PMID- 27272779
OWN - NLM
STAT- MEDLINE
DCOM- 20170126
LR  - 20220331
IS  - 1791-7530 (Electronic)
IS  - 0250-7005 (Linking)
VI  - 36
IP  - 6
DP  - 2016 Jun
TI  - Activation of the PERK-eIF2alpha Pathway Is Associated with Tumor-infiltrating 
      Lymphocytes in HER2-Positive Breast Cancer.
PG  - 2705-11
AB  - BACKGROUND: We evaluated endoplasmic reticulum stress and unfolded protein 
      response (UPR) activation, as possible mechanisms for influx of tumor 
      infiltrating lymphocytes (TILs), and the correlation between UPR activation and 
      mammalian target of rapamycin (mTOR) pathway activation. MATERIALS AND METHODS: 
      TILs and the immunohistochemical expression of protein kinase RNA-like 
      endoplasmic reticulum kinase (PERK), phospho-eukaryotic translation initiation 
      factor 2alpha (p-eIF2alpha) and phosphorylated S6 (pS6) were evaluated in 447 human 
      epidermal growth factor receptor 2 (HER2)-positive breast cancer tissues. 
      RESULTS: High expression of PERK, p-eIF2alpha and pS6 was observed in 270 (60.4%), 
      259 (57.9%), and 187 (41.8%) cases, respectively, and was significantly 
      associated with a high histological grade, high numbers of TILs, peritumoral 
      lymphocytic infiltration, and tertiary lymphoid structures in HER2-positive 
      breast cancer tissues. CONCLUSION: The results suggest endoplasmic reticulum 
      stress and UPR activation as possible mechanisms for the influx of TILs in 
      HER2-positive breast cancer. Evaluation of PERK and p-eIF2alpha expression might be 
      important in identifying targets for cancer therapies in modulating endoplasmic 
      reticulum stress.
CI  - Copyright(c) 2016 International Institute of Anticancer Research (Dr. John G. 
      Delinassios), All rights reserved.
FAU - Kim, Joo Young
AU  - Kim JY
AD  - Department of Pathology, Korea University Anam Hospital, Korea University College 
      of Medicine, Seoul, Republic of Korea.
FAU - Heo, Sun-Hee
AU  - Heo SH
AD  - Department of Pathology, University of Ulsan College of Medicine, Asan Medical 
      Center, Seoul, Republic of Korea.
FAU - Song, In Hye
AU  - Song IH
AD  - Department of Pathology, University of Ulsan College of Medicine, Asan Medical 
      Center, Seoul, Republic of Korea.
FAU - Park, In Ah
AU  - Park IA
AD  - Department of Pathology, University of Ulsan College of Medicine, Asan Medical 
      Center, Seoul, Republic of Korea.
FAU - Kim, Young-Ae
AU  - Kim YA
AD  - Department of Pathology, University of Ulsan College of Medicine, Asan Medical 
      Center, Seoul, Republic of Korea.
FAU - Gong, Gyungyub
AU  - Gong G
AD  - Department of Pathology, University of Ulsan College of Medicine, Asan Medical 
      Center, Seoul, Republic of Korea.
FAU - Lee, Hee Jin
AU  - Lee HJ
AD  - Department of Pathology, University of Ulsan College of Medicine, Asan Medical 
      Center, Seoul, Republic of Korea backlila@gmail.com.
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.10.1 (ERBB2 protein, human)
RN  - EC 2.7.10.1 (Receptor, ErbB-2)
RN  - EC 2.7.11.1 (EIF2AK3 protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (eIF-2 Kinase)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Breast Neoplasms/mortality/*pathology
MH  - Endoplasmic Reticulum Stress
MH  - Female
MH  - Humans
MH  - Lymphocytes, Tumor-Infiltrating/*physiology
MH  - Middle Aged
MH  - Receptor, ErbB-2/*analysis
MH  - Signal Transduction/*physiology
MH  - TOR Serine-Threonine Kinases/physiology
MH  - Unfolded Protein Response
MH  - eIF-2 Kinase/*physiology
OTO - NOTNLM
OT  - Breast cancer
OT  - HER2
OT  - PERK
OT  - p-eIF2alpha
OT  - pS6
OT  - tumor-infiltrating lymphocytes
EDAT- 2016/06/09 06:00
MHDA- 2017/01/27 06:00
CRDT- 2016/06/09 06:00
PHST- 2016/04/06 00:00 [received]
PHST- 2016/05/12 00:00 [accepted]
PHST- 2016/06/09 06:00 [entrez]
PHST- 2016/06/09 06:00 [pubmed]
PHST- 2017/01/27 06:00 [medline]
AID - 36/6/2705 [pii]
PST - ppublish
SO  - Anticancer Res. 2016 Jun;36(6):2705-11.