugs that 
      selectively target cancer-promoting pathways may complement conventional 
      therapeutic approaches. However, studies on genetic alterations and EGFR and Her2 
      status of apocrine-eccrine carcinomas are few in number. In addition, hormonal 
      studies have not been comprehensive and performed only on certain subsets of 
      apocrine-eccrine carcinomas. To investigate whether apocrine-eccrine carcinomas 
      express hormonal receptors or possess activation of oncogenic pathways that can 
      be targeted by available chemotherapeutic agent we performed immunohistochemistry 
      for AR, PR, ER, EGFR, and HER2 expression; fluorescence in situ hybridization 
      (FISH) for EGFR and ERBB2 gene amplification; and molecular analyses for 
      recurrent mutations in 15 cancer genes including AKT-1, EGFR, PIK3CA, and TP53 on 
      54 cases of apocrine-eccrine carcinomas. They include 10 apocrine carcinomas, 7 
      eccrine carcinomas, 9 aggressive digital papillary adenocarcinomas, 10 
      hidradenocarcinomas, 11 porocarcinomas, 1 adenoid cystic carcinoma, 4 malignant 
      chondroid syringomas, 1 malignant spiradenoma, and 1 malignant cylindroma. AR, 
      ER, PR, EGFR and HER2 expression was seen in 36% (19/53), 27% (14/51), 16% 
      (8/51), 85% (44/52) and 12% (6/52), respectively. Polysomy or trisomy of EGFR was 
      detected by FISH in 30% (14/46). Mutations of AKT-1, PIK3CA, and TP53 were 
      detected in 1, 3, and 7 cases, respectively (11/47, 23%). Additional 
      investigation regarding the potential treatment of rare cases of apocrine-eccrine 
      carcinomas with PI3K/Akt/mTOR pathway inhibitors, currently in clinical testing, 
      may be of clinical interest.
FAU - Le, Long P
AU  - Le LP
AD  - Department of Pathology, Massachusetts General Hospital, Boston, United States of 
      America.
FAU - Dias-Santagata, Dora
AU  - Dias-Santagata D
FAU - Pawlak, Amanda C
AU  - Pawlak AC
FAU - Cosper, Arjola K
AU  - Cosper AK
FAU - Nguyen, Anh Thu
AU  - Nguyen AT
FAU - Selim, M Angelica
AU  - Selim MA
FAU - Deng, April
AU  - Deng A
FAU - Horick, Nora K
AU  - Horick NK
FAU - Iafrate, A John
AU  - Iafrate AJ
FAU - Mihm, Martin C Jr
AU  - Mihm MC Jr
FAU - Hoang, Mai P
AU  - Hoang MP
LA  - eng
PT  - Journal Article
DEP - 20121009
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.10.1 (Receptor, ErbB-2)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Apocrine Glands/*metabolism/*pathology
MH  - Carcinoma/*metabolism/*pathology
MH  - Eccrine Glands/*metabolism/*pathology
MH  - ErbB Receptors/genetics/metabolism
MH  - Female
MH  - Humans
MH  - Immunohistochemistry/*methods
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Middle Aged
MH  - Receptor, ErbB-2/genetics/metabolism
MH  - Young Adult
PMC - PMC3467209
COIS- Competing Interests: DDS and AJI submitted a patent application (pending) for the 
      SNaPshot(r) genotyping methods used in this study, and are consultants for 
      BioReference Laboratories Inc. The remaining authors have no conflicts of 
      interest to declare. This does not alter the authors' adherence to all the PLOS 
      ONE policies on sharing data and materials.
EDAT- 2012/10/12 06:00
MHDA- 2013/06/01 06:00
PMCR- 2012/10/09
CRDT- 2012/10/12 06:00
PHST- 2012/06/12 00:00 [received]
PHST- 2012/09/13 00:00 [accepted]
PHST- 2012/10/12 06:00 [entrez]
PHST- 2012/10/12 06:00 [pubmed]
PHST- 2013/06/01 06:00 [medline]
PHST- 2012/10/09 00:00 [pmc-release]
AID - PONE-D-12-17581 [pii]
AID - 10.1371/journal.pone.0047290 [doi]
PST - ppublish
SO  - PLoS One. 2012;7(10):e47290. doi: 10.1371/journal.pone.0047290. Epub 2012 Oct 9.