A National Cancer Institute-designated Comprehensive Cancer Center

Make an appointment: 800-826-HOPE
Forman, Stephen J., M.D., F.A.C.P. Bookmark and Share

Laboratory of Stephen J. Forman, M.D., F.A.C.P.

Advances in surgery, radiation therapy and chemotherapy over the last decade have increased the cure rates of a variety of malignancies. For patients whose tumors are not eradicated, however, the impediment most frequently encountered is the inability to fully eliminate the minimal residual disease that frequently has acquired resistance to conventional treatment modalities.
 
A conceptually attractive strategy for targeting minimal residual disease is the manipulation of immunologic effector cells to specifically recognize tumor targets. Animal models and an increasing number of clinical trials have implicated the T lymphocyte as a pivotal immunologic effector cell in antitumor immunity. Technologies are now available for identifying immunogenic T-cell target epitopes expressed by human tumors, isolating antigen-specific T-cell clones and expanding these clones ex vivo to large numbers for reinfusion. Initial clinical trials for malignant glioma employing adoptive transfer of glioma-specific cytolytic T lymphocytes have commenced at City of Hope.
 
Lab Members:
 
Research Group
Christine Brown, Ph.D.
Assistant Research Scientist
cbrown@coh.org
626-256-HOPE (4673),ext. 63977
 
Julie Ostberg, PhD.
Assistant Research Scientist
jostberg@coh.org
626-256-HOPE (4673),ext. 65249
 
Xiuli Wang, M.D., Ph.D.
Assistant Research Scientist
xiuwang@coh.org
626-256-HOPE (4673),ext. 63511
 
Wen Chung Chang, M.S.
Support Scientist
wchang@coh.org
626-256-HOPE (4673),ext. 64155
 
Brenda Aguilar, B.S.
Senior Research Associate
baguilar@coh.org
626-256-HOPE (4673),ext. 6392
 
Renate Starr, M.S.
Research Associate II
rstarr@coh.org
626-256-HOPE (4673),ext. 61135
 
Sean Cho, B.S.
Research Associate I
scho@coh.org
626-256-HOPE (4673),ext. 63048 
 
Hao Hong, Ph.D.
Research Fellow
hhong@coh.org
626-256-HOPE (4673),ext. 63927
 
Leonor Velasco
Research Lab Technician
lvelasco@coh.org
626-256-HOPE (4673),ext. 64181
 
T-cell Therapeutics and Research Lab
Araceli Hamlett, B.A.
Senior Research Associate
ahamlett@coh.org
626-256-HOPE (4673),ext. 64181
 
Jamie Wagner, B.A.
Senior Research Associate
jwagner@coh.org
626-256-HOPE (4673),ext. 64181
 
Winnie Wong, B.S.
Research Associate I
wiwong@coh.org
626-256-HOPE (4673),ext. 64181
 
Regulatory Affairs
Merle Alvarez
Consultant
mealvarez@coh.org
626-256-HOPE (4673),ext. 65684    
 
Graduate Students
Michelle Hunter, B.S.
Graduate Student
mhunter@coh.org
626-256-HOPE (4673),ext. 62153
 
Mahesh Jonnalagadda, DVM, MS
Graduate Student
mjonnalagadda@coh.org
626-256-HOPE (4673),ext. 64181
 
Megan Prosser, B.S.
Graduate Student
mprosser@coh.org
626-256-HOPE (4673),ext. 62153
 

Stephen J. Forman, M.D., F.A.C.P. Research

Adoptive Immunotherapy
Advances in surgery, radiation therapy and chemotherapy over the last decade have increased the cure rates of a variety of malignancies. For patients whose tumors are not eradicated, however, the impediment most frequently encountered is the inability to fully eliminate the minimal residual disease that often has acquired resistance to conventional treatment modalities. An attractive strategy for targeting minimal residual disease is the manipulation of immunologic effector cells to specifically recognize tumor targets. Animal models and an increasing number of clinical trials have implicated the T lymphocyte as a pivotal immunologic effector cell in anti-tumor immunity. This has led to our overall interest in using adoptive immunotherapy of T-cells to target cancer, specifically leukemia/lymphoma, brain tumors and neuroblastoma. Areas of focus in our research program are outlined below.
 
Glioma tumor cells are killed by therapeutic T-cells
Scanning of zetakine redirected cytolytic T-cell lysis of a glioma tumor cell.
 
Genetic Modification of T-cells for Redirected Tumor Recognition
Technologies are now available for identifying immunogenic T-cell target epitopes expressed by human tumors, isolating antigen-specific T-cells and expanding them ex vivo to large numbers for reinfusion. However, to overcome the difficulties of isolating tumor-reactive T-cells from cancer patients, we have developed technology to take T-cells from a cancer patient and reprogram them to target a patient’s cancer through genetic engineering strategies using DNA electroporation and/or lentiviral transduction. Previous studies by our laboratory have provided proof of principle that CTL can be engineered to specifically target lymphoma, neuroblastoma, and glioma tumors via expression of tumor-specific chimeric immunoreceptors resulting in MHC-independent killing of target tumor cells (Cooper et al, Blood 2003; Park et al, Mol Therapy 2007; Kahlon et al, Cancer Res 2004). More recently, we have completed pre-clinical studies of cytotoxic T-cells (CTLs) genetically modified to express an IL13-zetakine chimeric immunoreceptor to target cell-surface IL13Rα2 on medulloblastoma/primitive neuroectodermal tumors, the most common type of brain tumor in children (Stastny et al, J Ped Hematol Oncol 2007). Overall, we are currently involved in studying the potential clinical utility of adoptively transferring T-cells that have been genetically redirected to recognize CD19 (on leukemia and lymphoma); IL13Ra2 (on glioblastoma and medulloblastoma); L1-CAM (on neuroblastoma, lung cancer, and renal cell carcinoma); HER2 (on breast cancer, brain metastases and medulloblastoma); or alpha-3 integrin (on medulloblastoma).
 
 
Murine Xenograft ModelsSurgical suite
To monitor the therapeutic objectives of adoptive T-cell transfer before entering the clinical setting, our lab has developed multiple murine xenograft models. For example, we are now routinely performing stereotactic surgeries in mice for the intracranial injection of human brain tumors to mimic the situation of our patients. In addition, we have also developed lymphoma, neuroblastoma, and medulloblastoma murine xenograft models. Bioluminescent strategies have also been developed by our group for the in vivo imaging of both T-cells and tumors. Our utilization of the firefly and renilla luciferase genes (ffLuc and rLuc, respectively) along with the Xenogen system for serial imaging of anesthetized mice has been critically important for evaluating our animal studies. Specifically, these animal model systems are being used for studying the efficacy of immunotherapy, T-cell trafficking from tail vein injections, contralateral homing of T-cells to tumors within the parenchyma of the brain, and studies of T-cell persistence and proliferation.
 
Trafficking of Adoptively Transferred T-cells
To exert a therapeutic effect, adoptively transferred tumor-specific cytotoxic T-cells (CTLs) must traffic to sites of tumor burden, exit the circulation, and infiltrate the tumor microenvironment. T-cells are able to respond to migration directing chemicals, called chemokines, that are produced by tumor cells. Thus our group has begun to examine the ability of adoptively transferred human CTLs to traffic to tumors. Using a combination of in vivo tumor tropism studies, and in vitro biophotonic chemotaxis assays, we observed that tumors that produce CCL2/MCP1 (>10ng/ml), such as cell lines derived from glioma and medulloblastoma, efficiently chemoattract ex vivo expanded primary human T-cells. These studies suggest that the capacity of adoptively transferred T-cells to home to tumors may be influenced in part by the species and amounts of tumor-derived chemokines, in particular MCP-1 (Brown et al, J Immunol 2007).
 
Targeting Tumor Progenit or Cells with Genetically Engineered Effector T-Cells
Recent hypotheses that tumors arise from cancer stem cells which appear to be resistant to radiation treatment and chemotherapy have also led us to begin to isolate and expand stem cells from human glioma to assess the vulnerability of these cells to T-cell mediated killing in our adoptive immunotherapy models. Our initial studies demonstrate that chimeric immunoreceptor redirected IL13Rα2-specific CTL, currently being evaluated in an FDA-approved pilot Phase I trial for the treatment of recurrent/refractory malignant glioma, can kill cancer stem/progenitor cells in vitro, and reduce engrafted potential of the glioma stem/progenitor population in an orthotopic murine tumor model. Current models now predict that curative therapies for many cancers might require the elimination of the stem/progenitor population, and these studies lay the foundation for an immunotherapy approach to achieve this goal.
 
Development of Strategies to Optimize T-cell Anti-Tumor Activity in Vivo
Our group has also begun to investigate the expression of additional gene products in T-cells that may serve to overcome constraints on T-cell effector function and survival in vivo. For example, we are currently examining the efficacy of providing co-stimulatory signaling to T-cells through integration of costimulatory signaling domains within a tumor targeting chimeric antigen receptor.  Our recent studies in this area demonstrate that integrating costimulation with activation signaling events is important for fully activating CD4+ anti-tumor effector cells, resulting in sustained function in the tumor microenvironment.
 
Another strategy we are currently examining is the utility of genetically modifying T-cells which have first been selected for specificity to viruses such as CMV or EBV, which would allow for endogenous stimulation of these T-cells upon their transfer to patients infected with these viruses that are frequently reactivated in infected hosts. We would also predict that such a combinatorial bispecific T-cell strategy would permit the selective isolation of virus specific memory T-cells as recipients of chimeric antigen receptor genes for improved in vivo persistence following adoptive transfer. In fact, studies on the unique engraftment potential of memory T-cells are also being carried out in primates in collaboration with Dr. Berger at the Fred Hutchison Cancer Research Center in Seattle, WA. Because tumors can avoid immune-mediated elimination by production of immunosuppressive cytokines (e.g., TGF-b), our group is also evaluating strategies by which T-cells may be rendered resistant to such immunosupression. One project is the development of interference RNA sequences that could decrease this susceptibility of T-cells to tumor-mediated suppression. In collaboration with Sangamo Biosciences in Richmond, CA, we are also interested in studying the effects of genetically blocking glucocorticoid sensitivity of the tumor specific T-cells because post-operative brain cancer patients are routinely treated with immunosuppressive steroids (i.e., glucocorticoids) to reduce clinical symptoms of edema.
 
Lastly, another group of projects underway in the lab are examining ways of generating gene products that influence the expression of cytokines such as IL-2 and IL-7 which help promote the survival of T-cells and are critical for generating T-cell memory responses. A new collaboration with Dr. Smolke in the Chemical Engineering Department at CalTech involves the development of RNA regulating systems that are inducible by drugs such as tetracycline to control the expression of cytokines in T-cells which will promote their proliferation and survival.
 
Overall, the recent progress and current directions of Dr. Forman’s research group have generated much enthusiasm and support at City of Hope. The laboratory and office space in the Arnold and Mabel Beckman Center for Cancer Immunotherapeutics & Tumor Immunology is located in the heart of City of Hope. This state-of-the-art center is dedicated to immunotherapy and facilitates collaboration between lab researchers and clinicians, and rapidly moves scientific discoveries from the lab to patients.
 
 

Forman, Stephen J., M.D., F.A.C.P.

Laboratory of Stephen J. Forman, M.D., F.A.C.P.

Advances in surgery, radiation therapy and chemotherapy over the last decade have increased the cure rates of a variety of malignancies. For patients whose tumors are not eradicated, however, the impediment most frequently encountered is the inability to fully eliminate the minimal residual disease that frequently has acquired resistance to conventional treatment modalities.
 
A conceptually attractive strategy for targeting minimal residual disease is the manipulation of immunologic effector cells to specifically recognize tumor targets. Animal models and an increasing number of clinical trials have implicated the T lymphocyte as a pivotal immunologic effector cell in antitumor immunity. Technologies are now available for identifying immunogenic T-cell target epitopes expressed by human tumors, isolating antigen-specific T-cell clones and expanding these clones ex vivo to large numbers for reinfusion. Initial clinical trials for malignant glioma employing adoptive transfer of glioma-specific cytolytic T lymphocytes have commenced at City of Hope.
 
Lab Members:
 
Research Group
Christine Brown, Ph.D.
Assistant Research Scientist
cbrown@coh.org
626-256-HOPE (4673),ext. 63977
 
Julie Ostberg, PhD.
Assistant Research Scientist
jostberg@coh.org
626-256-HOPE (4673),ext. 65249
 
Xiuli Wang, M.D., Ph.D.
Assistant Research Scientist
xiuwang@coh.org
626-256-HOPE (4673),ext. 63511
 
Wen Chung Chang, M.S.
Support Scientist
wchang@coh.org
626-256-HOPE (4673),ext. 64155
 
Brenda Aguilar, B.S.
Senior Research Associate
baguilar@coh.org
626-256-HOPE (4673),ext. 6392
 
Renate Starr, M.S.
Research Associate II
rstarr@coh.org
626-256-HOPE (4673),ext. 61135
 
Sean Cho, B.S.
Research Associate I
scho@coh.org
626-256-HOPE (4673),ext. 63048 
 
Hao Hong, Ph.D.
Research Fellow
hhong@coh.org
626-256-HOPE (4673),ext. 63927
 
Leonor Velasco
Research Lab Technician
lvelasco@coh.org
626-256-HOPE (4673),ext. 64181
 
T-cell Therapeutics and Research Lab
Araceli Hamlett, B.A.
Senior Research Associate
ahamlett@coh.org
626-256-HOPE (4673),ext. 64181
 
Jamie Wagner, B.A.
Senior Research Associate
jwagner@coh.org
626-256-HOPE (4673),ext. 64181
 
Winnie Wong, B.S.
Research Associate I
wiwong@coh.org
626-256-HOPE (4673),ext. 64181
 
Regulatory Affairs
Merle Alvarez
Consultant
mealvarez@coh.org
626-256-HOPE (4673),ext. 65684    
 
Graduate Students
Michelle Hunter, B.S.
Graduate Student
mhunter@coh.org
626-256-HOPE (4673),ext. 62153
 
Mahesh Jonnalagadda, DVM, MS
Graduate Student
mjonnalagadda@coh.org
626-256-HOPE (4673),ext. 64181
 
Megan Prosser, B.S.
Graduate Student
mprosser@coh.org
626-256-HOPE (4673),ext. 62153
 

Research

Stephen J. Forman, M.D., F.A.C.P. Research

Adoptive Immunotherapy
Advances in surgery, radiation therapy and chemotherapy over the last decade have increased the cure rates of a variety of malignancies. For patients whose tumors are not eradicated, however, the impediment most frequently encountered is the inability to fully eliminate the minimal residual disease that often has acquired resistance to conventional treatment modalities. An attractive strategy for targeting minimal residual disease is the manipulation of immunologic effector cells to specifically recognize tumor targets. Animal models and an increasing number of clinical trials have implicated the T lymphocyte as a pivotal immunologic effector cell in anti-tumor immunity. This has led to our overall interest in using adoptive immunotherapy of T-cells to target cancer, specifically leukemia/lymphoma, brain tumors and neuroblastoma. Areas of focus in our research program are outlined below.
 
Glioma tumor cells are killed by therapeutic T-cells
Scanning of zetakine redirected cytolytic T-cell lysis of a glioma tumor cell.
 
Genetic Modification of T-cells for Redirected Tumor Recognition
Technologies are now available for identifying immunogenic T-cell target epitopes expressed by human tumors, isolating antigen-specific T-cells and expanding them ex vivo to large numbers for reinfusion. However, to overcome the difficulties of isolating tumor-reactive T-cells from cancer patients, we have developed technology to take T-cells from a cancer patient and reprogram them to target a patient’s cancer through genetic engineering strategies using DNA electroporation and/or lentiviral transduction. Previous studies by our laboratory have provided proof of principle that CTL can be engineered to specifically target lymphoma, neuroblastoma, and glioma tumors via expression of tumor-specific chimeric immunoreceptors resulting in MHC-independent killing of target tumor cells (Cooper et al, Blood 2003; Park et al, Mol Therapy 2007; Kahlon et al, Cancer Res 2004). More recently, we have completed pre-clinical studies of cytotoxic T-cells (CTLs) genetically modified to express an IL13-zetakine chimeric immunoreceptor to target cell-surface IL13Rα2 on medulloblastoma/primitive neuroectodermal tumors, the most common type of brain tumor in children (Stastny et al, J Ped Hematol Oncol 2007). Overall, we are currently involved in studying the potential clinical utility of adoptively transferring T-cells that have been genetically redirected to recognize CD19 (on leukemia and lymphoma); IL13Ra2 (on glioblastoma and medulloblastoma); L1-CAM (on neuroblastoma, lung cancer, and renal cell carcinoma); HER2 (on breast cancer, brain metastases and medulloblastoma); or alpha-3 integrin (on medulloblastoma).
 
 
Murine Xenograft ModelsSurgical suite
To monitor the therapeutic objectives of adoptive T-cell transfer before entering the clinical setting, our lab has developed multiple murine xenograft models. For example, we are now routinely performing stereotactic surgeries in mice for the intracranial injection of human brain tumors to mimic the situation of our patients. In addition, we have also developed lymphoma, neuroblastoma, and medulloblastoma murine xenograft models. Bioluminescent strategies have also been developed by our group for the in vivo imaging of both T-cells and tumors. Our utilization of the firefly and renilla luciferase genes (ffLuc and rLuc, respectively) along with the Xenogen system for serial imaging of anesthetized mice has been critically important for evaluating our animal studies. Specifically, these animal model systems are being used for studying the efficacy of immunotherapy, T-cell trafficking from tail vein injections, contralateral homing of T-cells to tumors within the parenchyma of the brain, and studies of T-cell persistence and proliferation.
 
Trafficking of Adoptively Transferred T-cells
To exert a therapeutic effect, adoptively transferred tumor-specific cytotoxic T-cells (CTLs) must traffic to sites of tumor burden, exit the circulation, and infiltrate the tumor microenvironment. T-cells are able to respond to migration directing chemicals, called chemokines, that are produced by tumor cells. Thus our group has begun to examine the ability of adoptively transferred human CTLs to traffic to tumors. Using a combination of in vivo tumor tropism studies, and in vitro biophotonic chemotaxis assays, we observed that tumors that produce CCL2/MCP1 (>10ng/ml), such as cell lines derived from glioma and medulloblastoma, efficiently chemoattract ex vivo expanded primary human T-cells. These studies suggest that the capacity of adoptively transferred T-cells to home to tumors may be influenced in part by the species and amounts of tumor-derived chemokines, in particular MCP-1 (Brown et al, J Immunol 2007).
 
Targeting Tumor Progenit or Cells with Genetically Engineered Effector T-Cells
Recent hypotheses that tumors arise from cancer stem cells which appear to be resistant to radiation treatment and chemotherapy have also led us to begin to isolate and expand stem cells from human glioma to assess the vulnerability of these cells to T-cell mediated killing in our adoptive immunotherapy models. Our initial studies demonstrate that chimeric immunoreceptor redirected IL13Rα2-specific CTL, currently being evaluated in an FDA-approved pilot Phase I trial for the treatment of recurrent/refractory malignant glioma, can kill cancer stem/progenitor cells in vitro, and reduce engrafted potential of the glioma stem/progenitor population in an orthotopic murine tumor model. Current models now predict that curative therapies for many cancers might require the elimination of the stem/progenitor population, and these studies lay the foundation for an immunotherapy approach to achieve this goal.
 
Development of Strategies to Optimize T-cell Anti-Tumor Activity in Vivo
Our group has also begun to investigate the expression of additional gene products in T-cells that may serve to overcome constraints on T-cell effector function and survival in vivo. For example, we are currently examining the efficacy of providing co-stimulatory signaling to T-cells through integration of costimulatory signaling domains within a tumor targeting chimeric antigen receptor.  Our recent studies in this area demonstrate that integrating costimulation with activation signaling events is important for fully activating CD4+ anti-tumor effector cells, resulting in sustained function in the tumor microenvironment.
 
Another strategy we are currently examining is the utility of genetically modifying T-cells which have first been selected for specificity to viruses such as CMV or EBV, which would allow for endogenous stimulation of these T-cells upon their transfer to patients infected with these viruses that are frequently reactivated in infected hosts. We would also predict that such a combinatorial bispecific T-cell strategy would permit the selective isolation of virus specific memory T-cells as recipients of chimeric antigen receptor genes for improved in vivo persistence following adoptive transfer. In fact, studies on the unique engraftment potential of memory T-cells are also being carried out in primates in collaboration with Dr. Berger at the Fred Hutchison Cancer Research Center in Seattle, WA. Because tumors can avoid immune-mediated elimination by production of immunosuppressive cytokines (e.g., TGF-b), our group is also evaluating strategies by which T-cells may be rendered resistant to such immunosupression. One project is the development of interference RNA sequences that could decrease this susceptibility of T-cells to tumor-mediated suppression. In collaboration with Sangamo Biosciences in Richmond, CA, we are also interested in studying the effects of genetically blocking glucocorticoid sensitivity of the tumor specific T-cells because post-operative brain cancer patients are routinely treated with immunosuppressive steroids (i.e., glucocorticoids) to reduce clinical symptoms of edema.
 
Lastly, another group of projects underway in the lab are examining ways of generating gene products that influence the expression of cytokines such as IL-2 and IL-7 which help promote the survival of T-cells and are critical for generating T-cell memory responses. A new collaboration with Dr. Smolke in the Chemical Engineering Department at CalTech involves the development of RNA regulating systems that are inducible by drugs such as tetracycline to control the expression of cytokines in T-cells which will promote their proliferation and survival.
 
Overall, the recent progress and current directions of Dr. Forman’s research group have generated much enthusiasm and support at City of Hope. The laboratory and office space in the Arnold and Mabel Beckman Center for Cancer Immunotherapeutics & Tumor Immunology is located in the heart of City of Hope. This state-of-the-art center is dedicated to immunotherapy and facilitates collaboration between lab researchers and clinicians, and rapidly moves scientific discoveries from the lab to patients.
 
 
Our Scientists

Our research laboratories are led by the best and brightest minds in scientific research.
 

Beckman Research Institute of City of Hope is internationally  recognized for its innovative biomedical research.
City of Hope is one of only 41 Comprehensive Cancer Centers in the country, the highest designation awarded by the National Cancer Institute to institutions that lead the way in cancer research, treatment, prevention and professional education.
Learn more about City of Hope's institutional distinctions, breakthrough innovations and collaborations.
Develop new therapies, diagnostics and preventions in the fight against cancer and other life-threatening diseases.
 
Support Our Research
By giving to City of Hope, you support breakthrough discoveries in laboratory research that translate into lifesaving treatments for patients with cancer and other serious diseases.
 
 
 
 


NEWS & UPDATES
  • Cancer cells are voracious eaters. Like a swarm of locusts, they devour every edible tidbit they can find. But unlike locusts, when the food is gone, cancer cells can’t just move on to the next horn o’ plenty. They have to survive until more food shows up — and they do. Mei Kong, Ph.D., assistant […]
  • On Jan. 1, 2015, six City of Hope patients who have journeyed through cancer will welcome the new year with their loved ones atop City of Hope’s Tournament of Roses Parade float. The theme of the float is “Made Possible by HOPE.” The theme of the parade is “Inspiring Stories.” Repr...
  • When 25-year-old Angelina Mattos was diagnosed with Stage 4 oral cancer earlier this year, she learned that her only hope of survival was through the removal of her tongue, a surgery that leaves people without the ability to talk or eat normally, sometimes permanently ending their ability to speak. After hearin...
  • Two years ago, Joselyn Miller and her family sat together as stem cells from her brother’s bone marrow were infused into her – a precious gift of life that the family is excited to have the chance to pass to another patient in need. Today, the stem cell recipient is healthy. Her 23-year-old son Rex, who […...
  • Even as the overall rate of oral cancers in the United States steadily declines, the rate of tongue cancer is increasing — especially among white females ages 18 to 44. An oral cancer diagnosis, although rare, is serious. Only half of the people diagnosed with oral cancer are still alive after five years, accor...
  • Sometimes cancer found in the lungs is not lung cancer at all. It can be another type of cancer that originated elsewhere in the body and spread, or metastasized, to the lungs through the bloodstream or lymphatic system. These tumors are called lung metastases, or metastatic cancer to the lungs, and are not the...
  • When it comes to research into the treatment of hematologic cancers, City of Hope scientists stand out. One study that  they presented this week at the annual meeting of the American Society of Hematology suggests a new standard of care for HIV-associated lymphoma, another offers promise for the treatment of re...
  • Patients with HIV-associated lymphoma may soon have increased access to the current standard of care for some non-HIV infected patients – autologous stem cell transplants. Impressive new data, presented Monday at the annual meeting of the American Society of Hematology (ASH) in San Francisco, indicate that HIV-...
  • On Jan. 1, 2015, six City of Hope patients who have journeyed through cancer will welcome the new year with their loved ones atop City of Hope’s Tournament of Roses Parade float. The theme of the float is “Made Possible by HOPE.” The theme of the Rose Parade is “Inspiring Stories.”...
  • The holidays can create an overwhelming urge to give to people in need — especially to sick children and families spending the holidays in a hospital room. That’s a good thing. Holiday donations of toys and gifts can bolster the spirits, and improve the lives, of people affected by illness, and hospitals ...
  • On Jan. 1, 2015, six City of Hope patients who have journeyed through cancer will welcome the new year with their loved ones atop City of Hope’s Tournament of Roses Parade float. The theme of the float is “Made Possible by HOPE.” The theme of the parade is “Inspiring Stories.” Here...
  • Cancer has a way of “talking” to the immune system and corrupting it to work on its own behalf instead of defending the body. Blocking this communication would allow the immune system to see cancer cells for what they are – something to be fought off – and stop them from growing. A breakthrough Scientists [R...
  • On Jan. 1, 2015, six City of Hope patients who have journeyed through cancer will welcome the new year with their loved ones atop City of Hope’s Tournament of Roses Parade float. The theme of the float is “Made Possible by HOPE.” The theme of the parade is “Inspiring Stories.” By V...
  • On Jan. 1, 2015, six City of Hope patients who have journeyed through cancer will welcome the new year with their loved ones atop City of Hope’s Tournament of Roses Parade float. The theme of the float is “Made Possible by HOPE.” The theme of the parade is “Inspiring Stories.” The ...
  • On Jan. 1, 2015, six City of Hope patients who have journeyed through cancer will welcome the new year with their loved ones atop City of Hope’s Tournament of Roses Parade float. The theme of the float is “Made Possible by HOPE.” The theme of the parade is “Inspiring Stories.” In 2...