PMID- 36221879
OWN - NLM
STAT- MEDLINE
DCOM- 20230519
LR  - 20230521
IS  - 1874-4702 (Electronic)
IS  - 1874-4672 (Linking)
VI  - 16
IP  - 5
DP  - 2023
TI  - Prevalence of Hepatocellular Carcinoma in Men and the Contribution of Androgen 
      and its Receptor in Pathogenesis and Therapy.
PG  - 559-563
LID - 10.2174/1874467215666221010092825 [doi]
AB  - BACKGROUND: Hepatocellular carcinoma (HCC) is a solid cancer with high 
      predominance in males. Liver tissue of both genders has saturable specific 
      oestrogen receptors. Androgen and its receptor (AR) have been suggested to 
      contribute to the predominance in men. Anti-oestrogens, like tamoxifen may reduce 
      the expression of oestrogen receptors, sustaining cellular in HCC. In vitro and 
      human, studies confirmed that both testosterone and dihydrotestosterone (DHT) 
      enhanced the growth and proliferation of hepatic normal and tumour cells. 
      Although the activity of AR is escalated by the chemical induction of 
      hepatocarcinogenesis; clinical trials with AR-targeted agents alone failed to 
      generate survival benefits. PURPOSE: This review will outline the possible 
      pathophysiological mechanisms by which both androgen and AR contribute to 
      hepatocarcinogenesis and to which extent this pathway can be responsible for the 
      male prevalence and if they could be pharmacological targets in HCC management. 
      CONCLUSION: Influencing factors that seem to be responsible for male prevalence 
      include testosterone, dihydrotestosterone and androgen receptors, as well as, 
      proteomic deficiency of DNA packaging, nuclear proteins and homeostasis-related 
      functional proteins. Understanding the reasons for males, rather than females the 
      HCC prevalence may help in suggesting new approaches by improving the anti-AR 
      therapies through co-targeting of AR and protein kinase B (Akt)/mammalian target 
      of rapamycin (mTOR) pathway.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Abdel-Hamid, Nabil Mohie
AU  - Abdel-Hamid NM
AD  - Department of Biochemistry, Faculty of Pharmacy, Kafrelsheikh University, 
      Kafrelsheikh, Egypt.
FAU - Al-Quzweny, Rawaa Muayad
AU  - Al-Quzweny RM
AD  - Department of Medical Lab Technique, Faculty of Pathological Analysis, 
      Al-Farahidi University, Baghdad, Iraq.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Curr Mol Pharmacol
JT  - Current molecular pharmacology
JID - 101467997
RN  - 0 (Androgens)
RN  - 08J2K08A3Y (Dihydrotestosterone)
RN  - 0 (Receptors, Estrogen)
RN  - 0 (Receptors, Androgen)
RN  - 3XMK78S47O (Testosterone)
SB  - IM
MH  - Humans
MH  - Male
MH  - Female
MH  - *Carcinoma, Hepatocellular/drug therapy/epidemiology
MH  - Androgens/therapeutic use
MH  - *Liver Neoplasms/drug therapy
MH  - Dihydrotestosterone/pharmacology/therapeutic use
MH  - Prevalence
MH  - Proteomics
MH  - Receptors, Estrogen/therapeutic use
MH  - Receptors, Androgen/genetics/metabolism/therapeutic use
MH  - Testosterone/therapeutic use
OTO - NOTNLM
OT  - Liver cancer
OT  - androgen receptors
OT  - anti-androgen therapy
OT  - incidence
OT  - oestrogen
OT  - sex hormoness
EDAT- 2022/10/13 06:00
MHDA- 2023/05/19 06:42
CRDT- 2022/10/12 02:33
PHST- 2022/05/22 00:00 [received]
PHST- 2022/08/28 00:00 [revised]
PHST- 2022/09/09 00:00 [accepted]
PHST- 2023/05/19 06:42 [medline]
PHST- 2022/10/13 06:00 [pubmed]
PHST- 2022/10/12 02:33 [entrez]
AID - CMP-EPUB-126866 [pii]
AID - 10.2174/1874467215666221010092825 [doi]
PST - ppublish
SO  - Curr Mol Pharmacol. 2023;16(5):559-563. doi: 10.2174/1874467215666221010092825.