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Posts Tagged ‘discovery of the PD-1/PD-L1 and PD-L2 pathway’

2026 Tang Prize in Biopharmaceutical Science Awarded to Three Pioneers of Cellular Immunotherapy Revolutionizing Treatments for Blood Cancers and Solid Tumors

Reporter: Stephen J. Williams, Ph.D.

From the Tang Prize Committee Anouncement

Source: https://www.tang-prize.org/en/media_detail.php?id=2097

On June 16, the Tang Prize in Biopharmaceutical Science announced its 2026 laureates. The prize, whose laureates from previous cycles have subsequently received Nobel Prize honors, has drawn wide international attention. Three leading scientists in the field of cellular immunotherapy, Drs. Steven A. Rosenberg, Michel Sadelain, and Carl H. June, have been named joint laureates “for the discovery and development of tumor-infiltrating lymphocyte (TIL) and chimeric antigen receptor T-cell (CAR-T) therapies, which have revolutionized treatment for blood cancers and solid tumors.

Immunosuppression in the Tumor Microenvironment (TME) can lead to exhaustion of T cells, which are responsible for identifying and attacking cancer cells. Cellular immunotherapy uses a patient’s own immune cells, including genetically engineered CAR-T, to recognize and destroy cancer cells, and has emerged as one of the most transformative advances in cancer treatment in recent years. The contributions of the three laureates have laid the foundation for a new era of “living drugs,” turning the patient’s immune system into a powerful medicine with far-reaching impact.

Since the first FDA approval in 2017, CAR-T therapy has already benefited over 30,000 patients with blood cancers worldwide. These therapies provide life-saving options for patients with recurrent and/or refractory blood cancers. Furthermore, TIL therapy has established a new option for treating advanced solid tumors, especially metastatic melanoma. Recent advances in CAR-T therapy in 2026 have also expanded into areas such as CRISPR-Cas9-based cell engineering, treatment of autoimmune diseases such as systemic lupus erythematosus, cardiac injury repair, and research targeting senescence.

Academician Wen-Chang Chang, Chair of the Tang Prize Selection Committee in Biopharmaceutical Science, noted that the Tang Prize in Biopharmaceutical Science recognizes successful drug development, as well as medical and technological research that leads to clinical treatment breakthroughs. In the field of tumor immunology, the inaugural Tang Prize laureates, Drs. James P. Allison and Tasuku Honjo, respectively identified CTLA-4 and PD-1 as key inhibitory immune checkpoints, paving the way for the development of antibody drugs known as immune checkpoint inhibitors and bringing major advances to the treatment of many cancers, particularly certain solid tumors. This year’s three laureates specialize in cellular immunotherapy. From Dr. Rosenberg’s pioneering clinical work with TILs, to the foundational advances by Dr. Sadelain and Dr. June that brought CAR-T therapy toward maturity and clinical application, the three scientists helped turn the human immune system into a powerful anti-cancer medicine, creating breakthrough treatments for malignant blood diseases such as leukemia, lymphoma, and multiple myeloma.

 

The pioneering work in this field was fundamentally established by Dr. Steven A. Rosenberg, widely known as the “Father of Cancer Immunotherapy.” As Chief of the Surgery Branch at the National Cancer Institute (NCI) since 1974, he has built the foundational clinical framework for adoptive cell therapy (ACT) 1. In the 1980s, Dr. Rosenberg showed that high-dose interleukin-2 (IL-2) could stimulate T cell proliferation and enhance their ability to kill cancer cells, leading to regression of metastatic tumors — the first clinical proof of T cells’ anti-cancer potential, leading to the FDA approval of IL-2 as the first cancer immunotherapy agent. He also demonstrated that TILs could induce regression of metastatic melanoma. In the 1990s, he achieved another milestone by receiving the first regulatory approval to introduce foreign genes into humans3.

From The National Cancer Institute

Source: https://ccr.cancer.gov/staff-directory/steven-a-rosenberg 

Dr. Rosenberg has pioneered the development of effective immunotherapies for patients with advanced cancer. His studies of cell transfer immunotherapy using tumor infiltrating lymphocytes (TIL) have resulted in durable complete remissions in patients with advanced solid cancers. He has also pioneered the development of gene therapy and was the first to successfully insert foreign genes into humans. His recent studies of the adoptive transfer of genetically modified lymphocytes using chimeric antigen receptors (CAR) or conventional T-cell receptors (TCR) have resulted in the regression of metastatic cancer in patients with lymphomas and solid cancers. His current research is aimed at defining the host immune response of patients to their cancers. These studies emphasize the ability of human lymphocytes to recognize unique cancer antigens and the identification of anti-tumor T-cell receptors that can be exploited to develop new cell transfer immunotherapies. As Chief, Dr. Rosenberg also oversees the Branch’s extensive clinical program aimed at translating scientific advances into effective immunotherapies for patients with advanced cancers arising from the breast, gastrointestinal tract, and pancreas.

Please Watch VIDEO

Dr. Michel Sadelain and Dr. Carl H. June are two leading pioneers in the development of CAR-T cell therapy. In the early development of antigen receptor engineering, research teams incorporated the intracellular CD3ζ chain4— responsible for transmitting activation signals — which Dr Sadelain found to be ineffective on its own.  He discovered that integrating an additional CD28 co-stimulatory domain2 directly into the receptor yielded T cells with therapeutic potential, thereby establishing the core architecture that has become standard framework for all subsequently FDA-approved CAR-T therapies. In addition, Dr. Sadelain identified a molecule named CD19 as a potential target for treating B cell malignancies, which include leukemias and lymphomas, and provided the first demonstration that human CD19 CAR T cells could treat cancer in mice. In 2013, his team at Memorial Sloan Kettering Cancer Center (MSKCC) reported the first significant therapeutic responses to CD19 CAR-T cells in adults with relapsed and refractory acute lymphoblastic leukemia (ALL).

Dr. June made the key breakthroughs that carried CAR-T therapy toward clinical success. He helped demonstrate that CD28 co-stimulation2 as essential for T-cell activation and applied the anti-CD3 and anti-CD28 bead expansion protocol, which has become the global manufacturing standard for CAR-T cells. He also engineered CAR constructs incorporating the 4-1BB (CD137) co-stimulatory domain and the T-cell receptor-zeta chain (TCR-ζ) to enhance the proliferation and long-term survival of transferred T cells, while also addressing the challenges of large-scale manufacturing. Dr. June then led the first successful clinical trials of CD19-targeted CAR-T cells, achieving durable remissions in patients with chronic lymphocytic leukemia (CLL) and acute lymphoblastic leukemia (ALL). His partnership with Novartis culminated in Kymriah becoming the first FDA-approved CAR-T therapy in 2017, marking a major step in bringing CAR-T therapy from research into clinical medicine.

Among the many patients who have benefited from CAR-T therapy, the story of Emily Whitehead is especially compelling. She was the first pediatric patient to receive CAR-T therapy. Diagnosed with ALL at just 5 years old in 2010, she underwent more than 16 months of chemotherapy without success before receiving CAR-T therapy in 2012. After treatment, her cancer went into complete remission, and she has remained healthy for 14 years. Over the years, Emily has continued to share her story publicly, advocating and raising funds for leukemia patients every year. Her recovery has moved and inspired countless patients and families.

Please Watch VIDEO on Dr. June

Footnotes:

  1. Adoptive cell transfer (ACT) is a form of immunotherapy in which a patient’s own immune cells  are collected, expanded or modified outside the body, and then reinfused into the patient to attack cancer.
  2. CD28 is a co-stimulatory receptor on T cells that provides a crucial “second signal” for T-cell activation, proliferation, and survival.
  3. Because gene-transfer research raises ethical and safety concerns, it had long been subject to strict regulation. The 1990 approval laid an important foundation for later genetically modified immune cell therapies.
  4. The CD3ζ chain is an intracellular signaling chain in T cells that helps initiate T-cell activation and immune-killing responses.

 

About the Tang Prize

Since the advent of globalization, humanity has enjoyed unprecedented benefits from advances in civilization and science. Yet a multitude of challenges, such as climate change, the emergence of new infectious diseases, the widening wealth gap, and moral degradation, have surfaced along the way. Against this backdrop, Dr. Samuel Yin established the Tang Prize in December 2012. It consists of four award categories: Sustainable Development, Biopharmaceutical Science, Sinology, and Rule of Law. Every two years, four independent and professional selection committees, comprising many internationally renowned experts, scholars, and Nobel laureates, choose Tang Prize laureates who have made substantive contributions and generated a far-reaching impact on the world, regardless of race, nationality, gender, or religion. A cash prize of NT$50 million (approximately US$1.6 million) is allocated to each category, with NT$10 million (approximately US$320,000) of it being a grant intended for research or educational outreach programs to encourage professionals in every field to examine mankind’s most urgent needs in the 21st century, and become leading forces in the sustainable development of human society through their outstanding research outcomes and active civic engagement.

 

For more articles on Tumor Infiltrating Lymphocytes and CAR-T Therapy on this Open Access Scientific Journal please see:

Tumor Infiltrating Lymphocytes (TIL) as a first of kind FDA approved immunotherapy for cancer
2018 Albany Medical Center Prize in Medicine and Biomedical Research goes to NIH’s Dr. Rosenberg and fellow immunotherapy researchers James P. Allison, Ph.D., and Carl H. June, M.D.
2018 Nobel Prize in Physiology or Medicine for contributions to Cancer Immunotherapy to James P. Allison, Ph.D., of the University of Texas, M.D. Anderson Cancer Center, Houston, Texas. Dr. Allison shares the prize with Tasuku Honjo, M.D., Ph.D., of Kyoto University Institute, Japan

 

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Lectures by The 2017 Award Recipients of Warren Alpert Foundation Prize in Cancer Immunology, October 5, 2017, HMS, 77 Louis Paster, Boston

Reporter: Aviva Lev-Ari, PhD, RN

Article ID #242: LIVE: Lectures by The 2017 Award Recipients of Warren Alpert Foundation Prize in Cancer Immunology, October 5, 2017, HMS, 77 Louis Paster, Boston. Published on 9/8/2017

WordCloud Image Produced by Adam Tubman

Top, from left: James Allison and Lieping Chen. Bottom, from left: Gordon Freeman, Tasuku Honjo (NOT ATTENDED), Arlene Sharpe.

Aviva Lev-Ari, PhD, RN was in attendance and covered this event LIVE

The 2017 Warren Alpert Foundation Prize has been awarded to five scientists for transformative discoveries in the field of cancer immunology.

Collectively, their work has elucidated foundational mechanisms in cancer’s ability to evade immune recognition and, in doing so, has profoundly altered the understanding of disease development and treatment. Their discoveries have led to the development of effective immune therapies for several types of cancer.

The 2017 award recipients are:

  • James Allison, professor of immunology and chair of the Department of Immunology, The University of Texas MD Anderson Cancer Center – Immune checkpoint blockage in Cancer Therapy strictly Genomics based drug
  1. 2017 FDA approved a genomics based drug
  2. and co-stimulatory signals
  3. CTLA-4 blockade, CD28, AntiCTLA-4 induces regression of Transplantable Murine tumor
  4. enhance tumor-specific immune response
  5. Fully antibody human immune response in 10,000 patients – FDA approved 2011
  6. Metastatic melanoma – 3 years survival, programmed tumor death, PD-1, MHC-A1
  7. Ipi/Nivo vs. Ipi – combination – 60% survival vs Ipi alone
  8. Anti CTA4 vs Anti-PD-1
  9. responsive T cell population – MC38 TILs
  10. MC38 Infiltrating T cell populations: T-reg, CD4, Effector, CD8, NKT/gamma-delta
  11. Checkpoint blockage modulates infiltrating T cell population frequencies
  12. T reg correlated with Tumor growth
  13. Combination therapy lead to CURE survival at 80% rate vs CTAL-4 40% positive outcome

Not Attended — Tasuku Honjo, professor of immunology and genomic medicine, Kyoto University – Immune regulation of Cancer Therapy by PD-1 Blockade

 

  • Lieping Chen, United Technologies Corporation Professor in Cancer Research and Professor of immunobiology, of dermatology and of medicine, Yale University – Adoptive Resistance: Molecular Pathway t Cancer Therapy – focus on solid tumors
  1. Enhancement – Enhance normal immune system – Co-stimulation/Co-inhibition Treg, and Cytokines, adoptive cell therapy, Lymphoid organs stores
  2. Normalization – to correct defective immune system – normalizing tumor immunity, diverse tumor escape mechanisms
  3. Anti-PD therapy: regression of large solid tumors: normalizing tumor immunity targeting tumor microenvironment: Heterogeneity, functional modulation, cellular and molecular components – classification by LACK of inflamation, adaptive resistance, other inhibitory pathways, intrinsic induction
  4. avoid autoimmune toxicity,
  5. Resetting immune response (melanoma)
  6. Understad Resistance: Target missing resistance or Adaptive resistance Type II= acquired immunity
  • Gordon Freeman, professor of medicine, Dana-Farber Cancer Institute, Harvard Medical School – PD-L1/PD-1 Cancer Immunotherapy
  1. B7 antibody
  2. block pathway – checkpoint blockage, Expand the T cells after recognition of the disease. T cell receptor signal, activation, co -stimulatory: B71 molecule, B72 – survival signals and cytokine production,.Increased T cell proliferation,
  3. PDL-1 is a ligand of PD 1. How T cell die? genes – PD1 Gene was highly expressed,
  4. Interferon gamma upregulate PD-L1 expression
  5. Feedback loop Tumor – stimulating immune response, interferon turn off PD1
  6. PD-L1 and PD-L2 Expression: Interferom
  7. Trancefuctor MHC, B7-2
  8. PD-L! sisgnat inhibit T-cell activation: turn off Proliferation and cytokine production — Decreasing the immune response
  9. T cell DNA Content: No S-phase devided cell
  10. PD-L1 engagement of PD-1 results in activation : Pd-1 Pathway inhibits T Cell Actiivation – lyposite motility,
  11. Pd-L2 is a second ligand for PD-1 and inhibits T cell activation
  12. PDl-1 expression: BR CA, Ovarian, Colonol-rectal, tymus, endothelial
  13. Blockage of the Pathway – Immune response enhanced
  14. Dendritic cells express PD-L1, PD-L2 and combination of Two, Combination was best of all by increase of cytokine production, increasing the immune response.
  15. PD-L1 blockade enhanced the immune response , increase killing and increased production of cytokines,
  16. anti-tumor efficacy of anti-PD-1/Pd-L1
  17. Pancreatic and colono-rector — PD-L, PDL1, PDL2 — does not owrkd.
  18. In menaloma: PD-1 works better than CYLA-4
  19. Comparison of Targeted Therapy: BRAF TKI vs Chemo high % but short term
  20. Immunotherapy – applies several mechanism: pre-existing anti-therapy
  21. Immune desert: PD=L does not work for them
  22. COMBINATION THERAPY: BLOCK TUMOR INVASION THEN STIMULATE IMMUNE RESPONSE — IT WILL WORK
  23. PD blockage + nutrients and probiotic
  24. Tumor Genome Therapy
  25. Tumore Immuno-evasion Score
  26. Antigens for immune response – choose the ones
  27. 20PD-1 or PD-L1 drugs in development
  28. WHO WILL THE DRUG WORK FOR?

 

  • Arlene Sharpe, the George Fabyan Professor of Comparative Pathology, Harvard Medical School; senior scientist, department of pathology, Brigham and Women’s Hospital – Multi-faceted Functionsof the PD-1 Pathway
  1. function of the pathway: control T cell activation and function of maintain immune tolerance
  2. protect tissues from damage by immune response
  3. T cell dysfunction during cancer anf viral infection
  4. protection from autoimmunity, inflammation,
  5. Mechanism by which PD-1 pathway inhibits anti-tumor immunity
  6. regulation of memoryT cell responce of PD-1
  7. PD-1 signaling inhibit anti-tumor immunity
  8. Compare: Mice lacking CD8-Cre- (0/5) cleared vs PD-1-/-5/5 – PD-1 DELETION: PARTIAL AND TIMED: DELETION OF PD-1 ON HALF OG TILS STARTING AT DAY 7 POSTTUMOR IMPLANTATION OF BOTH PD-1 AND PD-1 TILS: – Tamoxifen days 7-11
  9. Transcription profile: analysis of CD8+ TILs reveal altered metabolism: Fatty Acid Metabolism vs Oxidative Phosphorylation
  10. DOes metabolic shift: WIld type mouth vs PD-1-/_ P14: analyze Tumor cell killingPD-1-/- enhanced FAO increases CD8+ T cell tocicity
  11. Summary: T cell memory development and PD-1: T effectors vs T cell memory: Primary vs Secondary infection: In the absent of PD-1, CD8+ T cels show increase expansion of T cells
  12. INFLUENZA INFECTION: PRIMARY more virus in lung in PD-1 is lacking
  13. Acute infection: PD-1 controls memory T cell differentiation vs PD-1 increase expansion during effector phase BUT impaired persistence during memory phase: impaired cytokine production post re-challenge
  14. PD-1 immunotherapy work for patients with tumor: Recall Response and Primary response
  15. TIL density Primary vs Long term survivor – 5 days post tumor implantation – rechallenged long term survival
  16. Hot tumor vs Cold tumor – Deletion of PD-1 impairs T memory cell development

Opening Remarks: George Q. Daley, MD, PhD, DEAN, HMS

  • Scientific collaboration check point – avoid the body attacking itself, sabotaging the immune system
  • 1987 – Vaccine for HepB
  • Eight of the awardees got the Nobel Prize

 

Moderated by Joan Brugge, PhD, HMS, Prof. of Cell Biology

  • Evolution of concepts of Immunotherapy: William Coley’s Toxin streptoccocus skin infection.
  • 20th century: Immuno-surveilence, Immune response – field was dead in 1978 replaced by Immunotherapy
  • Rosenberg at NIH, high dose of costimulatory molecule prevented tumor reappearanceantbody induce tumor immunity–>> immune theraphy by check point receptor blockade – incidence of tumor in immune compromised mice – transfer T cell
  • T cell defficient, not completely defficient, self recognition of tumor,
  • suppress immmune – immune evasion
  • Michael Atkins, MD, Detupy Director, Georgetown-Lombardi, Comprehensive Cancer Center Clinical applications of Checkpoint inhibitors: Progress and Promise
  1. Overwhelm the Immune system, hide, subvert, Shield, defend-deactivating tumor trgeting T cells that ATTACK the immune system
  2. Immune system to TREAT the cancer
  3. Monotherapy – anti PD1/PD-L1: Antagonist activity
  4. Evading immune response: prostate, colcn
  5. MMR deficiency
  6. Nivolumab in relaped/Refractory HODGKIN LYMPHOMAS – over expression of PD-L1 and PDL2in Lymphomas
  7. 18 month survival better with Duv in Lung cancer stage 3 – anti PD-1- adjuvant therapy with broad effectiveness
  8. Biomarkers for pD-L1 Blockage
  9. ORR higher in PD-L1
  10. Improve Biomarkers: Clonality of T cells in Tumors
  11. T-effector Myeloid Inflammation Low – vs Hogh:
  12. Biomarker Model: Neoantigen burden vs Gene expression vs CD8+
  13. Tissue DIagnostic Labs: Tumor microenveironmenr
  14. Microbiome
  15. Combination: Nivo vs Nivo+Ipi is superior: DETERMINE WHEN TO STOP TREATMENT
  16. 15/16 stopped treatment – Treatment FREE SURVIVAL
  17. Sequencing with Standard Therapies
  18. Brain metastasis – Immune Oncology Therapy – crosses the BBB
  19. Less Toxic regimen, better toxicity management,
  20. Use Immuno therapy TFS
  21. combination – survival must be justified
  22. Goal: to make Cancer a curable disease vs cancer becoming a CHronic disease

Closing Remarks: George Q. Daley, MD, PhD, DEAN, HMS

The honorees will share a $500,000 prize and will be recognized at a day-long symposium on Oct. 5 at Harvard Medical School.

The Warren Alpert Foundation, in association with Harvard Medical School, honors trailblazing scientists whose work has led to the understanding, prevention, treatment or cure of human disease. The award recognizes seminal discoveries that hold the promise to change our understanding of disease or our ability to treat it.

“The discoveries honored by the Warren Alpert Foundation over the years are remarkable in their scope and potential,” said George Q. Daley, dean of Harvard Medical School. “The work of this year’s recipients is nothing short of breathtaking in its profound impact on medicine. These discoveries have reshaped our understanding of the body’s response to cancer and propelled our ability to treat several forms of this recalcitrant disease.”

The Warren Alpert Foundation Prize is given internationally. To date, the foundation has awarded nearly $4 million to 59 scientists. Since the award’s inception, eight honorees have also received a Nobel Prize.

“We commend these five scientists. Allison, Chen, Freeman, Honjoand Sharpe are indisputable standouts in the field of cancer immunology,” said Bevin Kaplan, director of the Warren Alpert Foundation. “Collectively, they are helping to turn the tide in the global fight against cancer. We couldn’t honor more worthy recipients for the Warren Alpert Foundation Prize.”

The 2017 award: Unraveling the mysterious interplay between cancer and immunity

Understanding how tumor cells sabotage the body’s immune defenses stems from the collective work of many scientists over many years and across multiple institutions.

Each of the five honorees identified key pieces of the puzzle.

The notion that cancer and immunity are closely connected and that a person’s immune defenses can be turned against cancer is at least a century old. However, the definitive proof and demonstration of the steps in this process were outlined through findings made by the five 2017 Warren Alpert prize recipients.

Under normal conditions, so-called checkpoint inhibitor molecules rein in the immune system to ensure that it does not attack the body’s own cells, tissues and organs. Building on each other’s work, the five award recipients demonstrated how this normal self-defense mechanism can be hijacked by tumors as a way to evade immune surveillance and dodge an attack. Subverting this mechanism allows cancer cells to survive and thrive.

A foundational discovery made in the 1980s elucidated the role of a molecule on the surface of T cells, the body’s elite assassins trained to seek, spot and destroy invaders.

A protein called CTLA-4 emerged as a key regulator of T cell behavior—one that signals to T cells the need to retreat from an attack. Experiments in mice lacking CTLA-4 and use of CTLA-4 antibodies demonstrated that absence of CTLA-4 or blocking its activity could lead to T cell activation and tumor destruction.

Subsequent work identified a different protein on the surface of T cells—PD-1—as another key regulator of T cell response. Mice lacking this protein developed an autoimmune disease as a result of aberrant T cell activity and over-inflammation.

Later on, scientists identified a molecule, B7-H1, subsequently renamed PD-L1, which binds to PD-1, clicking like a key in a lock. This was followed by the discovery of a second partner for PD-1—the molecule PD-L2—which also appeared to tame T-cell activity by binding to PD-1.

The identification of these molecules led to a set of studies showing that their presence on human and mouse tumors rendered the tumors resistant to immune eradication.

A series of experiments further elucidated just how tumors exploit the interaction between PD-1 and PD-L1 to survive. Specifically, some tumor cells appeared to express PD-L1, essentially “wrapping” themselves in it to avoid immune recognition and destruction.

Additional work demonstrated that using antibodies to block this interaction disarmed the tumors, rendering them vulnerable to immune destruction.

Collectively, the five scientists’ findings laid the foundation for antibody-based therapies that modulate the function of these molecules as a way to unleash the immune system against cancer cells.

Antibody therapy that targets CTLA-4 is currently approved by the FDA for the treatment of melanoma. PD-1/PD-L1 inhibitors have already shown efficacy in a broad range of cancers and have been approved by the FDA for the treatment of melanoma; kidney; lung; head and neck cancer; bladder cancer; some forms of colorectal cancer; Hodgkin lymphoma and Merkel cell carcinoma.

In their own words

“I am humbled to be included among the illustrious scientists who have been honored by the Warren Alpert Foundation for their contributions to the treatment and cure of human disease in its 30+ year history.  It is also recognition of the many investigators who have labored for decades to realize the promise of the immune system in treating cancer.”
        -James Allison


“The award is a great honor and a wonderful recognition of our work.”
         Lieping Chen



I am thrilled to have made a difference in the lives of cancer patients and to be recognized by fellow scientists for my part in the discovery of the PD-1/PD-L1 and PD-L2 pathway and its role in tumor immune evasion.  I am deeply honored to be a recipient of the Alpert Award and to be recognized for my part in the work that has led to effective cancer immunotherapy. The success of immunotherapy has unleashed the energies of a multitude of scientists to further advance this novel strategy.”
                                        -Gordon Freeman


I am extremely honored to receive the Warren Alpert Foundation Prize. I am very happy that our discovery of PD-1 in 1992 and subsequent 10-year basic research on PD-1 led to its clinical application as a novel cancer immunotherapy. I hope this development will encourage many scientists working in the basic biomedical field.”
-Tasuku Honjo


“I am truly honored to be a recipient of the Alpert Award. It is especially meaningful to be recognized by my colleagues for discoveries that helped define the biology of the CTLA-4 and PD-1 pathways. The clinical translation of our fundamental understanding of these pathways illustrates the value of basic science research, and I hope this inspires other scientists.”
-Arlene Sharpe

Previous winners

Last year’s award went to five scientists who were instrumental in the discovery and development of the CRISPR bacterial defense mechanism as a tool for gene editing. They were RodolpheBarrangou of North Carolina State University, Philippe Horvath of DuPont in Dangé-Saint-Romain, France, Jennifer Doudna of the University of California, Berkeley, Emmanuelle Charpentier of the Max Planck Institute for Infection Biology in Berlin and Umeå University in Sweden, and Virginijus Siksnys of the Institute of Biotechnology at Vilnius University in Lithuania.

Other past recipients include:

  • Tu Youyou of the China Academy of Chinese Medical Science, who went on to receive the 2015 Nobel Prize in Physiology or Medicine with two others, and Ruth and Victor Nussenzweig, of NYU Langone Medical Center, for their pioneering discoveries in chemistry and parasitology of malaria and the translation of their work into the development of drug therapies and an anti-malarial vaccine.
  • Oleh Hornykiewicz of the Medical University of Vienna and the University of Toronto; Roger Nicoll of the University of California, San Francisco; and Solomon Snyder of the Johns Hopkins University School of Medicine for research into neurotransmission and neurodegeneration.
  • David Botstein of Princeton University and Ronald Davis and David Hogness of Stanford University School of Medicine for contributions to the concepts and methods of creating a human genetic map.
  • Alain Carpentier of Hôpital Européen Georges-Pompidou in Paris and Robert Langer of MIT for innovations in bioengineering.
  • Harald zur Hausen and Lutz Gissmann of the German Cancer Research Center in Heidelberg for work on the human papillomavirus (HPV) and cancer of the cervix. Zur Hausenand others were honored with the Nobel Prize in Physiology or Medicine in 2008.

The Warren Alpert Foundation

Each year the Warren Alpert Foundation receives between 30 and 50 nominations from scientific leaders worldwide. Prize recipients are selected by the foundation’s scientific advisory board, which is composed of distinguished biomedical scientists and chaired by the dean of Harvard Medical School.

Warren Alpert (1920-2007), a native of Chelsea, Mass., established the prize in 1987 after reading about the development of a vaccine for hepatitis B. Alpert decided on the spot that he would like to reward such breakthroughs, so he picked up the phone and told the vaccine’s creator, Kenneth Murray of the University of Edinburgh, that he had won a prize. Alpert then set about creating the foundation.

To award subsequent prizes, Alpert asked Daniel Tosteson (1925-2009), then dean of Harvard Medical School, to convene a panel of experts to identify scientists from around the world whose research has had a direct impact on the treatment of disease.

SOURCE

https://hms.harvard.edu/news/warren-alpert-foundation-honors-pioneers-cancer-immunology

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