See this information may help you.

   CAR T CELL target CD19, a B cell–specific protein.Adoptive T cell transfer therapy typically is done after standard treatment for lymphoma or leukemia cancer. 

Traditional method of making CARs is to use viral transfection to modify the T cells’ antigen receptors. After the antigen receptors are modified, the chimeric T cells are cultured with antigen-presenting cells that express CD19. These antigen-presenting cells stimulate the transformed T cells and cause them to proliferate.

CAR-T cells can be designed  for each type of cancer  antigens. 

Just yesterday, I attended a very interesting talk by Michel Sadelain on that fascinating topic. Maybe you check some of his recent reviews, several groups appear to have estonishing success rates on CD19 bearing B-cell malignancies. Future approaches may help to treat many solid tumors on any  cancer neoantigen or new combinations of normal antigens on tumor cells.

http://cancerdiscovery.aacrjournals.org/content/early/2015/10/30/2159-8290.CD-15-0583.abstract

CAR T-cell therapy  has succeed   for B-cell acute lymphoblastic leukemia (B-ALL).

Great responses so far and for an overview of CAR's structure/generations, CAR-T's manufacturing/administration and tumor cell killing mechanism, next-generation CARs and landmark developments in cancer immunotherapy including of that of B cell malignancies, you may review Novus' Chimeric Antigen Receptor (CAR)-T Cell in Immunotherapy wall poster at https://www.novusbio.com/support/car-t-cell-immunotherapy-poster

Major advances and results of CAR-T cell therapy have been obtained so far in B-cell malignancies, mostly applying anti-CD19 (pan-B cell surface marker) CAR-T cells in pre-B/B-ALL and B-cell NHL. Moreover, anti-BCMA CARs have been applied with considerable success in phase I/II studies in multiple myeloma (MM), since the CD19 pan-B cell antigen is lost at the normal plasma cell stage of B-cell differentiation and in most abnormal myeloma plasma cells. In contrast, BCMA (B-cell maturation antigen) is a member of the tumor necrosis factor superfamily of proteins that is primarily expressed by malignant and normal plasma cells and some mature B cells, making it a potential target for multiple myeloma. Until today, despite the fact that CAR-T cells in the above lymphoid malignancies are not tumor (leukemia/lymphoma/myeloma) specific, but rather lineage specific, they induce on-target, off-tumor specific effects, such as, B-cell depletion with resultant normal Ig production deficiency, that can be easily controlled by monthly infusions of IVIG as replacement therapy.

In solid tumors there are currently trials [currently over 270 CAR T cell trials registered at the U.S. National Library of Medicine (ClinicalTrials.gov)], mostly phase I/II, of CAR-T cells, such as against EGFRvIII in recurrent Glioblastoma/Sarcoma, CD171 and GD2 in neuroblastoma, ErbB in head & neck cancer (intra-tumoral), FAP (fibroblast activation protein alpha) in malignant pleural mesothelioma (MPM), GPC-3 (glypican-3) in pediatric solid tumors and hepatocellular carcinoma, HER2 intra-cerebral in relapsed/refractory (r/r) pediatric CNS tumors/sarcoma/glioblastoma, IL13Rα2 in glioblastoma & r/r brain neoplasms, Mesothelin in breast/cervical/pancreatic/ovarian/lung cancer & MPM, MUC-16 ectodomain in recurrent ovarian/primary peritoneal/fallopian tube carcinomas (systemically and intraperitoneally), PSCA in prostate and pancreatic cancer and ROR1 (a tyrosine kinase orphan receptor expressed on cancer stem cells) in triple negative breast cancer & NSCLC.

Another important issue is that while on-target, off-tumor toxicities of CD19 and BCMA specific CARs, in the form of B cell and plasma cell aplasia, are usually manageable in patients with hematological malignancies, in contrast, on-target, off-tumor toxicities of CARs for solid cancers can lead to fatal outcomes (Morgan RA, et al. Mol Ther 2010; 18: 843–51). Potential reasons for this may include overlapping antigen expression on epithelial tissues, which most solid tumors originate from. The problem is that tumor and normal tissue are not targeted by an antibody as in MoAb therapy, where antigen expression differs quantitatively in favor of the tumor cells, but are rather targeted by a "living drug", that is to say, by T cells that have memory, can multiply and expand exponentially and attack even normal cells with low antigen expression and antigen density on their surfaces.