PMID- 17611654
OWN - NLM
STAT- MEDLINE
DCOM- 20070911
LR  - 20181201
IS  - 1021-335X (Print)
IS  - 1021-335X (Linking)
VI  - 18
IP  - 2
DP  - 2007 Aug
TI  - Differential levels of human leukocyte antigen-class I, multidrug-resistance 1 
      and androgen receptor expressions in untreated prostate cancer cells: the 
      robustness of prostate cancer.
PG  - 343-6
AB  - Tumors are highly robust and maintain their proliferative potential against a 
      wide range of both host-defense mechanisms and anticancer therapies. One of the 
      approaches to overcome cancer robustness could be combined therapy in which each 
      modality imposes independent selective pressures against the acquired mutation of 
      cancer. To develop such a therapy, it is crucial to understand the magnitude of 
      acquired mutations. In this study, we investigated the levels of human leukocyte 
      antigen (HLA)-class I, multidrug-resistance 1 (MDR1), and androgen receptor (AR) 
      expressions in untreated prostate cancers harvested by radical prostatectomy. The 
      mean percentages of cancer cells expressing HLA-class I, MDR and AR among the 10 
      cancer samples were 41, 35 and 74%, respectively. In addition, double-staining of 
      HLA and MDR revealed the four definite populations (HLA+/MDR+, HLA+/MDR-, 
      HLA-/MDR+ and HLA-/MDR-) in cancer tissues from the majority of cancer patients 
      tested, and the mean percentages of cells expressing these combinations were 13, 
      29, 22 and 38%, respectively. Similar results were obtained by double-staining of 
      HLA and AR, except for 2 cases in which HLA-/AR+ cancer cells predominated. These 
      results indicated that untreated prostate cancer cells acquired a wide range of 
      genomic mutations, which may have been caused by internal host pressure to 
      eliminate malignant cells, and would provide evidence of the robustness of 
      untreated prostate cancer.
FAU - Homma, Shigenori
AU  - Homma S
AD  - Department of Immunology, Kurume University School of Medicine, Fukuoka 830-0011, 
      Japan.
FAU - Komohara, Yoshihiro
AU  - Komohara Y
FAU - Harada, Mamoru
AU  - Harada M
FAU - Saya, Hideyuki
AU  - Saya H
FAU - Todo, Satoru
AU  - Todo S
FAU - Itoh, Kyogo
AU  - Itoh K
FAU - Noguchi, Masanori
AU  - Noguchi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (ABCB1 protein, human)
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B)
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 1)
RN  - 0 (HLA Antigens)
RN  - 0 (Receptors, Androgen)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B
MH  - ATP Binding Cassette Transporter, Subfamily B, Member 1/*biosynthesis
MH  - Aged
MH  - HLA Antigens/*biosynthesis
MH  - Humans
MH  - Immunohistochemistry
MH  - Male
MH  - Middle Aged
MH  - Prostatic Neoplasms/metabolism/*pathology
MH  - Receptors, Androgen/*biosynthesis
EDAT- 2007/07/06 09:00
MHDA- 2007/09/12 09:00
CRDT- 2007/07/06 09:00
PHST- 2007/07/06 09:00 [pubmed]
PHST- 2007/09/12 09:00 [medline]
PHST- 2007/07/06 09:00 [entrez]
PST - ppublish
SO  - Oncol Rep. 2007 Aug;18(2):343-6.