PMID- 11062756
OWN - NLM
STAT- MEDLINE
DCOM- 20001211
LR  - 20131121
IS  - 0250-7005 (Print)
IS  - 0250-7005 (Linking)
VI  - 20
IP  - 5A
DP  - 2000 Sep-Oct
TI  - Induction of tumor-specific antitumor immunity after chemotherapy with cisplatin 
      in mice bearing MOPC-104E plasmacytoma by modulation of MHC expression on tumor 
      surface.
PG  - 3293-9
AB  - Chemotherapy sometimes results in induction of specific antitumor immunity. We 
      investigated the mechanisms responsible for the induction of antitumor immunity 
      in mice bearing MOPC-104E plasmacytoma after chemotherapy with cisplatin (CDDP), 
      especially the effects of CDDP on the expression of MHC on the tumor surface. 
      BALB/c mice were subcutaneously (s.c.) inoculated with MOPC-104E cells on day 0, 
      then intravenously (i.v.) treated with CDDP at 3.6 mg/kg on day 7. The tumors 
      disappeared completely on day 35 and the mice rejected a second challenge with 
      MOPC-104E, but did not reject syngeneic Meth-A fibrosarcoma. The tumors did not 
      regress, however, when MOPC-104E was s.c. transplanted in nude mice, or when 
      anti-T-cell monoclonal antibodies were i.v. injected into BALB/c mice before CDDP 
      treatment on day 6. To determine which of the mice or tumor were affected by 
      CDDP, BALB/c mice were inoculated with CDDP-treated (12.5 micrograms/ml for 3 
      hours in vitro) MOPC-104E cells on day 0, 7 and 14. The potential to reject 
      MOPC-104E was lower in mice immunized with ethanol-treated MOPC-104E cells than 
      in those immunized with CDDP-treated cells. CDDP-treated or -untreated MOPC-104E 
      cells ultrasonicated and fractionated into soluble and insoluble fractions by 
      centrifuging, also induced antitumor immunity. Flow cytometry demonstrated that 
      the expression of MHC-class-I antigens H-2Dd and H-2Kd was enhanced after 
      CDDP-treatment, but that of class-II antigens I-Ad and I-Ed was not, suggesting 
      that CDDP induced tumor-specific antitumor immunity by enhancing the expression 
      of MHC-class-I antigens.
FAU - Nio, Y
AU  - Nio Y
AD  - First Department of Surgery, Shimane Medical University, Izumo, Japan. 
      fsurgery@shimane-med.ac.jp
FAU - Hirahara, N
AU  - Hirahara N
FAU - Minari, Y
AU  - Minari Y
FAU - Iguchi, C
AU  - Iguchi C
FAU - Yamasawa, K
AU  - Yamasawa K
FAU - Toga, T
AU  - Toga T
FAU - Tamura, K
AU  - Tamura K
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - 0 (Antineoplastic Agents)
RN  - 0 (H-2 Antigens)
RN  - 0 (H-2K(K) antigen)
RN  - 0 (Histocompatibility Antigen H-2D)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (I-Ad antigen)
RN  - 0 (I-E-antigen)
RN  - Q20Q21Q62J (Cisplatin)
SB  - IM
MH  - Animals
MH  - Antineoplastic Agents/*therapeutic use
MH  - Cell Cycle
MH  - Cell Fractionation
MH  - Cisplatin/*therapeutic use
MH  - Flow Cytometry
MH  - H-2 Antigens/biosynthesis
MH  - Histocompatibility Antigen H-2D
MH  - Histocompatibility Antigens Class II/biosynthesis
MH  - Lymphocyte Depletion
MH  - *Major Histocompatibility Complex
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Nude
MH  - Neoplasm Transplantation
MH  - Plasmacytoma/*drug therapy/*immunology
MH  - Solubility
MH  - T-Lymphocytes/immunology
MH  - Vaccination
EDAT- 2000/11/04 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/11/04 11:00
PHST- 2000/11/04 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/11/04 11:00 [entrez]
PST - ppublish
SO  - Anticancer Res. 2000 Sep-Oct;20(5A):3293-9.