Targeting An Ancient Retrovirus In Tumor Using Engineered T Cells

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4206-4206
Author(s):  
Janani Krishnamurthy ◽  
Brian Rabinovich ◽  
Simon Olivares ◽  
Mi Teijuan ◽  
Kirsten Switzer ◽  
...  
Keyword(s):  
Clinical Trials ◽  
T Cells ◽  
Tumor Cells ◽  
Treatment Strategy ◽  
Conflicts Of Interest ◽  
Sleeping Beauty ◽  
Normal Organ ◽  
Car T Cells ◽  
Car T ◽  
Env Protein

Abstract Human endogenous retroviruses (HERVs) are ancient viruses forming 8% of human genome. One subset of HERVs, the HERV-K has recently been found to be expressed on tumor cells including melanoma, breast cancer and lymphoma but not on normal body cells. Thus, targeting HERV-K protein as a tumor associated antigen (TAA) may be a potential treatment strategy for tumors that are resistant to conventional therapies. One approach to improve therapeutic outcome is by infusing T cells rendered specific for such TAAs preferentially expressed on tumor cells. Recognition of cell-surface TAAs independent of major histocompatibility complex can be achieved by introducing a chimeric antigen receptor (CAR) on T cells using gene therapy. This approach is currently being used in our clinical trials adoptively transferring CD19-specific CAR+ T cells into patients with B-lineage malignancies. Preliminary analysis of HERV-K env protein expression in 268 melanoma samples and 139 normal organ donor tissues using immunohistochemistry demonstrated antigen expression in tumor cells and absence of expression in normal organ tissues. The scFv region from a mouse monoclonal antibody to target HERV-K env was used to generate a CAR and cloned into Sleeping Beauty (SB) plasmid for stable expression in T cells. HERV-K-specific CAR+T cells were selectively propagated ex vivo on artificial antigen presenting cells (aAPC) using an approach already in our clinical trials. Indeed, after genetic modification of T cells and selection on HERV-K+ aAPC, over 95% of propagated T cells stably expressed the introduced HERV-K-specific CAR and exhibited redirected specificity for HERV-K+ melanoma (Figure 1). Further, the adoptive transfer of HERV-K-specific CAR+T cells killed metastatic melanoma in a mouse xenograph model. While we have chosen melanoma as our tumor model, this study has the potential to be applied to other malignancies, including lymphoma and myeloma due to restricted expression of HERV-K envelope (env) protein on these tumor cells. These data demonstrate that it is feasible to generate T cells expressing a HERV-K-specific CAR using a clinically-appealing approach as a treatment strategy for HERV-K env+ tumors. Disclosures: No relevant conflicts of interest to declare.

scholarly journals New Generation Chimeric Antigen Receptor T-Cell Therapy (CoupledCAR) Induces High Rate Remissions in Solid Tumor

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 4631-4631
Author(s):  
Lei Xiao
Keyword(s):  
Clinical Trials ◽  
T Cells ◽  
Thyroid Cancer ◽  
T Cell ◽  
Cell Therapy ◽  
Solid Tumors ◽  
Tumor Cells ◽  
T Cell Therapy ◽  
Car T Cells ◽  
Car T

New Generation Chimeric Antigen Receptor T-Cell Therapy ( CoupledCAR ) Induces High Rate Remissions in Solid Tumor Yu Liu1,Song Li2,Youli Luo3,Haixia Song4,Chengfei Pu5, Zhiyuan Cao 5, Cheng Lu5,Yang Hang5,Xi Huang5,Xiaogang Shen5 ,Xiaojun Hu3 , Renbin Liu1,Xiuwen Wang2,Junjie Mao3,Shihong Wei4 ,Zhao Wu5and Lei Xiao5* 1.The Third Affiliated Hospital, SUN YAT-SEN University 2.Qilu Hospital of Shandong University 3.The Fifth Affiliated Hospital, SUN YAT-SEN University 4.Gansu Procincial Cancer Hospital 5.Innovative Cellular Therapeutics *Corresponding to: Lei Xiao, [email protected] Chimeric antigen receptor (CAR) T cell therapy made significant progress for treating blood cancer such as leukemia, lymphoma, and myeloma. However, the therapy faces many challenges, such as physical barrier, tumor microenvironment immunosuppression, tumor heterogeneity, target specificity, and cell expansion in vivo for treatment of solid tumors Conventional CAR T cell therapy showed weak CAR T expansion in patients and thus achieved no or little response for treating solid tumors. Here, we generated "CoupledCAR" T cells including an anti-TSHR CAR molecule. Compared with conventional CART cells,these "CoupledCAR" T cells successfully improved the expansion of CART cells more than 100 times and enhanced CAR T cells' migration ability, allowing the CAR T cells to resist and infiltrate the tumor microenvironment and killed tumor cells. To verify the effect of "CoupledCAR" T cells on solid tumors, we have completed several clinical trials for different solid tumors, including two patients with thyroid cancer. Immunohistochemistry (IHC) results showed that thyroid stimulating hormone receptors (TSHR) were highly expressed in thyroid cancer cells. In vitro co-culture experiments showed that TSHR CAR T cells specifically recognized and killed TSHR-positive tumor cells. Animal experiments showed that TSHR CAR T cells inhibited the proliferation of TSHR-positive tumor cells. Therefore, we designed "CoupledCAR" T cells expressing a binding domain against TSHR. Further,we did clinical trials of two group patients that were successfully treated using conventional TSHR CAR T cells and the "CoupledCAR" T cells, respectively. In the first group using conventional TSHR CAR T cells, patients showed weak cell expansion and less migration ability. In the group using TSHR "CoupledCAR" T cells, patients showed rapid expansion of CAR T cells and killing of tumor cells. One month after infusion (M1), the patient was evaluated as PR(Partial Response): the lymph node metastasis disappeared, and thoracic paratracheal tumors decreased significantly. Three months after infusion (M3), the patient was evaluated as a durable response, and the tumor tissue was substantially smaller than M1. Further, two patients with colonrectal cancer were enrolled in this trial and infused "CoupledCAR" T cells. One patient achieved PR and the other one achieved SD (Stable Disease). Therefore, "CoupledCAR" T cells can effectively promote expansion, migration and killing ability of CAR T cells in patients with thyroid cancer. "CoupledCAR" T cell technology is a technological platform, which may be used to treat other cancer types. Next, we are recruiting more patients with solid tumors in clinical trials using "CoupledCAR" T cells. Disclosures No relevant conflicts of interest to declare.

Synergistic Antitumor Effects of Chimeric Antigen Receptor-Modified T Cells and Oncolytic Virotherapy

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 5808-5808 ◽  
Author(s):  
Xingbing Wang ◽  
Stephen Gottschalk ◽  
Xiao-Tong Song
Keyword(s):  
T Cells ◽  
Vaccinia Virus ◽  
Tumor Cells ◽  
Chimeric Antigen Receptor ◽  
Conflicts Of Interest ◽  
Synergistic Effects ◽  
Antigen Receptor ◽  
Antitumor Effects ◽  
Car T Cells ◽  
Car T

Abstract Oncolytic vaccinia virus (VV) therapy has shown promise in preclinical models and in clinical studies. However their use has been limited by constraints on delivery and effective tumor targeting. The combination of VV therapy with Chimeric Antigen Receptor-modified T cells (CAR-T cells) might overcome these limitations, since CAR-T cells can direct VV to the tumors. In our previous studies, we have developed a novel T-cell Engager Armed Vaccinia Virus (TEA-VVs) strategy that expresses secretory bispecific antibodies that bind both to CD3 and a tumor cell surface antigen EphA2. We demonstrated that EphA2-TEA-VV displays significantly enhanced antitumor activity by inducing bystander killing of tumor cells that are not infected with virus, compared to non-modified VV. In this study, we aimed to evaluate the efficacy of combination therapy of HER2-CAR-T cells with EphA2-TEA-VV. This combinational therapy should exerts its anti-tumor activity through three mechanisms: i) HER2-CAR-T cells recognize and lyse HER2-positive tumor cells, ii) VV infect, replicate in, and lyse tumor cells, and iii) bi-specific antibody expressed by EphA2-TEA-VV directs T cells to recognize EphA2 and kill tumor cells, overcoming tumor heterogeneity. In our preliminary studies, we demonstrated that EphA2-TEA-VV can effectively infect and replicated in HER2-CAR-T cells. In coculture assays, preinfectin of HER2-CAR-T cells with EphA2-TEA-VV resulted in strongly enhanced killing of HER2+EphA2+ A549 tumor cells. These results illustrate the potential of combining CAR-T cells and TEA-VV for synergistic effects that more effectively treat cancer.  Disclosures No relevant conflicts of interest to declare.

IL-7 as a Membrane-Bound Molecule for the Costimulation of Tumor-Specific T Cells.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3035-3035 ◽  
Author(s):  
Lenka V. Hurton ◽  
Harjeet Singh ◽  
Simon Olivares ◽  
Sonny O. Ang ◽  
Susan Staba Kelly ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Conflicts Of Interest ◽  
Therapeutic Potential ◽  
Sleeping Beauty ◽  
Specific Lysis ◽  
Car T Cells ◽  
Car T ◽  
Membrane Bound

Abstract Abstract 3035 Poster Board II-1011 Redirecting specificity to a selected cell surface tumor-associated antigen can be accomplished by the genetic modification of T cells to express a chimeric antigen receptor (CAR). Despite systematic modifications to the CAR endodomains to provide T cells with competent signaling, CAR-dependent T-cell activation may remain incomplete resulting in inferior in vivo persistence leading to a suboptimal therapeutic response. To improve T-cell survival and therefore an anti-tumor response, investigators have co-infused soluble recombinant cytokines such as IL-2 and IL-7. IL-7 is a homeostatic cytokine for T cells and supports survival of memory T cells. To provide IL-7 mediated signaling to T cells in the tumor microenvironment and thus enhance the proliferation and survival of CAR+ T cells, we constructed a version of IL-7 as a novel membrane-bound molecule (mIL7) designed to stimulate T cells in cis and trans. The mIL7 construct was electro-transferred with a CD19-specific CAR (on day 0) into primary T cells via multiple transposition of Sleeping Beauty DNA plasmids. These genetically modified T cells could be numerically expanded ex vivo without additional soluble cytokine supplementation on CD19+ artificial antigen presenting cells (aAPC) derived from K562. This resulted in the preferential outgrowth of T cells expressing both mIL7 and CAR (Figure A and B) while CAR+ T cells receiving no soluble cytokine supplementation did not sustain proliferation (Figure B). These mIL7+CAR+ T cells exhibited redirected specific lysis of CD19+ tumor targets. Significantly, the kinetics of propagation of mIL7+CAR+ T cells in the absence of exogenous cytokine was comparable to CAR+ T cells that were numerically expanded in the presence of soluble IL-2. Signaling by IL-7 receptor signal induction in mIL7+CAR+ T cells appeared comparable to signaling by soluble IL-7 in CAR+ T cells, as assessed by phosphorylation of signal transducer and activator of transcription 5 (STAT5). These data demonstrate that mIL7 can be expressed by CAR+ tumor-redirected T cells to enhance their proliferation without the need for additional cytokine support. These results have implications for the design of clinical trials to evaluate whether mIL7+CAR+ T cells can exhibit enhanced persistence and thus improved therapeutic potential. Disclosures No relevant conflicts of interest to declare.

scholarly journals CD19 CAR-T Cells Treatment Conferred a Sustained Remission in Patients with Chemotherapy-Refractory MRD in B-ALL

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 48-48
Author(s):  
Wenyi Lu ◽  
Yunxiong Wei ◽  
Yaqing Cao ◽  
Xia Xiao ◽  
Qing Li ◽  
...  
Keyword(s):  
Clinical Trials ◽  
T Cells ◽  
Conflicts Of Interest ◽  
Residual Disease ◽  
Lymphoblastic Leukemia ◽  
Sustained Remission ◽  
Car T Cells ◽  
Car T ◽  
Duration Of Response ◽  
Cell Acute Lymphoblastic Leukemia

Background: The persistence or recurrence of minimal residual disease (MRD) after chemotherapy predicts relapse of B-cell acute lymphoblastic leukemia (B-ALL). CD19-directed chimeric antigen receptor-modified T (CD19 CAR-T) cells have shown excitable response in B-ALL. Recently, some studies have shown that ALL patients with lower burden had higher CR rate and lower risk of CRS after CAR-T therapy (Park, et al, NEJM. 2018; 378(5):439-448. Lee, et al, Blood.128 (22):Abstract 218.). However, its role in chemotherapy-refractory MRD-positive B-ALL remains unclear. Here we aimed to assess the effectiveness and safety of CD19 CAR-T in MRD-positive B-ALL patients. Methods: Since January 2018, a total of 14 B-ALL patients with persistent (n=8) or recurrent (n=6) MRD were enrolled in the CAR-T clinical trials (ChiCTR-ONN- 16009862 and ChiCTR1800015164). The patients were from two different clinical trials about CAR-T. If patients were treated in an MRD positive state, they would be included in this analysis. All the patients received one or more infusions of autogenous CD19 CAR-T. Results: Median age was 37.5 (13-62) years and 7 patients were female. The median dose of infused CAR-T cells was 6.78´106cells/kg, and 5 patients received more than one infusion. After one cycle of CAR-T infusion, 12 patients achieved MRD-negative remission, leading a response rate of 85.7%. Of the subgroup of 5 Ph-positive patients who subsequently underwent transplantation, 2 patients died due to transplant-related toxic effects, whereas the other 3 patients all currently alive without leukemia. Of the subgroup of 9 Ph-negative patients, 8 patients did not undergo subsequent transplantation (Figure 1). Three patients finally suffered CD19-positive relapse and 1 patient suffered CD19-negative relapse. Importantly, 4 patients (50%) are in ongoing molecular remission without transplantation, with a duration of response averaging 22.9 months (range: 12.1-28.6 months). The most frequent adverse events were fever and hematopoietic toxicities. Ten patients (71.4%) had grade 1 or 2 cytokine release syndrome (CRS) and no patients died of CRS. At a median follow-up time of 599.5 days (range: 172-915 days), the probability of 2-year relapse-free survival and 2-year overall survival was 61.2%±14.0% and 78.6%±11.0%, respectively. Conclusion: In conclusion, pre-emptive CD19 CAR-T treatment is an effective and safe approach and may confer a sustained remission in B-ALL patients with chemotherapy-refractory MRD. Disclosures No relevant conflicts of interest to declare.

scholarly journals 121 ICAM-1-specific affinity tuned CAR T cells expressing SSTR2 for real-time imaging

2021 ◽  
Vol 9 (Suppl 3) ◽  
pp. A130-A130
Author(s):  
Jingmei Hsu ◽  
Eric von Hofe ◽  
Michael Hsu ◽  
Koen Van Besien ◽  
Thomas Fahey ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Phase I ◽  
Tumor Cells ◽  
Somatostatin Receptor ◽  
Laboratory Animals ◽  
Therapeutic Window ◽  
Car T Cells ◽  
Car T

BackgroundThe use of CAR T cells for solid tumors has a number of challenges, such as lack of tumor-specific targets, CAR T cell exhaustion, and the immunosuppressive tumor microenvironment. To address these challenges, AffyImmune has developed technologies to affinity tune and track CAR T cells in patients. The targeting moiety is affinity tuned to preferentially bind to tumor cells overexpressing the target while leaving normal cells with low basal levels untouched, thereby increasing the therapeutic window and allowing for more physiological T cell killing. The CAR T cells are designed to express SSTR2 (somatostatin receptor 2), which allows for the tracking of CAR T cells in vivo via PET/CT scan using FDA-approved DOTATATE.MethodsAIC100 was generated by affinity tuning the I-domain of LFA-1, the physiological ligand to ICAM-1. Various mutants with 106-fold difference in affinity were evaluated for affinity. This allowed structure activity relationships to be conducted using CAR T cells expressing the various affinity mutants against targets with varying antigen densities. The variant with micromolar affinity was clearly the most effective in non-clinical animal models. AIC100 is currently being evaluated to assess safety, CAR T expansion, tumor localization, and preliminary activity in patients with advanced thyroid cancer in a phase I study (NCT04420754). Our study uses a modified toxicity probability interval design with three dosage groups of 10 x 106, 100 x 106, and 500 x 106 cells.ResultsPreclinical studies demonstrated greater in vivo anti-tumor activity and safety with lower affinity CAR T cells. A single dose of AIC100 resulted in tumor elimination and significantly improved survival of animals. AIC100 activity was confirmed in other high ICAM-1 tumor models including breast, gastric, and multiple myeloma. In a Phase I patient given 10-million CAR T cells, near synchronous imaging of FDG and DOTATATE revealed preliminary evidence of transient CAR T expansion and tumor reduction at multiple tumor lesions, with the peak of CAR T density coinciding with the spike in CAR T numbers in blood.ConclusionsWe have developed affinity tuned CAR T cells designed to selectively target ICAM-1 overexpressing tumor cells and to spatiotemporally image CAR T cells. Near-synchronous FDG and DOTATATE scans will enhance patient safety by early detection of off-tumor CAR T activity and validation of tumor response. We anticipate that our ‘tune and track’ technology will be widely applicable to developing potent yet safe CAR T cells against hard-to-treat solid cancers.Trial RegistrationNCT04420754Ethics ApprovalIRB number19-12021154IACUC (animal welfare): All animal experiments were performed in accordance with the National Institute of Health’s Guide for the Care and Use of Laboratory Animals. Animal handling protocols were approved by the Institutional Laboratory Animal Use and Care Committee of Weill Cornell Medicine (Permit Number: 2012–0063).

scholarly journals Safety and Efficacy of Anti-Bcma CAR-T Cells for Relapsed/Refractory Multiple Myeloma: A Systematic Review of Literature

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 5-6
Author(s):  
Israr Khan ◽  
Abdul Rafae ◽  
Anum Javaid ◽  
Zahoor Ahmed ◽  
Haifza Abeera Qadeer ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Multiple Myeloma ◽  
Clinical Trials ◽  
T Cells ◽  
Partial Response ◽  
Residual Disease ◽  
Safety And Efficacy ◽  
Refractory Multiple Myeloma ◽  
Car T Cells ◽  
Car T

Background: Multiple myeloma (MM) is a plasma cell disorder and demonstrates overexpression of B cell maturation antigen (BCMA). Our objective is to evaluate the safety and efficacy of chimeric antigen receptor T cells (CAR-T) against BCMA in patients with relapsed/refractory multiple myeloma (RRMM). Methods: We conducted a systematic literature search using PubMed, Cochrane, Clinicaltrials.gov, and Embase databases. We also searched for data from society meetings. A total of 935 articles were identified, and 610 were screened for relevance. Results: Data from thirty-one original studies with a total of 871 patients (pts) were included based on defined eligibility criteria, see Table 1. Hu et al. reported an overall response rate (ORR) of 100% in 33 pts treated with BCMA CAR-T cells including 21 complete response (CR), 7 very good partial response (VGPR), 4 partial response (PR). Moreover, 32 pts achieved minimal residual disease (MRD) negative status. Chen et al. reported ORR of 88%, 14% CR, 6% VGPR, and 82% MRD negative status with BCMA CAR-T therapy in 17 RRMM pts. In another clinical trial by Han et al. BCMA CAR-T therapy demonstrated an ORR of 100% among 7 evaluable pts with 43% pts having ≥ CR and 14% VGPR. An ORR of 100% with 64% stringent CR (sCR) and 36% VGPR was reported with novel anti-BCMA CART cells (CT103A). Similarly, Li et al. reported ORR of 87.5%, sCR of 50%, VGPR 12.5%, and PR 25% in 16 pts. BCMA targeting agent, JNJ-4528, showed ORR of 91%, including 4sCR, 2CR, 10MRD, and 7VGPR. CAR-T- bb2121 demonstrated ORR of 85%, sCR 36%, CR 9%, VGPR 57%, and MRD negativity of 100% (among 16 responsive pts). GSK2857916, a BCMA targeting CAR-T cells yielded ORR of 60% in both clinical trials. Three studies utilizing bispecific CART cells targeting both BCMA & CD38 (LCARB38M) reported by Zhao et al., Wang et al., and Fan et al. showed ORR of 88%, 88%, & 100% respectively. Topp et al. reported ORR of 31% along with 5 ≥CR and 5 MRD negative status in 42 pts treated with Bi T-cells Engager BiTE® Ab BCMA targeting antigen (AMG420). One clinical trial presented AUTO2 CART cells therapy against BCMA with an ORR of 43%, VGPR of 14%, and PR of 28%. CT053CAR-BCMA showed 14sCR and 5CR with a collective ORR of 87.5% and MRD negative status of 85% in 24 and 20 evaluable pts, respectively. Likewise, Mikkilineni et al. reported an ORR of 83%, sCR of 16.7%, and VGPR & PR of 25% and 41% in 12 pts treated with FHVH-BCMA T cells. Similar results are also reported in other clinical trials of BCMA targeting CART therapy (Table 1). The most common adverse effects exhibited were grade 1-3 hematologic (cytopenia) and cytokine release syndrome (CRS) (mostly reversible with tocilizumab). Conclusion: Initial data from ongoing clinical trials using BCMA targeting CAR-T therapy have yielded promising results both in terms of improved outcome and tolerable toxicity profiles. Although two phase 3 trails are ongoing, additional data is warranted to further ensure the safety and efficacy of anti-BCMA CAR-T cells therapy in pts with RRMM for future use. Disclosures Anwer: Incyte, Seattle Genetics, Acetylon Pharmaceuticals, AbbVie Pharma, Astellas Pharma, Celegene, Millennium Pharmaceuticals.: Honoraria, Research Funding, Speakers Bureau.

scholarly journals Sustained B cell depletion by CD19-targeted CAR T cells is a highly effective treatment for murine lupus

2019 ◽  
Vol 11 (482) ◽  
pp. eaav1648 ◽  
Author(s):  
Rita Kansal ◽  
Noah Richardson ◽  
Indira Neeli ◽  
Saleem Khawaja ◽  
Damian Chamberlain ◽  
...  
Keyword(s):  
Clinical Trials ◽  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Depletion ◽  
B Cell Depletion ◽  
Murine Lupus ◽  
Car T Cells ◽  
Car T

The failure of anti-CD20 antibody (Rituximab) as therapy for lupus may be attributed to the transient and incomplete B cell depletion achieved in clinical trials. Here, using an alternative approach, we report that complete and sustained CD19+ B cell depletion is a highly effective therapy in lupus models. CD8+ T cells expressing CD19-targeted chimeric antigen receptors (CARs) persistently depleted CD19+ B cells, eliminated autoantibody production, reversed disease manifestations in target organs, and extended life spans well beyond normal in the (NZB × NZW) F1 and MRLfas/fas mouse models of lupus. CAR T cells were active for 1 year in vivo and were enriched in the CD44+CD62L+ T cell subset. Adoptively transferred splenic T cells from CAR T cell–treated mice depleted CD19+ B cells and reduced disease in naive autoimmune mice, indicating that disease control was cell-mediated. Sustained B cell depletion with CD19-targeted CAR T cell immunotherapy is a stable and effective strategy to treat murine lupus, and its effectiveness should be explored in clinical trials for lupus.

Abstract 6591: Antibody-based redirection of meditope-CAR T cells selectively kill antigen bearing tumor cells

2020 ◽  
Author(s):  
Yi-Chiu Kuo ◽  
Jeremy D. King ◽  
Cheng-Fu Kuo ◽  
Victor Kenyon ◽  
Miso Park ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Cells ◽  
Car T Cells ◽  
Car T

scholarly journals CHIMERIC ANTIGEN RECEPTOR FOR CHRONIC LYMPHOCYTIC LEUKEMIA - A REVIEW

2019 ◽  
Vol 12 (1) ◽  
pp. 62
Author(s):  
Kiruthiga Raghunathan ◽  
Brindha Devi P
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Radiation Therapy ◽  
Chronic Lymphocytic Leukemia ◽  
Tumor Cells ◽  
Chimeric Antigen Receptor ◽  
Lymphocytic Leukemia ◽  
Normal Cells ◽  
Car T Cells ◽  
Car T

Chronic lymphocytic leukemia cancer is a deadly one which affects the bone marrow from making it to produce more amounts of white blood cells in the humans. This disease can be treated either by radiation therapy, bone marrow transplantation, chemotherapy, or immunotherapy. In radiation therapy, the ionizing radiation is used toward the tumor cells, but the main drawback is the radiation may affect the normal cells as well. To overcome this drawback, immunotherapy chimeric antigen receptor (CAR) is used. These CAR cells will target only the antigen of the tumor cells and not damage the normal cells in the body. In this therapy, the T-cells are taken either from the patients or a healthy donor and are engineered to express the CARs which are called as CAR-T-cells. When these CAR-T-cells come in contact with the antigen present on the surface of the tumor cells, they will get activated and become toxic to the tumor cells. This new class of therapy is having a great prospect in cancer immunotherapy.

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