Gene therapy trials cancer

Log in. Gene Therapy Clinical Trial Databases Wiley database on Gene Therapy Trials Worldwide The Journal of Gene Medicine clinical trial site presenting charts and tables showing the number of approved, ongoing or completed clinical trials worldwide.

A searchable database is also present with detailed information on individual trials. Beware that information on some trials is incomplete as some countries regulatory agencies simply do not disclose any information. See also: Gene therapy clinical trials worldwide to - an update. Gene Med. The database is a registry of federally and privately supported clinical trials conducted in the United States and around the world.

GeMCRIS - NIH Genetic Modification Clinical Research Information GeMCRIS allows users to access an array of information about human gene transfer trials registered with the NIH, including medical conditions under study, institutions where trials are being conducted, investigators carrying out these trials, gene products being used, route of gene product delivery, and summaries of study protocols.

In addition, the registry contains more than 16, abstracts of clinical trial protocols that have been completed or are closed to patient accrual. The information on the website is collected and entered by national medicine regulatory authorities or by the addressee of a PIP decision for trials conducted outside the European Union. They are required by European Union law to enter details of clinical trials into a database called EudraCT.

The information stored in this database is now being made publicly available through a new website, the EU Clinical Trials Register. The mammalian mitochondria are responsible for metabolic functions. Nearly of the known mutations causing metabolic diseases are secondary to disorders affecting the mitochondrial genome [ 23 ].

Several approaches have been used to transfer genes successfully into cell mitochondria. It has become apparent that the immune system is a crucial element in cancer regression or progression. There are two types of immune responses: humoral immunity and cellular immunity. Furthermore, the tumor microenvironment plays an important role in host immune effects against cancer cells [Table 1 ].

Humoral immunity is mediated by antibodies released by B-cells with a high-binding affinity to specific tumor antigens. The Food and Drug Administration in the United States FDA approved several antibodies against malignant cells, which include trastuzumab for breast cancer [ 70 ], rituximab for indolent lymphoma [ 71 ], cetuximab for lung cancer [ 72 ], and bevacizumab for various solid tumors [ 49 , 73 ], and many others [ 74 ] [Table 2 ].

Cellular immunity is mediated by cell-to-cell contact that leads to antigen recognition and cell destruction of a target cell. Based on the intensity of tumor-associated antigens TAAs on the surface of tumor cells, they are recognized by the host immune system [ 75 ].

Dendritic cells are specialized in antigen recognition as well as mediation of immune responses against infectious agents or malignant cells, through direct stimulation or inhibition of immune effector cells such as T-cells, B-cells, and natural killer NK cells [ 76 ]. Dendritic cells are derived from the bone marrow and migrate to lymph nodes and distant tissue, looking for those foreign antigens [ 49 ].

Cancer cells can evade the immune system by secreting immunosuppressive cytokines that can downregulate major histocompatibility molecules, can recruit regulatory T-cells, and can kill reactive cytotoxic lymphocytes. Thus, the tumor microenvironment is highly immunosuppressive, which allows a tumor to grow and metastasize [ 77 ]. Several efforts have been undertaken to manipulate the tumor microenvironment in order to induce tumor regression.

Most tumor cells express antigens that can mediate antitumor immune responses [ 78 ]. Earlier studies on antigens for therapeutic targeting were based on shared antigens that are expressed on self-tissue or peripheral cells, which can lead to immunologic tolerance for the interaction between antigen peptide, major histocompatibility complex MHC , and T-cell antigen receptor TCR.

Generated immunologic responses were restricted with low therapeutic efficacy [ 78 ]. Recently, it has been found that neoantigens generated by point mutation in normal genes, which are unique to particular tumors, can result in much more potent antitumor T-cell response.

Some cancers display hundreds or even thousands of mutations in coding exons, representing a large resource of potential targets for recognition by the immune system. However, despite such a plethora of antigens, most cancers progress and evade immune-system mediated destruction [ 78 ]. Antigens recognition by dendritic cells induce a T-cell inflamed reaction consisting of infiltrating T-cells, a broad chemokine profile, and type I interferon signature indicative of innate immune activation.

Recent investigations have suggested two explanations for tumor escape recognition by host immune system, based primarily on cellular and molecular characteristics of the tumor microenvironment [ 78 ]. One explanation is that tumors resist immune attacks through inhibitory effects mediated by immune system suppressive pathways. This was evident in some tumors such as melanoma with high expression of PD-LI and indoleamine-2,3-dioxygenase IDO [ 82 ], leading to T-cell anergy and dysfunction with subsequent immune escape detection [ 83 ].

The presence of transcription factor forkhead box 03 proteins Fox3 in the peritumoral microenvironment leads to the inhibition of tumor-infiltrating dendritic cell stimulatory functions [ 84 ].

Mechanism of action of monoclonal antibody ipilimumab. Generation of an immune signal requires presentation of tumor antigen by major histocompatibility complex MHC class I or II molecules, on an antigen presenting cell APC such as dendritic cell. However, T-cell activation and proliferation requires a second signal, typically generated by CD28 antigen.

Ipilimumab blocks cytotoxic T-lymphocyte antigen-4 CTLA-4 receptor, thus prevents such inhibitory effect, and allows T-cell to proliferate and mediate an immune reaction against malignant cells. Other regulatory checkpoints with the potential for modulation include the coinhibitory molecule PD-1, as well as costimulatory molecules such as OX40 and BB. Analysis of overall survival comparing monoclonal antibody ipilimumab plus dacarbazine to placebo plus dacarbazine in metastatic melanoma patients.

The survival curves reach a plateau beginning at approximately three years after initiation of treatment. Continued survival follow-up of more than four years demonstrates a long-term survival benefit that is consistent with the results of other ipilimumab studies.

The other mechanism is immune system exclusion or ignorance with subsequent poor or no T-cell inflammatory reaction. Radiations of tumors have shown to induce productions of interferon-beta and augment function of intratumoral dendritic cells with improved accumulation of T-cells leading to tumor regression [ 87 ]. Imatinib in gastrointestinal stromal cell tumors may cause down-modulation of IDO with improved antitumor response [ 88 ].

In patients with malignant melanoma, inhibition of R-Raf enzyme activity with vemurafenib can induce a T-cell infiltration within 1—2 weeks of therapy with some tumor responses [ 89 ]. It has been suggested that combination regimens consisting of strategies to improve innate immune system activation, T-cell trafficking in the tumor microenvironment, vaccination or adoptive T-cell transfer, and blockage of immune inhibitory pathways may be necessary to achieve clinical benefit in patients with a non-inflamed tumor phenotype.

Such an approach is presently being tested in clinical trials [ 90 , 91 ]. Immunotherapy in cancer can be classified into four major categories [ 92 ]. Active immunotherapy includes strategies that directly sensitize the host immune system to tumor-specific antigens, exemplified as cancer vaccines. Passive immunotherapy utilizes humanized or chimeric antibodies to specifically target tumor antigens without direct activation of the immune system.

Immune enhancement therapy aims to augment co-stimulatory molecules or block inhibitory molecules. Immune-based therapy may include one or more of the above approaches, either as distinct immunotherapy treatment, or in combination with other modalities of cancer therapy [Table 1 ]. Adoptive T-cell therapy has been shown to induce tumor regression in some patients with solid malignancies.

In a recent study on patients with human papilloma virus HPV -induced metastatic cervical cancer who failed to respond to chemotherapy and radiation, and were selected for HPV-E6 and HPV-E7 reactivity, researchers collected tumor-infiltrating T-cell lymphocytes TIL , and infused them back to patients.

This was preceded by a non-myeloablative conditioning regimen and followed by a high-dose of bolus aldesleukin interleukin Three out of six patients with HPV reactivity achieved objective tumor responses, including two patients with metastatic disease that achieved complete tumor regression for 18 and 11 months after therapy.

Side effects were minimal [ 93 ]. Host T-cell lymphocytes have been found to be successful in controlling metastatic cancer with transient side effects. The first commercially available vaccine was modified dendritic cells, sipuleucel-T Provenge Dendron Corporation , which was approved by the FDA for minimally symptomatic castration-resistant metastatic prostate cancer.

CD54 T-cell lymphocytes were obtained from the patients using density gradient centrifugation, and then activated ex vivo with a prostatic specific antigen in addition to granulocyte macrophage colony stimulating factor GM-CSF to form sipuleucel-T. Autologous activated T-cell lymphocytes, at a dose of at least fifty million CD54 cells were infused back to the patient, intravenously over 60 minutes, every two weeks for three infusions.

Premedications included acetaminophen and diphenhydramine. Side effects included transient fever, chills, fatigue, asthenia, backaches, and headaches. However, infusion-induced hypersensitivity reactions with cerebrovascular events have been reported in 3.

Compared to a control group treated with a placebo, there were significant improvements in the survival of The adoptive transfer of lymphokine-activated lymphocytes can mediate the cellular immune response against cancer cells, which may lead to tumor regression.

However, clinical trials have led to limited success. An alternative approach is to use genetically modified T-cells by altering their receptor for better recognition of tumor antigens. In such an approach, T-cells are collected from patient apheresis using density gradient centrifugation. As resting T-cell lymphocytes are non-dividing, refractory to gene therapy with lentiviral vectors, they need to be stimulated using cytokines such as interleukin T-cells are then exposed to lentiviral vectors with the attached gene for 1—2 days of gene transfer.

After transduction by the lentivirus, cells are then stimulated further to obtain a therapeutically effective number of cells. Genetically modified T-cell lymphocytes are then re-infused back into the patient [ 95 ]. The high-affinity of modified T-cells in detecting very low levels of tumor antigens is an extremely potent approach against tumor cells.

However, it may also destroy normal cells. In another study using T-cell receptor gene-modified cells against melanoma differentiated antigens led to higher responses in patients with malignant melanoma [ 96 ]. It also destroyed normal melanocytes leading to vitiligo skin depigmentation , uveitis, and hearing impairment [ 97 ]. Unfortunately, for many B-lineage leukemias and lymphomas, the resident immune system of patients remains incapable of controlling tumor growth, since autologous T-cells lack expression of the required receptors and tumor cells have adapted to evade immunological recognition [ 98 ].

It has been demonstrated that a chimeric antigen receptor CAR integrated into T-cells from patient or even from healthy individuals , can directly recognize the CD19 molecule expressed on the cell surface of B-cell malignancies independent of major histocompatibility complex [ 99 ]. Recently, CDspecific chimeric antigen receptor redirected T-lymphocytes have been utilized as gene therapy for patients with B-cell malignancies.

One approach is to use a microelectroporator to achieve high throughput non-viral gene transfer of naked DNA plasmid, of in vitro transcribed CAR mRNA into human T cells that had been numerically expanded ex vivo using interleukin Preserved T-cells can then be re-infused into patient as an effector form of adoptive immunotherapy [ 98 ] [Figure 4 ].

Similar approaches have been used against other B-lineage restricted antigens such as CD20 in lymphoma, the light chain of human immunoglobulins, or CD30 expressed by Reed-Sternberg Cells in Hodgkin lymphoma [ ]. Adding costimulatory endodomain within the chimeric receptors such as CD28, BB, or their combination, usually leads to enhancement of T-cell functions through the release of interleukin-2, interleukin-7 or interleukin cytokines [ ].

Excellent results in patients with B-cell malignancies have been reported [ — ]. CAR-modified allogeneic T-cells, such as those obtained from healthy individuals, have the potential to act as universal effector cells, which can be administered to any patient regardless of MHC type.

Such universal effector cells could be used as an 'off-the-shelf' cell-mediated treatment for cancer [ , ]. Chimeric antigen receptor modified T-lymphocyte therapy for B-cell malignancies. Generation of tumor-specific T cells by repeated antigen stimulation or genetic modification to express a tumor-targeting receptor. PBMC collected from a patient or healthy individual can be stimulated in vitro with tumor antigen at regular intervals to induce gradual enrichment of antigen-specific T cells blue.

Multiple stimulations followed by additional enrichment or expansion strategies are required to ensure sufficient antigen-specific T cells are generated. The entire process may take 2—3 months. In contrast, approaches that utilize genetic modification to redirect T cell specificity to a tumor antigen are much more rapid.

The enriched CAR-modified tumor-reactive T cells red can be infused into the patient in as little as 1—2 weeks. Dendritic cells are the most powerful antigen-presenting cells APCs for antigen identification, T-cell costimulation and cytokine production by T lymphocytes [ ]. When cultured in the presence of granulocyte-macrophage colony-stimulating factor GM-CSF plus interleukin-4, monocytes develop into immature dendritic cells in 3—5 days. Cells are then exposed to a variety of different stimuli over another 2 days in culture media to become mature dendritic cells, which are more effective in stimulating T-cells [ ].

To target a specific tumor, mature dendritic cells are incubated with certain peptides, proteins, or irradiated tumor cells. An alternative approach is genetic modification of dendritic cells through viral and non-viral gene transfer vectors, resulting in dendritic cells that are more potent in antitumor immunity.

Dendritic cell vaccines have a favorable safety profile, with toxicities limited to a local inflammatory reaction, flu-like symptoms, and vitiligo-like skin changes [ ]. Despite numerous clinical trials, clinical outcomes have been modest.

Emphasis has been shifted in using therapy on patients with a lower tumor burden, such as those after surgery, or following successful chemotherapy or radiation therapy. Indeed, significant synergy has been observed for chemotherapy and dendritic cell vaccines [ ].

Previous attempts to use tumor cells or their products as a vaccine have not been successful. Subsequently, clinical trials have been conducted using methods to increase tumor antigenicity in order to enhance the immune-mediated tumor lysis by T-cells. One approach is to obtain tumor cells, infect them with a viral vector such as recombinant poxvirus that contains multiple costimulatory molecules to enhance the immunogenicity of tumor cells, and subsequently use those modified tumor cells as a vaccine.

An alternative approach is to directly administer the poxviral vector into the tumor. Such an approach enhances tumor antigenicity and subsequent antigen-specific T-cell response, leading to an antitumor effect. A Phase-III clinical trial is presently in progress. DNA plasmids containing a genetic sequence that encodes a desired antigen with other transcriptional elements have been considered as a mode of cancer vaccine.

It readily accesses the nucleus of a transfected cell, transcribed into a peptide or protein, and may lead to cellular and humoral immune response [ ]. The technique is considered to be relatively safe compared to viral or bacterial vectors, does not cause infection or autoimmune disorders, and is easy to develop and produce commercially [ ].

However, its effectiveness wanes with time. Hence, the need for frequent booster immunizations. Although therapy was well tolerated, responses were minimal and transient. Using a multiple-antigens plasmid-based vaccine leads to broadly specific, long lasting, and multifunctional immune stimulation [ ]. Improved results were noticed [ , ]. The microenvironment around a tumor plays an important role in tumor progression and metastases. It includes stromal tissue, fibroblasts, and vascular endothelial cells.

Interfering with such a microenvironment will lead to tumor regression. The most important target is angiogenesis, which is essential for tumor growth and metastases. It is mediated by tumor-derived pro-angiogenic cytokines, such as the vascular endothelial growth factor and fibroblast growth factor. These factors stimulate the proliferation of microvasculature around a tumor, with subsequent tumor progression and metastases.

Using an anti-angiogenic genes, such as angiostatin and endostatin , delivered by an adeno-associated virus vector, has led to tumor regression with minimal side effects [ 24 ]. As with other modes of cancer therapies, multimodality treatment frequently yields, better results compared to monotherapy. This is similarly true for gene therapy, and is evident when gene therapy is administered after maximum tumor load reduction following radical surgery or successful chemotherapy.

Gene therapy has a synergistic effect when combined with chemotherapy, with higher tumor responses and lower therapy-related toxicities. This is a new strategy in cancer management that aims to reduce the side effects of chemotherapy. With such an approach, a gene that expresses a nontoxic enzyme into cancer cells is first delivered to the cells, followed by the systemic administration of a pro-drug that can be converted into a toxic compound by the enzyme, leading to selective tumor cell death, with lower adverse effects on normal tissues [ ].

Cell-to-cell diffusion of toxic metabolites may damage nearby and adjacent tumor cells bystander effect [ ]. Release of tumor cell necrotic material in the circulation may activate the immune system in response to the tumor antigen, with subsequent regression of distant tumor cells, such as metastatic nodules distant bystander effect [ ].

Examples include the use of a retroviral vector, such as suicide gene therapy and herpes simplex virus carrying the thymidine kinase enzyme, to the interior of tumor cells. The enzyme has a fold greater efficiency to selectively phosphorylate the acyclovir-derived pro-drug ganciclovir [ ]. Following the systemic administration of ganciclovir, the drug is metabolized in tumor cells leading to cell death.

The system has been tried in several clinical trials [ ]. Replacing ganciclovir with a penciclovir drug, modified to generate radiolabeled analog, will also allow a closer follow-up of therapy results, using high-quality positron emission tomography imaging studies [ ].

Several studies have used a gene transfer approach that aims to enhance chemotherapy and radiation effects against cancer cells, while protecting normal tissue against therapy mediated toxicities. Such gene transfer may also be used in the protection against HIV virus by making normal cells resistant to viral invasion, or correction of genetic disorders such as sickle cell anemia or metabolic disorders. Hence, it is a risky approach in gene therapy.

Few clinical trials have recently been conducted in this regards. The MDR1 gene is minimally expressed in malignant cells; thus, chemotherapeutic medications entering the cytoplasm will remain at a higher concentration, leading to cell death. Other drug-resistant genes include methyl guanine methyltransferase MGMT for alkylating chemotherapy [ , ], and glutathione transferase GSTP1 for cisplatin, doxorubicin, and cyclophosphamide [ , , ].

In a combined diagnostic and therapeutic system theranostic , gene therapy may also be combined with other diagnostic measures to help diagnose, treat and monitor the response to therapy. For example, a small interfering double-stranded RNA siRNA delivery system can be labelled with imaging agents such as dextran-coated superparamagnetic nanoparticles for simultaneous noninvasive imaging of siRNA delivery to tumors, using magnetic resonance imaging MRI [ 59 ]. The siRNA delivery system can also be labeled with other imaging agents to closely monitor therapy, and may even predict the outcome of therapy long before any anatomical changes [ ].

Such molecular diagnostic approaches have been evolving relatively fast in the last few years, and may become an important avenue in cancer diagnosis sometime in the near future [ 59 ].

The most frequent side effects following gene therapy include transient fever and flu-like symptoms [ 24 ]. A grade-3 hypersensitivity reaction following intravenous administration is usually transient and managed with the usual supportive measures. Leukocytopenia, and in particular, lymphopenia, may represent cellular redistribution of white blood cells to target tissue such as tumors.

Mild transient anemia has also been reported [ ]. However, toxicity, mutagenicity and immunogenicity associated with viral vector therapy have raised great concern [ 12 ]. Retroviral such as lentiviruses mediated gene therapy leads to viral integration into host genome, thus, it may cause mutagenic events with possible second malignancies.

This was reported in earlier studies on the murine leukemia retrovirus vector in the treatment of patients with severe combined immunodeficiency and five out of 30 cases developed leukemia [ ], though, no second malignancy has been reported so far, in gene therapy for cancer.

Such mutagenicity depends on the site of viral insertion. For this reason, the FDA has required all clinical trials involving genomic integrated viral vectors to report and analyzes viral vector insertion sites. Initial methodology was linear amplification mediated polymerase chain reaction [ ], but lately, high-throughput DNA sequencing methods have been used [ , ].

Clinical trials that initially or subsequently show evidence of higher mutagenicity are usually discontinued. Information obtained from such studies is of major significance in designing new and much safer therapeutic approaches [ 58 ]. Another major problem with gene therapy for cancer is the resistance to treatment with subsequent tumor recurrences and shorter survival. A potential mechanism is intrinsic, and possibly acquired, tumor cell resistance to therapy-induced cell death apoptosis by dysregulation and release of anti-apoptotic inhibitor of apoptosis protein or Bcl-2 proteins [ 24 ].

Recently, some pharmaceutical companies have developed several medications such as Novartis-LBH, cIAP1, and cIAP2 which inhibit the Bcl-2 protein, thus promoting cell death apoptosis and tumor regression, prevent or delay tumor resistance, and prolong remission following gene therapy.

These medications are presently in clinical trials [ 24 , ]. Gene therapy for cancer has evolved relatively fast in the last two decades, and presently, few drugs are commercially available while others are still in clinical trials. Most reports on gene therapy have shown good safety profiles with transient tolerable toxicities.

The lack of success in several clinical trials may partly be attributed to patient selection. Similar to initial chemotherapy outcomes thirty years ago, patients with advanced and therapy-resistant malignancies are presently enrolled in gene therapy trials. Perhaps, gene therapy maybe much more successful in patients with earlier stages of malignancies, or in those who have a lower tumor burden.

Alternatively, gene therapy may better be used after successful cancer therapy with maximum tumor load reduction, such as after radical surgery, following radiation therapy, or after successful chemotherapy.

In the future, the wide use of patient and tumor genomic analysis as well as the assessment of host humoral and cellular immunity, will facilitate a better selection of the most appropriate gene therapy per patient. Recent progress in developing safe and effective vectors for gene transfer, such as with synthetic viruses and non-viral methods, as well as the success in using autologous and allogenic chimeric antigen receptor integrated T-lymphocytes, even from healthy individuals, as universal effector cells in mediating adoptive immunotherapy, will increase the effectiveness and safety profile of gene therapy.

Furthermore, with the advancement in biological research, much cheaper gene vectors will become commercially available, which will make gene therapy readily available to the majority of cancer patients, worldwide. Treatment is expected to be fast, effective, relatively less toxic and inexpensive, with higher cure rates, and may even, cancer prevention.

The author is an internist and medical oncologist at a regional cancer center in the United States, with higher qualification from United Kingdom, Canada, and United States, previous academic title at Ohio State University, over thirty five years practice as a medical oncologist, and authored or co-authored over twenty five peer-reviewed papers on cancer management and research.

Competing interests. The author declare that he has no financial and non-financial competing interests. National Center for Biotechnology Information , U. Journal List Mol Cell Ther v. Mol Cell Ther. Published online Sep Magid H Amer.

Author information Article notes Copyright and License information Disclaimer. Magid H Amer, Email: moc. Corresponding author. Received Apr 9; Accepted Aug This article is published under license to BioMed Central Ltd. This article has been cited by other articles in PMC. Abstract Advancements in human genomics over the last two decades have shown that cancer is mediated by somatic aberration in the host genome.

Keywords: Adenoviruses, Clinical trials, Electroporation, Gene silencing, Gene transfer technique, Immunomodulation, Molecular targeted therapy, Oncolytic viruses, Retroviruses, Suicide transgenes.

Introduction Over the last two decades, cancer research and genomics have experienced considerable advancements. History The history of cancer therapy dates back to the eighteenth century, when surgery was the primary treatment for early stages of cancer, and patients suffered from frequent relapses [ 7 ].

Methods of gene therapy Gene therapy implies an approach that aims to modify, delete, or replace abnormal gene s at a target cell. Gene transfer delivery system Several methods have been developed to facilitate the entry of genetic materials transgenes into target cells, using various vectors. Table 1 Gene transfer and immunomodulation in cancer therapy. Open in a separate window. Physical mediated gene transfer DNA genetic material that is coated with nanoparticles from gold or other minerals, and with their kinetic energy supplemented by compressed air or fluid gene gun , or using ultrasound, can force the genetic material into the target cell, followed by the release of DNA into its nucleus.

Chemical mediated gene transfer Cationic liposomes are microscopic vesicles of synthetic phospholipids and cholesterol that can enter into cells by endocytosis [ 25 ], with the capability of carrying a variety of molecules such as drugs, nucleotides, proteins, plasmids and large genes [ 23 ]. Bacterial mediated gene transfer Some bacteria have the capability of specifically targeting tumor cells, leading to RNA interference RNAi and gene silencing with blockage of RNA functions, including cellular metabolism and protein synthesis.

Viral mediated gene transfer Viruses are small particles that contain either ribonucleic acid RNA or deoxyribonucleic acid DNA , and may be single-stranded ss or double-stranded ds. Adenoviruses Adenoviruses are double-stranded DNA viruses that usually cause mild respiratory, digestive and ocular infection in humans.

Adeno-associated virus This represents small, single-stranded DNA viruses, which do not usually cause infection without co-infection of a helper virus, such as adenovirus, or herpes simplex virus. Herpes simplex virus This is a large, enveloped double-stranded DNA virus kb , naturally neurotropic prefer nerve cells , that infects humans particularly at the oral and genital mucosa, but ultimately spreads to sensory nerves to replicate or become dormant at the sensory ganglions.

Companies such as Novartis and Roche are developing cancer gene therapies that have high adoption of viral as well as non-viral vectors, thereby proving beneficial for the segmental growth. These companies also conduct clinical trials that raises the demand for vectors, hence fostering the segmental growth. Significant country growth can be attributed to the rising awareness regarding the availability of advanced therapies for treating cancer.

Furthermore, increasing government initiatives and funds motivate the researchers and scientists for carrying out extensive research activities associated with cancer gene therapy that will positively influence the country growth.

Above mentioned factors coupled with increasing prevalence of cancer will further stimulate the industry growth. Cancer gene therapy industry is dominated by few major players. Cancer gene therapy industry is still in the developing phase, therefore, players involved in thie market focus on integrating advanced technology to promote developments in the therapies.

The players also implement certain strategic initiatives such as merger, acquisitions and product launches for acquiring competitive advantage. For instance, in , Celgene and bluebird bio collaborated to introduce innovations in gene therapies.

Such collaborations will provide both the companies to gain competitive advantage over others. About Us: Market Study Report. We streamline the purchase of your market research reports and services through a single integrated platform by bringing all the major publishers and their services at one place. Our customers partner with Market Study Report.