Androgens and esophageal cancer: What do we know?

Table 1 Androgen receptor expression in esophageal cancer

Ref.	No. of patients	Male:female	Histological type	AR	Conclusion
Matsuoka et al[74], 1987	NA	NA	SCC cell line	2.2 fmol/mg	Proliferation of KSE-1 cell line is inhibited by estrogen and enhanced by testosterone
Tihan et al[19], 2001	25	21:4	AC (n = 11)SCC (n = 14)	7 males and 1females, 5 EAC and 3 SCC were positive	Presence of AR in human esophageal cancer is an impetus for further studies to assess anti-androgen therapy for treatment and or prevention of these tumors.
Yang et al[20], 2001	31	26:5	SCC	Cancer tissues: 40.56 ± 18.19 fmol/mg, normal tissues: 7.84 ± 3.21 fmol/mg	AR and estrogen receptors have close relationship with the biologic behavior and prognosis of esophageal SCC
Tiffin et al[80], 2003	20	10:10	AC (ND)BE (ND)	Very weakly positive in 1 male with EAC and 1 female with BE	Androgen receptors are not implicated in BE or AC
Awan et al[17], 2007	23	20:3	AC (n = 18)SCC (n = 5)	16 samples (EAC = 13, SCC = 3) showed positive nuclear staining. AC occurred in 12 males and 1 female, while in SCC 2 males and 1 female	AR expressed in the stroma of esophageal AC may induce paracrine effects following stimulation by androgens (including tumor-derived), possibly via FGFs
Nordenstedt, et al[18], 2012	30	20:10	BE (n = 10)Controls (n = 20)	All BE cases were negative. Only 1 male control was found AR expressed in squamous esophageal mucosa	AR were negative in BE warrants further research to find alternative explanations for the male predominance in BE and EAC

AR: Androgen receptor; EAC: Esophageal adenocarcinoma; SCC: Squamous cell cancer; BE: Barrett’s esophagus; NA: Not applicable; ND: Not described.