Cancer Forums and News by PhD's


News | Forums Register

Go Back   Cancer Forums and News by PhD's > Leukemia Forum

Reply
 
Thread Tools Display Modes
  #1  
Old 07-30-2013, 02:26 PM
gdpawel gdpawel is offline
Moderator
 
Join Date: Feb 2007
Location: Pennsylvania
Posts: 4,354
Default The Promise of T-Cell Immunotherapy

For patients with leukemia who have failed multiple therapies and experienced numerous recurrences, alternative options are limited and extended survival is unlikely.

However, recent research into a new form of immunotherapy for leukemia has shown great promise in battling, and in some cases curing, the disease in these patients with a poor prognosis (< 20% chance of survival).1

Investigators at the Seattle Children's Hospital opened a phase 1 clinical trial in December 2012, which recruited patients who had relapsed acute lymphoblastic leukemia (ALL) and were not responding to chemotherapy. In this study, patients were given genetically modified T cells—taken from their own blood— that had been reprogrammed to recognize and destroy leukemic cells.

“The reprogrammed T cells are genetically modified to zero in on the cancer cells and attack only those cells just like they would get rid of a viral infection,” said Michael Jensen, MD, Director of the Ben Towne Center for Childhood Cancer Research at Seattle Children's Research Institute.

What is, in essence, a genetically modified form of the HIV virus that can seek out and attack only cancer cells, leaves healthy cells untouched—meaning the patient can avoid side effects that often come with traditional chemotherapy and radiation treatment, such as anemia, alopecia, and nausea.1 At this stage, the trial seeks to determine the dose range that is tolerable for patients, as well as any potential toxicities of the treatment.

According to available research, a patient can expect to experience flu-like symptoms over a few weeks upon receiving the modified T cells, which is caused by cytokines produced by the T cells. These symptoms can be readily managed and may serve as a good indication that the cancer is being attacked.2

“It is our hope as we develop and refine this targeted form of immunotherapy we can become less reliant on chemotherapy and radiation therapy that often cause lifelong debilitating side effects,” Dr. Jensen added.

In fact, the first adult patient recruited on the study, a 23-year-old female with ALL, has already responded to the cellular immunotherapy. “Results show that [the patient] has had a positive response to the T-cell therapy and, at this time, we do not detect any leukemia cells,” said Rebecca Gardner, MD, Principal Investigator for the clinical trial. The next step for the patient will be a stem-cell transplant to remove any trace of cancer from her body.3

Last year, a 7-year-old patient with ALL went into complete remission 3 weeks after receiving the same type of T-cell immunotherapy (CTL019 therapy) at the University of Pennsylvania. After 11 months of follow-up, she was still disease-free, and the cancer fighting T cells remained in her body, albeit at lower levels. The pediatric trial in which this patient participated is still ongoing, but initial results released online in March 2013 revealed that CTL019 therapy could, in the near future, be an effective therapy for many patients with B cell cancers, including those with an aggressive, advanced form of the disease. 4

So what is the future for this type of targeted immunotherapy? Initial results seen in a small number of patients treated with T-cell therapy are certainly promising, but more research is needed to evaluate the response of this form of immunotherapy in other hematologic malignancies and in different patient populations. It is also important to continue to assess safety and toxicity levels associated with treatment to ensure that patients' quality of life is not compromised. Studies are still underway and clinicians at The University of Pennsylvania also plan to test the therapy on other forms of cancer, including mesothelioma, as well as ovarian and pancreatic cancer, which are notoriously difficult to treat.2

It is crucial that healthcare professionals continue to enroll their patients into these clinical trials in order to gather and analyze more detailed data. If the initial results can be duplicated in additional patients and with other cancers, the live-saving potential of this new therapy could be staggering.

References

1. Seattle Children's Hospital Website. One Step Closer to a Cure for Leukemia without Chemotherapy or Radiation.

[url]http://pulse.seattlechildrens.org/one-step-closer-to-a-cure-for-leukemia-without-chemotherapy-or-radiation.

2. HIV Used to Fight Cancer.

[url]http://news.discovery.com/human/health/hiv-used-to-fight-cancer-110914.htm.

3. Seattle Children's Hospital Website. Seattle Children's patient has positive response to new cancer treatment.

[url]http://pulse.seattlechildrens.org/seattle-childrens-patient-has-positive-response-to-new-cancer-treatment.

4. Grupp SA, Kalos M, Barrett D, et al. Chimeric Antigen Receptor–Modified T Cells for Acute Lymphoid Leukemia. N Engl J Med 2013; Apr 18;368(16):1509-18.

5. The Children's Hospital of Philadelphia Website. First Pediatric Patients Treated in T cell therapy Clinical Trial (CTL019, formerly CART19).

[url]http://www.chop.edu/service/oncology/pediatric-cancer-research/t-cell-therapy.html.

Citation: Chemotherapy Advisor "Harnessing the Power of HIV to Kill Cancer" July 24, 2013
__________________
Gregory D. Pawelski
Reply With Quote
  #2  
Old 07-30-2013, 02:27 PM
gdpawel gdpawel is offline
Moderator
 
Join Date: Feb 2007
Location: Pennsylvania
Posts: 4,354
Default More Promise With Immunotherapy in Pediatric Leukemia

T-cells, one of the centerpieces of the immune system, can be genetically engineered to attack leukemia in children, according to research presented here at the American Association for Cancer Research (AACR) 104th Annual Meeting.

The immunotherapy, known as anti-CD19 chimeric antigen receptor (CAR) T-cell therapy, puts a patient's own immune cells through a laboratory process that results in the number of T-cells being greatly expanded, "fully activated," and then reinfused, explained Daniel W. Lee, MD, from the Pediatric Oncology Branch of the National Cancer Institute.

"Anti-CD19 CAR T-cell therapy is a completely new way to attack childhood leukemia," Dr. Lee told reporters at a meeting press briefing.

In a phase 1 trial, the experimental therapy demonstrated antileukemia activity in 3 of 3 children with acute lymphocytic leukemia (ALL).

A 13-year-old boy, who had relapsed after bone marrow transplantation, had a complete response that lasted several months.

A 16-year-old girl, who had also relapsed after bone marrow transplantation, had an early transient complete response, but is not yet fully evaluable.

Surprisingly, an 11-year-old girl, who had not undergone transplantation, had never been in remission, and was refractory to all treatment, including chemotherapy, had a complete response. "Hopefully, it will be curative for her," said Dr. Lee. The response allowed the girl to return to her primary oncologist for bone marrow transplantation, he noted.

"Anti-CD19 CAR T-cell therapy can induce complete remission even when chemotherapy cannot," said Dr. Lee.

A fourth patient, a 10-year-old girl with B-cell lymphoma who had relapsed after bone marrow transplantation, did not respond to the new therapy and has had progressive disease.

Dr. Lee described the 11-day treatment process his team used. Researchers collected T-cells from the patient and modified them in the laboratory so that they attach to a protein (CD19) expressed by the ALL cells and attack the cancers. The number of modified T-cells — or anti-CD19 CAR T-cells — was expanded in the laboratory to counts of up to 1 million/kg; they were then returned to the patient. All patients were pretreated with fludarabine and cyclophosphamide prior to receiving the CAR-transduced T-cells.

The treatment was well tolerated and adverse effects were manageable; so far, there has been no evidence of graft-vs-host disease, Dr. Lee reported.

"Autologous collected anti-CD19 CAR T-cell therapy is a reasonable and potentially effective strategy," Dr. Lee and colleagues conclude in their abstract.

"This is a very hot area [in cancer research] — using chimeric antigen receptor T-cells," said press-briefing moderator Louis Weiner, MD, from the Georgetown Lombardi Comprehensive Cancer Center in Washington, DC. He was not involved in the research.

CAR-modified T-cells targeting CD19 have also been effective in adults with B-cell lymphomas and chronic lymphocytic leukemia, Dr. Lee and his colleagues note.

In a recent report of 2 children with relapsed chemotherapy-refractive ALL from the Children's Hospital of Philadelphia in Pennsylvania, CAR-modified T-cells produced complete remission, as reported by Medscape Medical News (N Engl J Med. Published online March 25, 2013).

However, in meeting press materials, Dr. Lee suggested that the process developed at the National Cancer Institute is superior in terms of timing.

"We wanted something that could be done in a more timely manner. We decided to collect the immune cells, which are called T-cells, directly from the patients, even though they'd had bone marrow transplants," he explained.

Given all of the advances in pediatric and adult cancers, Dr. Weiner proclaimed that immunotherapy should now be recognized as the "fourth modality" for cancer, along with chemotherapy, radiation, and surgery.

Immunotherapies, especially monoclonal antibodies, represent "the fulfillment of a century-long dream first had by Dr. Paul Ehrlich in the early twentieth century about creating so-called magic bullets," Dr. Weiner noted. These kind of agents include the experimental nivolumab (GlaxoSmithKline), which was highlighted here in an AACR plenary session, as reported by Medscape Medical News.

ALL Is Leading Killer

There is a substantial need for more effective treatments in ALL, said Dr. Lee. ALL is the most common childhood malignancy. Although more than 95% of children initially diagnosed with ALL achieve remission, treatment is long (averaging 2 to 3 years), toxic, and costly, he said. Furthermore, many children relapse and, at that point, have a poor prognosis because treatment is "very limited." ALL is the leading cause of cancer death among children.

Dr. Lee and colleagues are continuing to test their method in patients whose disease has returned after, or is refractory to, standard treatments, whether or not they have undergone bone marrow transplantation.

"We think that the children who have never had a transplant might experience different toxicities," he said.

In the 4 patients treated to date, the safety profile was "acceptable," Dr. Lee said. The primary adverse effects have been fever, low blood pressure, and low blood counts. But these lasted "only a few days," he said, and they were all manageable in a hospital setting.

The study was funded by the National Cancer Institute and the St. Baldrick's Foundation. Dr. Weiner reports financial relationships with a number of pharmaceutical companies.

American Association for Cancer Research (AACR) 104th Annual Meeting: Abstract LB-138. Presented April 8, 2013.

Citation: More Promise With Immunotherapy in Pediatric Leukemia. Medscape. Apr 16, 2013.

CAR T Cells: A Look Under the Hood and Down the Road

[url]http://www.medscape.com/viewarticle/831551
__________________
Gregory D. Pawelski

Last edited by gdpawel : 09-16-2014 at 09:36 PM. Reason: Add url address
Reply With Quote
  #3  
Old 04-17-2014, 05:42 PM
gdpawel gdpawel is offline
Moderator
 
Join Date: Feb 2007
Location: Pennsylvania
Posts: 4,354
Default Immunotherapy: A prematurely-abandoned treatment option

Larry Weisenthal, M.D., PhD.
Medical and Lab Director
Weisenthal Cancer Group; Huntington Beach, CA

Clinical trials are warranted to test macrophage-activating biologic response modifiers administered following chemotherapy of ovarian and breast cancers. This is based on (1) striking in vitro findings in fresh human tumor cell culture assays, (2) supportive data from pilot clinical trials, and (3) a sound mechanistic rationale. I would advocate sequential administration of (1) assay-directed chemotherapy, (2) "non-specific" immunotherapy (e.g. antigens derived from bacteria), and (3) more "specific" cytokine therapy (e.g. interferon gamma).

In 1991, my colleagues and I published a study (1,2) in the Journal of the National Cancer Institute which I hoped would receive scrutiny and follow-up. This was a tumor immunology study which grew out of a contract research project. Continuing this research was at the time not an option, as my priorities were to establish a clinical laboratory to provide cell culture drug resistance testing.

In the 1991 study, we presented the concept of "in situ vaccination," based upon our studies of biologic response modifiers in the DISC assay. We found that there was a striking association between the activity of biologic response modifiers which activate macrophages and the prior treatment status of patients with breast and ovarian cancers. Color photomicrographs illustrating method.

[url]http://weisenthal.org/jnci83_38_91f1.jpg

The following agents were dramatically more active in fresh tumor specimens from previously-treated breast and ovarian cancer patients than against specimens from untreated patients:

1. ImuVert (a potent macrophage activator derived from Serratia marcescens)
2. Interferon gamma, and
3. Tumor necrosis factor

This greater activity in specimens from treated versus non-treated patients was not observed in adenocarcinomas known to be relatively resistant to chemotherapy (colon cancer, non-small cell lung cancer, etc.). Graphs showing representative results.

[url]http://weisenthal.org/jnci83_39_91.jpg

This differential activity was also not observed in agents which are not potent macrophage activators (interleukin-2 and interferon alpha).

Based on these findings (and supported by anecdotal studies in the clinical trials literature), we proposed that effective chemotherapy produces massive release and processing of tumor antigens, which leads to a state in which the human immune system is primed (via "in situ vaccination") to respond to exogenous macrophage-activation signals with potent, specific antitumor effects.

In the above-quoted study (1), I reviewed a diverse clinical trials literature which supported this concept. More recently published was a randomized trial in previously untreated ovarian cancer (3) , in which cisplatin/cyclophosphamide was compared to the same chemotherapy plus interferon gamma, administered subcutaneously three times a week, every other week, for the duration of chemotherapy (6 plannned treatment cycles). The study was prematurely closed because chemotherapy standard treatment had changed from platinum/cyclophosphamide to platinum/Taxol, but, even with the low power of the small numbers of patients accrued to show a difference, there was a significant advantage to combined treatment in progression-free survival and a soft trend for improved overall survival. The authors quoted our earlier work1 in providing a mechanism for their positive results and called for follow-up clinical trials. Progression-free survival curves.

[url]http://weisenthal.org/bjc82_1138_00.jpg

As noted above, my preferred trial design would be (1) first complete (preferably assay-directed) chemotherapy, then (2) administer non-specific immunotherapy to responders, then (3) provide more specific cytokine therapy, e.g. interferon gamma.

Literature Citation:

1. Weisenthal LM, Dill PL, Pearson FC (1991) Effect of prior cancer chemotherapy on human tumor-specific cytotoxicity in vitro in response to immunopotentiating biologic response modifiers. J Natl Cancer Inst 83: 37-42

2. Weisenthal LM (1991) Effect of prior chemotherapy on biologic response modifier activity. J Natl Cancer Inst 83: 790-791

3. Windbichler GH, Hausmaninger H, Stummvoll W, Graf AH, et al. (2000) Interferon-gamma in the first-line therapy of ovarian cancer: a randomized phase 3 trial. Br J Cancer 82:1138-1144, 2000.

Method for detecting immune-mediated cytotoxicity

ABSTRACT

A method for detecting the sensitivity of tumor cells to immune effector substances by using an assay that distinguishes living tumor cells from dead cells in mixed populations of cells. Acquired resistance to immune effectors used in therapy may be determined and used to identify methods to circumvent such resistance using the method.

[url]http://www.google.com/patents/US4996145
__________________
Gregory D. Pawelski
Reply With Quote
Sponsored Links
Advertisement
  #4  
Old 10-16-2014, 06:37 PM
gdpawel gdpawel is offline
Moderator
 
Join Date: Feb 2007
Location: Pennsylvania
Posts: 4,354
Default Chimeric Antigen Receptor T Cells for Sustained Remissions in Leukemia

Shannon L. Maude, M.D., Ph.D., Noelle Frey, M.D., Pamela A. Shaw, Ph.D., Richard Aplenc, M.D., Ph.D., David M. Barrett, M.D., Ph.D., Nancy J. Bunin, M.D., Anne Chew, Ph.D., Vanessa E. Gonzalez, M.B.A., Zhaohui Zheng, M.S., Simon F. Lacey, Ph.D., Yolanda D. Mahnke, Ph.D., Jan J. Melenhorst, Ph.D., Susan R. Rheingold, M.D., Angela Shen, M.D., David T. Teachey, M.D., Bruce L. Levine, Ph.D., Carl H. June, M.D., David L. Porter, M.D., and Stephan A. Grupp, M.D., Ph.D.

N Engl J Med 2014; 371:1507-1517October 16, 2014DOI:10.1056/NEJMoa1407222

BACKGROUND

Relapsed acute lymphoblastic leukemia (ALL) is difficult to treat despite the availability of aggressive therapies. Chimeric antigen receptor–modified T cells targeting CD19 may overcome many limitations of conventional therapies and induce remission in patients with refractory disease.

METHODS

We infused autologous T cells transduced with a CD19-directed chimeric antigen receptor (CTL019) lentiviral vector in patients with relapsed or refractory ALL at doses of 0.76×106 to 20.6×106 CTL019 cells per kilogram of body weight. Patients were monitored for a response, toxic effects, and the expansion and persistence of circulating CTL019 T cells.

RESULTS

A total of 30 children and adults received CTL019. Complete remission was achieved in 27 patients (90%), including 2 patients with blinatumomab-refractory disease and 15 who had undergone stem-cell transplantation. CTL019 cells proliferated in vivo and were detectable in the blood, bone marrow, and cerebrospinal fluid of patients who had a response. Sustained remission was achieved with a 6-month event-free survival rate of 67% (95% confidence interval [CI], 51 to 88) and an overall survival rate of 78% (95% CI, 65 to 95). At 6 months, the probability that a patient would have persistence of CTL019 was 68% (95% CI, 50 to 92) and the probability that a patient would have relapse-free B-cell aplasia was 73% (95% CI, 57 to 94). All the patients had the cytokine-release syndrome. Severe cytokine-release syndrome, which developed in 27% of the patients, was associated with a higher disease burden before infusion and was effectively treated with the anti–interleukin-6 receptor antibody tocilizumab.

CONCLUSIONS

Chimeric antigen receptor–modified T-cell therapy against CD19 was effective in treating relapsed and refractory ALL. CTL019 was associated with a high remission rate, even among patients for whom stem-cell transplantation had failed, and durable remissions up to 24 months were observed. (Funded by Novartis and others; CART19 ClinicalTrials.gov numbers, NCT01626495 and NCT01029366.)

[url]http://www.nejm.org/doi/full/10.1056/NEJMoa1407222
__________________
Gregory D. Pawelski
Reply With Quote
  #5  
Old 02-26-2015, 09:59 PM
gdpawel gdpawel is offline
Moderator
 
Join Date: Feb 2007
Location: Pennsylvania
Posts: 4,354
Default FDA Approves New Immunotherapy for Leukemia

Alexandra Mulvey
Cancer Research Institute

The FDA approved a new immunotherapy called Blincyto (blinatumomab) for use in the treatment of B cell acute lymphoblastic leukemia (ALL). The drug, manufactured by Amgen, is the first of a novel class of agents known as bispecific T cell engagers (BiTE), which consist of essentially two monoclonal antibodies joined together. One end of the BiTE binds to a molecule on T cells, and the other end binds to a molecule on cancer cells; by bringing the two together, the BiTE facilitates cancer cell killing. Blincyto (blinatumomab) is designed to treat cancers expressing a molecule called CD19—found on the surface of B cell ALL and also non-Hodgkin’s lymphoma. The FDA approval was based on a phase II clinical trial showing that, of the 185 patients evaluated, 41.6% achieved complete remission with Blincyto.

Blinctyo was a long time in the making and depended on the work of many scientists, a number of whom were funded by the Cancer Research Institute. Gert Riethmüller, M.D., a Scientific Advisory Council member and a member of the Academy of Cancer Immunology, conducted key research that led to a patent for blinatumomab. He was also involved in the clinical testing of the drug, as was Max S. Topp, M.D., a former CRI postdoctoral fellow and now a professor at Würzburg University Hospital in Germany. Topp was the first author on the phase I publication and the phase II American Society of Clinical Oncology abstract that showed that blinatumomab has anti-leukemia activity in this difficult-to-treat population.

BiTEs like Blincyto are the latest weapon in the immunotherapeutic arsenal against cancer. Along with checkpoint blockade antibodies, vaccines, and other immunotherapies, BiTEs are helping to turn our immune system into a powerful defense against this disease. One day—and one not too far away—immunotherapies will conquer cancer. Until that day comes, the Cancer Research Institute will continue to lead the way forward.

[url]http://meetinglibrary.asco.org/content/129500-144
__________________
Gregory D. Pawelski
Reply With Quote
Sponsored Links
Advertisement
  #6  
Old 04-30-2016, 12:06 AM
gdpawel gdpawel is offline
Moderator
 
Join Date: Feb 2007
Location: Pennsylvania
Posts: 4,354
Default CD4 T-cell Immunotherapy Shows Activity in Solid Tumors

Medscape Medical News
April 18, 2016

Alexander M. Castellino, PhD.

NEW ORLEANS ― For the first time, treatment with genetically engineered T-cells has used CD4 T-cells instead of the CD8 T-cells, which are used in the chimeric antigen receptor (CAR) T-cell approach. Early data suggest that this CD4 T-cell approach has activity against solid tumors, whereas the CAR T-cell approach so far has achieved dramatic success in hematologic malignancies.

In the new approach, CD4 T-cells were genetically engineered to target MAGE-A3, a protein found on many tumor cells. The treatment was found to be safe in patients with metastatic cancers, according to data from a phase 1 clinical study presented here at the American Association for Cancer Research (AACR) 2016 Annual Meeting.

"This is the first trial testing an immunotherapy using genetically engineered CD4 T-cells," senior author Steven A. Rosenberg, MD, PhD, chief of the Surgery Branch at the National Cancer Institute (NCI), told Medscape Medical News.

Most approaches use CD8 T-cells. Although CD8 T-cells are known be cytotoxic and CD4 T-cells are normally considered helper cells, CD4 T-cells can induce tumor regression, he said.

Louis M. Weiner, MD, director of the Lombardi Comprehensive Cancer Center at Georgetown University, in Washington, DC, indicated that in contrast with CAR T-cells, these CD4 T-cells target proteins on solid tumors. "CAR T-cells are not tumor specific and do not target solid tumors," he said.

Engineering CD4 Cells

Immunotherapy with engineered CD4 T-cells was personalized for each patient whose tumors had not responded to or had recurred following treatment with least one standard therapy. The immunotherapy was specific for patients in whom a specific human leukocyte antigen (HLA) — HLA-DPB1*0401 — was found to be expressed on their cells and whose tumors expressed MAGE-A3.

MAGE-A3 belongs to a class of proteins expressed during fetal development. The expression is lost in normal adult tissue but is reexpressed on tumor cells, explained presenter Yong-Chen William Lu, PhD, a research fellow in the Surgery Branch of the NCI.

Targeting MAGE-A3 is relevant, because it is frequently expressed in a variety of cancers, such as melanoma and urothelial, esophageal, and cervical cancers, he pointed out.

Researchers purified CD4 T-cells from the peripheral blood of patients. Next, the CD4 T-cells were genetically engineered with a retrovirus carrying the T-cell receptor (TCR) gene that recognizes MAGE-A3. The modified cells were grown ex vivo and were transferred back into the patient.

Clinical Results

Dr Lu presented data for 14 patients enrolled into the study: eight patients received cell doses from 10 million to 30 billion cells, and six patients received up to 100 billion cells.

This was similar to a phase 1 dose-finding study, except the researchers were seeking to determine the maximum number of genetically engineered CD4 T-cells that a patient could safely receive.

One patient with metastatic cervical cancer, another with metastatic esophageal cancer, and a third with metastatic urothelial cancer experienced partial objective responses. At 15 months, the response is ongoing in the patient with cervical cancer; after 7 months of treatment, the response was durable in the patient with urothelial cancer; and a response lasting 4 months was reported for the patient with esophageal cancer.

Dr Lu said that a phase 2 trial has been initiated to study the clinical responses of this T-cell receptor therapy in different types of metastatic cancers.

In his discussion of the paper, Michel Sadelain, MD, of the Memorial Sloan Kettering Cancer Center, New York City, said, "Although therapy with CD4 cells has been evaluated using endogenous receptor, this is the first study using genetically engineered CD4 T-cells."

Although the study showed that therapy with genetically engineered T-cells is safe and efficacious at least in three patients, the mechanism of cytotoxicity remains unclear, Dr Sadelain indicated.

Comparison With CAR T-cells

CAR T-cells act in much the same way. CARs are chimeric antigen receptors that have an antigen-recognition domain of an antibody (the V region) and a "business end," which activates T-cells. In this case, CD8 T-cells from the patients are used to genetically engineer T-cells ex vivo. In the majority of cases, dramatic responses have been seen in hematologic malignancies.

CARs, directed against self-proteins, result in on-target, off-tumor effects, Gregory L. Beatty, MD, PhD, assistant professor of medicine at the University of Pennsylvania, in Philadelphia, indicated when he reported the first success story of CAR T-cells in a solid pancreatic cancer tumor.

Side effects of therapy with CD4 T-cells targeting MAGE-A3 were different and similar to side effects of chemotherapy, because patients received a lymphodepleting regimen of cyclophosphamide and fludabarine. Toxicities included high fever, which was experienced by the majority of patients (12/14). The fever lasted 1 to 2 weeks and was easily manageable.

High levels of the cytokine interleukin-6 (IL-6) were detected in the serum of all patients after treatment. However, the elevation in IL-6 levels was not considered to be a cytokine release syndrome, because no side effects occurred that correlated with the syndrome, Dr Liu indicated.

He also indicated that future studies are planned that will employ genetically engineered CD4 T-cells in combination with programmed cell death protein 1–blocking antibodies.

This study was funded by Intramural Research Program of the National Institutes of Health. The NCI's research and development of T-cell receptor therapy targeting MAGE-A3 are supported in part under a cooperative research and development agreement between the NCI and Kite Pharma, Inc. Kite has an exclusive, worldwide license with the NIH for intellectual property relating to retrovirally transduced HLA-DPB1*0401 and HLA A1 T-cell receptor therapy targeting MAGE-A3 antigen. Dr Lu and Dr Rosenberg have disclosed no relevant financial relationships.

American Association for Cancer Research (AACR) 2016 Annual Meeting: Abstract CT003, presented April 17, 2016.

Citation: CD4 T-cell Immunotherapy Shows Activity in Solid Tumors. Medscape. Apr 18, 2016.

[url]http://www.abstractsonline.com/Plan/ViewAbstract.aspx?mID=4017&sKey=371fa616-a0cf-4bf8-993d-ce424853b52c&cKey=ba785b1a-668f-4459-8515-8ad2fc07f2b3&mKey=1d10d749-4b6a-4ab3-bcd4-f80fb1922267
__________________
Gregory D. Pawelski
Reply With Quote
Sponsored Links
Advertisement
Reply


Thread Tools
Display Modes

Posting Rules
You may not post new threads
You may not post replies
You may not post attachments
You may not edit your posts

vB code is On
Smilies are On
[IMG] code is On
HTML code is Off
Forum Jump


All times are GMT -5. The time now is 01:10 AM.