PMID- 2576640
OWN - NLM
STAT- MEDLINE
DCOM- 19900514
LR  - 20191022
IS  - 0753-3322 (Print)
IS  - 0753-3322 (Linking)
VI  - 43
IP  - 8
DP  - 1989
TI  - Lessons from past experience in cancer immunotherapy and their application to 
      cancer and AIDS treatment and prophylaxis.
PG  - 551-61
AB  - Passive immunotherapy which we attempted in 1957 using polyclonal antibodies from 
      immunized donors aggravated tumor evolution: we suspected that blocking by Ig, 
      tumor cell antigen epitopes which are necessary to enhance or even maintain the 
      T-lymphocyte effector role in anti-cancer immunity could be the reason for this 
      tumor aggravation by "specific" antibodies. Today the very limited results of 
      monoclonal antibodies in cancer treatment favors this hypothesis. The aggravation 
      of HIV by (some) antibodies suggests that the same phenomenon may also happen in 
      this condition. In 1957, on the other hand, we described the therapeutically 
      beneficial cytostatic targetting effect of polyclonal antibodies, an effect which 
      has often been quoted and widely confirmed. Does the reason for the poor results 
      of monoclonal antibody targetting in tumor treatment reside in cancer antigen 
      heterogeneity? This is what an experiment we conducted with Olsson on AkR 
      leukemia indicated, suggesting that several monoclonals should be simultaneously 
      combined for most patients, to be determined by the antigenic study not only of 
      each tumor but of each localisation. We shifted our cancer immunotherapy approach 
      to an adoptive form in 1959; a), after establishing partial and transient, then 
      total and permanent allogeneic marrow graft and chimerism in man; b), after 
      describing the graft versus leukemia (GvL) action of the graft versus host (GvH) 
      effect in leukaemic mice; c), and the same phenomenon in humans. Our observations 
      on human allogeneic grafted bone marrow GvH and GvL were statistically confirmed 
      in 1979 by the Seattle group. In the 1970s we attempted to induce strong GvL with 
      weak GvH by replacing allogeneic bone marrow graft by allogeneic lymphocyte 
      transfusions without host conditioning. Remarkable results were registered in 
      mice, and in patients with acute leukaemia--5 complete remissions out of 7 
      patients who developed moderate GvH, and only 3 out of 70 in those who did not 
      develop GvH. As we now know that CD4-, CD8+ lymphocytes are not all 
      MHCl-restricted, we consider that the allogeneic CTL approach is worth trying as 
      reinforcement treatment of (at least) severe hematopoietic malignancies. If it is 
      indeed worthwhile in some severe neoplasias to include the adoptive form of 
      immunotherapy in the multi-treatment program, the replacement of the patient's 
      bone marrow by engrafted allogeneic stem cells has not been proven necessary, as 
      the persistence in "ALL cured" chemotherapy patients of abnormally differentiated 
      cells does not reduce the expectancy of cure.(ABSTRACT TRUNCATED AT 400 WORDS)
FAU - Mathe, G
AU  - Mathe G
AD  - Institut du Cancer et d'Immunogenetique, Immunitaires et Tumorales, Hopital 
      Paul-Brousse, Villejuif, France.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
SB  - IM
MH  - Acquired Immunodeficiency Syndrome/immunology/prevention & 
      control/surgery/*therapy
MH  - Animals
MH  - Bone Marrow Transplantation
MH  - CD4-Positive T-Lymphocytes/transplantation
MH  - Humans
MH  - *Immunization, Passive
MH  - Mice
MH  - Neoplasms/immunology/prevention & control/surgery/*therapy
RF  - 112
EDAT- 1989/01/01 00:00
MHDA- 1989/01/01 00:01
CRDT- 1989/01/01 00:00
PHST- 1989/01/01 00:00 [pubmed]
PHST- 1989/01/01 00:01 [medline]
PHST- 1989/01/01 00:00 [entrez]
AID - 0753-3322(89)90032-2 [pii]
AID - 10.1016/0753-3322(89)90032-2 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 1989;43(8):551-61. doi: 10.1016/0753-3322(89)90032-2.