Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Cellular and humoral immunodeficiency in breast cancer patients resistant to hormone therapy

E Zavadova, M Vocka, J Spacek, B Konopasek, T Fucikova, L Petruzelka

. 2014 ; 61 (1) : 90-98.

Jazyk angličtina Země Slovensko

Perzistentní odkaz   https://www.medvik.cz/link/bmc17017083

Grantová podpora
NT13259 MZ0 CEP - Centrální evidence projektů

In view of the fact that insufficiency in immune response often correlates with poor prognosis, research in recent years has focused on the task of describing the precise status and function of the immune system and its possible effect on cancer patients. Although more than two thirds of treated patients respond to endocrine therapy, most patients with metastatic breast cancer develop a resistance to it. Estrogen modulates angiogenesis, partially through its effects on vascular endothelial growth factor (VEGF). It also appears that transforming growth factor-beta (TGF beta) could be another factor contributing to this resistance. TGF beta is a highly immunosuppressive factor that inhibits natural and specific immunity against tumors and stimulates the production of VEGF. The purpose of the study was to monitor immune responses in patients with hormone receptor-positive breast cancer who were resistant to hormone therapy. The examination of cellular components (CD4, CD8, HLA-DR, NK cells) and humoral immunity (IgG, IgG subclasses, IgA, IgM,). TGF beta and VEGF production were monitored with special attention, along with an analysis of the changes that occurred during the hormonal treatment. 68 patients included in the research project were implemented with routine cancer treatment with endocrine therapy. Basic parameters (the histological type and grade, the degree of expression of estrogen receptors (ER) and progesterone receptors (PR), human epidermal growth factor receptor 2 (HER2), and the proliferative marker) were established. Patients were evaluated by a cancer clinical immunologist to exclude immune disorders, allergic or autoimmune origin. TGF beta and VEGF were measured by ELISA and antitumor cellular immunity (CD4, CD8) was measured by flow cytometry. Patients who failed in the first line of hormone therapy treatment were considered as resistant to hormone therapy.Depression in cellular immunity was found especially in patients with resistance to endocrine therapy. In addition, immunoglobulin plasma levels were decreased (mainly IgG4 subtype). Most patients showed clinical symptoms of immunodeficiency (frequent infections of respiratory or urinary tract, herpetic infections). Significant increases in TGF beta and VEGF plasma were also detected.The correlation of these factors with resistance to hormonal therapy and the state of anticancer immunity could be helpful in the task of predicting resistance to hormonal therapy and could contribute to the selection of targeted immune therapy in cancer patients in the future.

000      
00000naa a2200000 a 4500
001      
bmc17017083
003      
CZ-PrNML
005      
20191014110309.0
007      
ta
008      
170518s2014 xo f 000 0|eng||
009      
AR
035    __
$a (PubMed)24195514
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xo
100    1_
$a Závadová, Eva $7 xx0083030
245    10
$a Cellular and humoral immunodeficiency in breast cancer patients resistant to hormone therapy / $c E Zavadova, M Vocka, J Spacek, B Konopasek, T Fucikova, L Petruzelka
520    9_
$a In view of the fact that insufficiency in immune response often correlates with poor prognosis, research in recent years has focused on the task of describing the precise status and function of the immune system and its possible effect on cancer patients. Although more than two thirds of treated patients respond to endocrine therapy, most patients with metastatic breast cancer develop a resistance to it. Estrogen modulates angiogenesis, partially through its effects on vascular endothelial growth factor (VEGF). It also appears that transforming growth factor-beta (TGF beta) could be another factor contributing to this resistance. TGF beta is a highly immunosuppressive factor that inhibits natural and specific immunity against tumors and stimulates the production of VEGF. The purpose of the study was to monitor immune responses in patients with hormone receptor-positive breast cancer who were resistant to hormone therapy. The examination of cellular components (CD4, CD8, HLA-DR, NK cells) and humoral immunity (IgG, IgG subclasses, IgA, IgM,). TGF beta and VEGF production were monitored with special attention, along with an analysis of the changes that occurred during the hormonal treatment. 68 patients included in the research project were implemented with routine cancer treatment with endocrine therapy. Basic parameters (the histological type and grade, the degree of expression of estrogen receptors (ER) and progesterone receptors (PR), human epidermal growth factor receptor 2 (HER2), and the proliferative marker) were established. Patients were evaluated by a cancer clinical immunologist to exclude immune disorders, allergic or autoimmune origin. TGF beta and VEGF were measured by ELISA and antitumor cellular immunity (CD4, CD8) was measured by flow cytometry. Patients who failed in the first line of hormone therapy treatment were considered as resistant to hormone therapy.Depression in cellular immunity was found especially in patients with resistance to endocrine therapy. In addition, immunoglobulin plasma levels were decreased (mainly IgG4 subtype). Most patients showed clinical symptoms of immunodeficiency (frequent infections of respiratory or urinary tract, herpetic infections). Significant increases in TGF beta and VEGF plasma were also detected.The correlation of these factors with resistance to hormonal therapy and the state of anticancer immunity could be helpful in the task of predicting resistance to hormonal therapy and could contribute to the selection of targeted immune therapy in cancer patients in the future.
590    __
$a bohemika - dle Pubmed
650    02
$a dospělí $7 D000328
650    02
$a nádory prsu $x farmakoterapie $x imunologie $x krev $7 D001943
650    12
$a chemorezistence $7 D019008
650    02
$a ženské pohlaví $7 D005260
650    02
$a lidé $7 D006801
650    02
$a buněčná imunita $7 D007111
650    02
$a humorální imunita $7 D056724
650    02
$a lidé středního věku $7 D008875
650    02
$a tamoxifen $x terapeutické užití $7 D013629
650    02
$a transformující růstový faktor beta $x krev $7 D016212
650    02
$a vaskulární endoteliální růstový faktor A $x krev $7 D042461
700    1_
$a Vočka, Michal $7 xx0181880
700    1_
$a Špaček, Jan $7 xx0181883
700    1_
$a Konopásek, Bohuslav, $d 1943- $7 jn19990209382
700    1_
$a Fučíková, Terezie, $d 1936- $7 jn20000400743
700    1_
$a Petruželka, Luboš, $d 1952- $7 jn19990209650
773    0_
$t Neoplasma $x 0028-2685 $g Roč. 61, č. 1 (2014), s. 90-98 $p Neoplasma $w MED00003470
910    __
$a ABA008 $b A 1194 $y 4 $z 0
990    __
$a 20170518135159 $b ABA008
991    __
$a 20191014110733 $b ABA008
999    __
$a ok $b bmc $g 1205664 $s 977893
BAS    __
$a 3
BMC    __
$a 2014 $b 61 $c 1 $d 90-98 $x MED00003470 $i 0028-2685 $m Neoplasma
GRA    __
$a NT13259 $p MZ0
LZP    __
$a NLK 2015-B/lp

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...