The B7-H1 (PD-L1) T lymphocyte-inhibitory molecule is expressed in breast cancer patients with infiltrating ductal carcinoma: correlation with important high-risk prognostic factors.
B7-H1 molecule increases the apoptosis of tumor-reactive T lymphocytes and reduces their immunogenicity. Breast cancer is the second most common cause of mortality after lung cancer. Direct evidence linking B7-H1 with cancer has been shown in several malignancies; however, its expression in breast cancer has not been investigated. We used immunohistochemistry to investigate the expression of the B7-H1 molecule in 44 breast cancer specimens and to study its correlation with patients' clinicopathological parameters. The expression of B7-H1 was shown in 22 of 44 patients and was not restricted to the tumor epithelium (15 of 44, 34% in tumor cells), but was also expressed by tumor-infiltrating lymphocytes (TIL; 18 of 44, 41%). Interestingly, intratumor expression of B7-H1 was significantly associated with histologic grade III-negative (P = .012), estrogen receptor-negative (P = .036), and progesterone receptor-negative (P = .040) patients. In addition, the expression of B7-H1 in TIL was associated with large tumor size (P = .042), histologic grade III (P = .015), positivity of Her2/neu status (P = .019), and severe tumor lymphocyte infiltration (P = .001). Taken together, these data suggest that B7-H1 may be an important risk factor in breast cancer patients and may represent a potential immunotherapeutic target using monoclonal antibody against the B7-H1 molecule.
Ghebeh
Hazem
H
Tumor Immunology Unit, Department of Biological and Medical Research, King Faisal Specialist Hospital and Research Center, PO Box 3354, Riyadh 11211, Saudi Arabia.
Mohammed
Shamayel
S
Al-Omair
Abeer
A
Qattan
Amal
A
Lehe
Cynthia
C
Al-Qudaihi
Ghofran
G
Elkum
Naser
N
Alshabanah
Mohamed
M
Bin Amer
Suad
S
Tulbah
Asma
A
Ajarim
Dahish
D
Al-Tweigeri
Taher
T
Dermime
Said
S
D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000032:analysis*; D060890:B7-H1 Antigen; D001943:Breast Neoplasms / Q000737:chemistry* / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology / Q000601:surgery; D018270:Carcinoma, Ductal, Breast / Q000737:chemistry* / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology / Q000601:surgery; D045744:Cell Line, Tumor / Q000737:chemistry / Q000276:immunology / Q000473:pathology; D003131:Combined Modality Therapy; D004847:Epithelial Cells / Q000378:metabolism; D004967:Estrogens; D005260:Female; D006801:Humans; D008207:Lymphatic Metastasis; D016246:Lymphocytes, Tumor-Infiltrating / Q000378:metabolism; D008408:Mastectomy; D008875:Middle Aged; D020360:Neoadjuvant Therapy; D009363:Neoplasm Proteins / Q000032:analysis*; D009376:Neoplasms, Hormone-Dependent / Q000737:chemistry / Q000188:drug therapy / Q000276:immunology / Q000473:pathology / Q000601:surgery; D011374:Progesterone; D011379:Prognosis; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D012307:Risk Factors; D012529:Saudi Arabia / Q000453:epidemiology; D047368:Tumor Burden; D019139:Tumor Escape / Q000276:immunology
D015703:Antigens, CD; D060890:B7-H1 Antigen; C423236:CD274 protein, human; D004967:Estrogens; D009363:Neoplasm Proteins; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D011374:Progesterone