Tag: University of Texas M. D. Anderson Cancer Center

MD Anderson’s Hagop Kantarjian, M.D., awarded highest honor from American Society of Clinical Oncology
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Newswise — The American Society of Clinical Oncology (ASCO) will present the 2023 David A. Karnofsky Memorial Award to Hagop Kantarjian, M.D., chair of Leukemia at The University of Texas MD Anderson Cancer Center, for his contributions to leukemia clinical research and his dedication to improving the lives of patients.

“Cancer research and patient care have been my life’s passion and mission and, I am honored to be recognized by ASCO with the society’s highest scientific award,” Kantarjian said. “I am grateful for all of the outstanding investigators in the Leukemia Department and outside colleagues whom I have had the privilege of working with throughout my career.”

The David A. Karnofsky Memorial Award has been presented annually since 1970 to recognize an oncologist who has made outstanding contributions to cancer research, diagnosis and/or treatment. Kantarjian will be presented with the award and will give a scientific lecture at the 2023 ASCO Annual Meeting.

For the past four decades, Kantarjian has led practice-changing national and international clinical trials at MD Anderson for the treatment of all leukemia subtypes. These trials resulted in multiple Food and Drug Administration (FDA)-approved drugs and delivered new standards of care across leukemias, significantly improving quality of life and survival rates across several leukemia subsets. Over the last two decades, Kantarjian has led national and international studies of innovative next-generation BCR-ABL tyrosine kinase inhibitors.

“Throughout a remarkable career, Dr. Kantarjian has contributed immensely to our mission of ending cancer. He not only advanced new treatments and furthered our knowledge of leukemia, but his leadership has inspired so many in the MD Anderson community,” said Peter WT Pisters, M.D., president of MD Anderson. “We congratulate Hagop on this exceptional achievement, and we thank him for the countless lives he has saved around the world.”

Among Kantarjian’s many contributions to the field of leukemia, highlights include:
- Developing the HYPER-CVAD regimen as a standard-of-care frontline therapy for adult patients with acute lymphoblastic leukemia (ALL). This regimen led to a change in the treatment approach to stop the disease from spreading to a patient’s central nervous system by administering a chemotherapy injection into the spinal fluid instead of treating with radiation therapy.
- Establishing clinical biology parameters of chronic myeloid leukemia (CML), including definitions of CML phases and cytogenetic responses as well as establishing new prognostic factors, which were subsequently adopted in studies of tyrosine kinase inhibitors.
- Leading the development of decitabine and epigenetic hypomethylation therapy for treating myelodysplastic syndromes (MDS) and older/unfit patients with acute myeloid leukemia (AML). He designed and conducted the Phase III trials that resulted in FDA approval of decitabine for MDS in 2006 and the European approval in older/unfit AML patients in 2012.
- Pioneering research with hypomethylating agents (HMAs) in combination with venetoclax, which resulted in FDA approval of HMA-venetoclax combinations in older/unfit patients with AML in 2017.
- Championing the development of clofarabine, conducting animal toxicology studies, and leading subsequent Phase I, Phase II and pivotal Phase III and Phase IV trials that resulted in FDA approval of clofarabine for pediatric patients with ALL.
- Developing several FLT3 inhibitors, IDH inhibitors and venetoclax, which all received FDA approvals for the treatment of AML and its subsets.
- Leading the clinical development of multiple monoclonal antibodies for treating ALL, including inotuzumab and blinatumomab, and leading the multi-institutional national studies of these monoclonal antibodies in adult patients with ALL.
- Developing regimens containing inotuzumab and blinatumomab combined with chemotherapy for adults with pre-B ALL.
- Working on the development of imatinib, dasatinib, nilotinib, bosutinib, ponatinib and omacetaxine, which all received FDA approval for CML therapy.
In addition to his own research contributions, Kantarjian has dedicated his career to the training and mentoring of clinicians and researchers focused on leukemia research and patient care, many of whom now provide exceptional treatment at institutions worldwide. These relationships have broadened Kantarjian’s impact in the field and helped to extend knowledge far beyond the walls of MD Anderson.

“Dr. Kantarjian’s long list of accomplishments and groundbreaking discoveries are a testament to his lifelong commitment to impactful cancer research and patient care,” said Giulio Draetta, M.D., Ph.D., chief scientific officer at MD Anderson. “As a community that strives to deliver cancer breakthroughs every day, we are immensely proud of him for receiving this well-deserved honor from ASCO.”

Since 1995, Kantarjian has served as chair of MD Anderson’s Department of Leukemia. In 2000, he established the MD Anderson Leukemia Fellowship Program, which now trains 10 fellows each year. To date, he has published over 2,400 peer-reviewed articles in many top peer-reviewed journals. Kantarjian has received many honors throughout his distinguished career, including the American Lebanese Medical Association’s Lifetime Achievement Award, the American Association for Cancer Research’s Joseph H. Burchenal Memorial Award, and the Leukemia Society of America’s Outstanding Service to Mankind Award. He also was named an ASCO Fellow and a Leukemia Society of America Special Fellow and Scholar.

He has served on multiple ASCO committees throughout the years and served on the ASCO Board of Directors from 2010-2015. In 2012, Kantarjian co-founded the Society of Hematologic Oncology, which focuses on the research and education of rising oncologists interested in hematologic malignacies.

Kantarjian has been a vocal advocate for key issues in patient-centered cancer care including issues pertaining to cancer drug shortages and costs. He currently is a non-resident fellow in health care at Rice University’s Baker Institute for Public Policy.
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University of Texas M. D. Anderson Cancer Center

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April 26, 2023
Targeted therapy momelotinib provides significant symptom and anemia improvements in patients with myelofibrosis

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Newswise — Patients with myelofibrosis had clinically significant improvement in disease-related symptoms, including anemia and spleen enlargement, when treated with the targeted therapy momelotinib, according to results from the international Phase III MOMENTUM trial led by researchers at The University of Texas MD Anderson Cancer Center.

The findings, published today in The Lancet, support the use of momelotinib – a potent ACVR1/ALK2 and JAK1/2 inhibitor – over the standard therapy danazol in treating myelofibrosis patients that were resistant, refractory or intolerant to firstline therapy, especially symptomatic patients and those with anemia.

“Current options for managing anemia in our myelofibrosis patients provide only modest and temporary benefits, so we are excited about these findings,” said study lead Srdan Verstovsek, M.D., Ph.D., professor of Leukemia. “The trial results suggest that momelotinib is safe, well-tolerated and can improve one of the most common and debilitating clinical problems for this patient population.”

Myelofibrosis is an uncommon bone marrow cancer that is part of a group of diseases known as myeloproliferative neoplasms. A hallmark of the disease is dysregulated JAK signaling, which disrupts the body’s normal production of blood cells and leads to common symptoms, including an enlarged spleen and anemia. Chronic anemia in these patients is associated with poor prognoses.

Currently approved JAK inhibitors can improve spleen responses and other disease-related symptoms, but they also can worsen anemia. In this trial, momelotinib improved anemia and reduced transfusion dependency in myelofibrosis patients previously treated with a JAK inhibitor. Momelotinib can be administered and maintained at full dose because it does not suppress bone marrow activity like other JAK inhibitors.

The MOMENTUM trial is the first randomized Phase III study to evaluate a JAK1/2 and ACVR1/ALK2 inhibitor in patients with myelofibrosis and anemia. The trial was designed to compare the clinical benefits of momelotinib to danazol, a synthetic androgen currently used to treat anemia in symptomatic myelofibrosis patients.

The study enrolled 195 adult patients from 107 research sites across 21 countries. Trial participants were randomly assigned (2:1) to receive momelotinib plus placebo or danazol plus placebo. Sixty-three percent of participants were male and 37% were female. The median age of participants for the momelotinib group was 71 years and for the danazol group 72 years.

The trial’s primary endpoint was symptom reduction after 24 weeks of treatment, defined as a 50% or more reduction in Myelofibrosis Symptom Assessment Form Total Symptom Score. A significantly greater proportion of patients who received momelotinib saw benefits in their disease symptoms (25%) compared to those receiving danazol (9%).

Patients treated with momelotinib also experienced a significant reduction in their spleen size, with 25% responding after 24 weeks of therapy. Additionally, these patients required fewer blood transfusions compared to those receiving danazol.

The safety profile of momelotinib was comparable to previous clinical trials. The most common non-hematological side effects experienced by trial participants in the momelotinib group included diarrhea, nausea, weakness and itching or irritated skin.

“If approved, momelotinib could offer an effective option for patients with myelofibrosis to improve anemia, splenomegaly and other disease-related symptoms over other approved medications so far,” Verstovsek said. “Momelotinib may also be an ideal partner for combinations with other investigational agents in development to further control myelofibrosis symptoms.”

Patient follow-up is ongoing and long-term survival continues to be monitored.

The research was supported by Sierra Oncology. A full list of collaborating authors and their disclosures can be found with the full paper here.

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University of Texas M. D. Anderson Cancer Center

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January 28, 2023
Study discovers triple immunotherapy combination as possible treatment for pancreatic cancer

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Newswise — HOUSTON ― Researchers at The University of Texas MD Anderson Cancer Center have discovered a novel immunotherapy combination, targeting checkpoints in both T cells and myeloid suppressor cells, that successfully reprogrammed the tumor immune microenvironment (TIME) and significantly improved anti-tumor responses in preclinical models of pancreatic cancer.

In this study, published today in Nature Cancer, researchers used comprehensive immune profiling in mouse and human pancreatic cancers to systematically identify mechanisms of immunotherapy resistance and investigate potential therapeutic targets. They found that neutralizing several distinct immunosuppressive mechanisms of the TIME dramatically improved survival rates in laboratory models, pointing to a potential treatment option for this notoriously lethal and unresponsive cancer.

“This triple combination therapy led to an unprecedented curative response in our models,” said corresponding author Ronald DePinho, M.D., professor of Cancer Biology. “The prevailing view has been that pancreatic cancer is impervious to immunotherapy, but this preclinical study shows that it can be vulnerable to the right combination therapy. Moreover, the presence of these targets in human pancreatic cancer specimens raises the exciting possibility that such therapeutic combinations could one day help our patients.”

Pancreatic cancer is one of the leading causes of cancer death in the United States, partially because 80% of cases are diagnosed at an advanced stage. Pancreatic cancer is also considered to be “non-immunogenic,” meaning it is unresponsive to commonly used anti-PD-1 and anti-CTLA-4 immune checkpoint inhibitors. This is due in part to the immunosuppressive conditions in the TIME, but the mechanisms behind this resistance are not fully understood.

The researchers used high-dimensional immune profiling and single-cell RNA sequencing to study how the TIME is affected by a variety of immunotherapies. They identified specific immune checkpoint proteins, 41BB and LAG, that were highly expressed in exhausted T cells.

In testing antibodies targeting these checkpoints, the researchers observed that models treated with a 41BB agonist and LAG3 antagonist in combination had slower tumor progression, higher levels of anti-tumor immunity indicators and significantly improved survival rates compared to treatment with either antibody alone or with other checkpoint inhibitors. Notably, these preclinical studies faithfully mirrored the human data in their lack of efficacy of anti-PD1 or anti-CTLA-4 therapy.

The researchers also confirmed these two therapeutic targets are present in human pancreatic cancer samples, with 81% and 93% of patients analyzed having T cells with 41BB and LAG3 expression, respectively.

Because this dual-therapy combination did not completely eliminate established tumors, the investigators also examined efforts to reprogram the TIME to further sensitize tumors to immunotherapy. At baseline, the TIME contained an abundance of myeloid-derived suppressor cells (MDSCs) expressing CXCR2, a protein associated with recruiting immunosuppressive cells. Inhibiting CXCR2 alone decreased MDSC migration and blocked tumor growth, but it was not curative. This prompted the investigators to consider a combination targeting 41BB, LAG3 and CXCR2.

It was this triple combination that resulted in complete tumor regression and improved overall survival in 90% of preclinical models. In a more stringent lab model that develops multiple spontaneously arising tumors with higher treatment resistance, the combination achieved complete tumor regression in over 20% of cases.

“These are encouraging results, especially considering the lack of effective immunotherapy options in pancreatic cancer,” DePinho said. “By targeting multiple synergistic mechanisms that get in the way of the immune response, we can give T cells a fighting chance to attack these tumors. Of course, we still need to see how this combination translates into a safe and effective regimen in the clinic, and we invite other researchers to build upon these results. We are optimistic that pancreatic cancers, and hopefully other non-immunogenic cancers, can ultimately be rendered vulnerable to combination immunotherapy.”

The authors point out that these particular immunotherapy agents currently are undergoing clinical trials as monotherapies, suggesting potential opportunities to rapidly translate this triple combination into clinical studies.

This work was supported by the National Institutes of Health/National Cancer Institute (P01 CA117969, RO1CA240526, RO1CA236864, R01CA231349, R01CA220236, P50CA221707), the Elsa U. Pardee Foundation, MD Anderson’s Advanced Scholar Program, the Eleanor Russo Fund for Pancreatic Research, Ralph A. Loveys Family Charitable Foundation, the Cultural & Charitable Club of Somerset Run, the New Jersey Health Foundation, the Sheikh Ahmed Bin Zayed Al Nahyan Center for Pancreatic Cancer Research, and MD Anderson’s Pancreatic Cancer Moon Shot^®. A full list of collaborating authors and their disclosures can be found with the full paper here.

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University of Texas M. D. Anderson Cancer Center

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December 30, 2022
Sotorasib shows clinically meaningful activity in KRAS G12C-mutated advanced pancreatic cancer

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Newswise — In the Phase I/II CodeBreaK 100 trial, the KRAS G12C inhibitor sotorasib achieved meaningful anticancer activity with an acceptable safety profile in heavily pretreated patients with KRAS G12C-mutated metastatic pancreatic cancer, according to researchers at The University of Texas MD Anderson Cancer Center.

The results of the trial, published today in the The New England Journal of Medicine, indicate an objective response rate of 21.1% and a median time-to-response of 1.5 months, with 84% of patients experiencing disease control. Median progression-free survival was 4 months and overall survival was 6.9 months.

“These are encouraging early data because they point toward establishing that KRAS inhibitors can work in pancreatic cancers, which have been difficult to crack from a targeted therapy standpoint,” said principal investigator David S. Hong, M.D., professor of Investigational Cancer Therapeutics. “We look forward to data from larger trials as we continue working to bring much-needed new therapies to these patients.”

The KRAS protein is part of a normal signaling pathway regulating growth and proliferation of cells, but activating mutations in KRAS drives abnormal growth in cancer. KRAS mutations are especially common in pancreatic cancers, occurring in about 90% of patients, while KRAS G12C mutations are present in 1-2% of cases.

Sotorasib is a small-molecule inhibitor that irreversibly binds the mutant KRAS G12C protein to lock it in an inactive state. In 2021, this targeted therapy was approved by the Food and Drug Administration for the treatment of KRAS G12C-mutated metastatic non-small cell lung cancer, based on previous data from another cohort of this study.

The pancreatic cancer cohort enrolled 38 patients with metastatic disease and a median of two prior lines of therapy. The median age of participants was 65.5, 76.3% were men and 55.3% had stage IV disease at initial diagnosis.

All patients experienced treatment-emergent adverse events, the most common of which were abdominal pain (36.8%), diarrhea and nausea (23.7% each). Treatment-related adverse events were reported in 42.1% of patients, of which 15.8% were grade 3. The most frequently occurring grade 3 toxicities were diarrhea and fatigue (5.3% each). No adverse events resulted in discontinuation of treatment.

According to Hong, these results may be a harbinger of success for other drugs in the pipeline targeting mutant KRAS that could potentially benefit far greater numbers of patients.

“It’s gratifying to see results like this, since targeting mutant KRAS seemed virtually impossible just a few years ago. Still, we must continue our research efforts to make progress against other common KRAS mutations found in pancreatic and other cancer types,” Hong said. “Trials have recently begun on drugs targeting KRAS G12D, a much more common mutation in pancreatic cancer, as well as some pan-RAS therapies, which target multiple mutations.”

This study was funded by Amgen. The work was also supported in part by the National Institutes of Health (P30 CA008748, P30 CA016672, 1UL1 TR003167), the Cancer Prevention and Research Institute of Texas (RP150535), and the Sheikh Khalifa Bin Zayed Al Nahyan Institute for Personalized Cancer Therapy at MD Anderson. A full list of authors and their disclosures can be found in the paper here.

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University of Texas M. D. Anderson Cancer Center

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December 21, 2022
Shorter Course of Radiation Therapy Yields Comparable Results for Patients with Non-Metastatic Soft Tissue Sarcoma

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Newswise — HOUSTON – Patients with non-metastatic soft tissue sarcoma (STS) who need pre-operative radiation therapy can safely receive hypofractionated treatment over three weeks instead of five, with comparable tumor control and no increased risk of major complications in wound healing, according to researchers at The University of Texas MD Anderson Cancer Center.

Results from the study, led by Ashleigh Guadagnolo, M.D., professor of Radiation Oncology, were published today in The Lancet Oncology. Guadagnolo also presented results at the 2022 American Society for Radiation Oncology (ASTRO) Annual Meeting.

On the single-arm, non-randomized trial, patients received hypofractionated radiation therapy, consisting of higher daily radiation therapy doses per treatment over fewer days relative to conventional therapy. Thirty-one percent of patients developed major wound complications within 120 days of surgery, while local tumor control was 93% at two-year follow-up — both comparable to historically reported rates with the longer treatment course.

“Our data indicate the three-week regimen offers patients a likely safe and effective alternative to the current standard of care with comparable outcomes in disease control and no increased risks of major wound complications,” Guadagnolo said. “We are excited by the current results of this study, which demonstrate the value of a hypofractionated approach to radiation therapy, which is more convenient for patients.”

A major side effect of pre-operative radiation therapy in patients with non-metastatic STS is an increased risk of wound-healing complications after surgery. Patients have a heightened risk of needing a second operation for wound repair, extensive wound management and readmission to the hospital.

On the current study, no patients experienced a serious adverse event or a grade 3 acute skin toxicity while on the study. The 31% rate of major wound complications is comparable to the historically observed 35% rate in patients treated with the standard five-week regimen.

“Research shows that patients receiving their treatment at cancer centers with sarcoma specialists have better survival and functional outcomes. Being able to shorten our patients’ treatment time from five to three weeks may improve care accessibility because patients would be able to reduce their time away from home if they do not live near a sarcoma specialty center,” Guadagnolo said.

The trial enrolled a total of 120 patients over the age of 18 with non-metastatic STS who had not previously undergone radiation therapy. All patients had STS in the extremity or superficial trunk; 65% of participants had lower extremity tumors; 17% had upper extremity tumors and 18% had tumors in the trunk.

All patients were treated with a three-week course of radiation consisting of 15 daily fractions of 2.85 Gray (Gy), totaling 42.75 Gy. The current standard dose is 50 Gy in 25 daily fractions, or a five-week course. Radiation therapy was followed by surgery four to eight weeks later. Researchers assessed major wound complications within 120 days of surgery among patients treated on the trial.

Long-term side effects, oncologic and functional outcomes using the hypofractionated regimen still are being assessed.

The research was supported by the National Cancer Institute (P30 CA016672). A full list of collaborating authors and their disclosures can be found with the full paper here.

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University of Texas M. D. Anderson Cancer Center

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November 4, 2022
MD Anderson’s Guillermina Lozano Receives AAMC Award for Distinguished Research in the Biomedical Sciences

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Newswise — HOUSTON ― In recognition of her trailblazing work uncovering the mechanisms of the p53 tumor suppressor, Guillermina “Gigi” Lozano, Ph.D., chair of Genetics at The University of Texas MD Anderson Cancer Center, has received the 2022 Award for Distinguished Research in the Biomedical Sciences by the Association of American Medical Colleges (AAMC).

Since its inception in 1947, the AAMC Award for Distinguished Research in the Biomedical Sciences has annually honored an individual or team of two individuals whose research has contributed to significant scientific discoveries benefitting human health and well-being, who participate in research beyond their own work through mentorship or review panels, and whose standards of professional ethics and scientific integrity are of the highest caliber. Lozano is the second MD Anderson researcher to be selected for this award, with James Allison, Ph.D., honored in 2014.

“Gigi’s key discoveries in the field of cancer biology are of tremendous importance, enabling a deeper understanding of the mechanisms that drive tumor development and treatment response. These breakthroughs are necessary for advancing the field and improving the care we bring to our patients,” said Giulio Draetta, M.D., Ph.D., chief scientific officer. “Her commitment to research excellence strengthens our entire MD Anderson community, and we applaud her for this well-deserved recognition.”

Lozano is internationally recognized as one of the world’s foremost cancer researchers. She was the first to establish p53 as a transcriptional activator of other genes and highlighted its mutation or deletion as a hallmark of more than 90% of cancers. She also identified the physiological roles of the Mdm2 and Mdm4 proteins as gatekeepers in cancer development and in regulating p53, providing the backbone for potentially using Mdm2/4 inhibitors as a novel targeted therapy approach .

“I am flattered to be recognized for our work on the p53 tumor suppressor pathway and want to thank members of my laboratory for all of their contributions,” Lozano said. “I look forward to continuing our exciting research and advancing new discoveries that will bring us closer to our mission to end cancer.”

Lozano also discovered the key mechanism through which breast cancers with mutant p53 respond better to chemotherapy than those with wild-type p53, and she led the development of laboratory models of mutant p53 that more accurately represent breast and pancreatic cancers. The Lozano laboratory at MD Anderson remains focused on understanding the effects of wild-type or mutant p53 on the tumor microenvironment and on genomic stability in cancer development and progression.

Lozano graduated magna cum laude with degrees in biology and mathematics from The University of Texas Rio Grande Valley. She received her Ph.D. in biochemistry from Rutgers University and the University of Medicine and Dentistry of New Jersey, continuing to Princeton University for a postdoctoral fellowship. She joined MD Anderson in 1987 and has published 261 articles in peer-reviewed journals, reviews and book chapters over the course of her 35 years at the institution, rising to her current position as chair of the department of Genetics. She has also mentored many young scientists, with 33 graduate students receiving their M.S. and Ph.D. degrees under her direction and 29 postdoctoral fellows having trained in her lab.

Lozano is an elected fellow of the American Association for the Advancement of Science (AAAS) and the American Association for Cancer Research (AACR) Academy. She has been elected to the National Academy of Medicine, the National Academy of Sciences, and the American Academy of Arts and Sciences. Among her many honors, she has received the Hubert L. Olive Stringer Distinguished Chair in Oncology in Honor of Sue Gribble Stringer in 2018, the AACR-Minorities in Cancer Research Jane Cooke Wright Lectureship and AACR-Women in Cancer Research Charlotte Friend Lectureship awards, and the 2018 MD Anderson President’s Leadership Award for Advancing Women and Minority Faculty.

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University of Texas M. D. Anderson Cancer Center

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October 27, 2022
MD Anderson hosts Leading Edge of Cancer Research Symposium
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Newswise — HOUSTON ― The University of Texas MD Anderson Cancer Center will host its virtual Leading Edge of Cancer Research Symposium from November 17-18, 2022, featuring presentations and discussions on important topics in discovery and translational research that will drive the next wave of cancer breakthroughs. The event also includes a virtual poster session; interested researchers are encouraged to submit abstracts by October 24, 2022.

The Leading Edge of Cancer Research Symposium will include keynote presentations from Tyler Jacks, Ph.D., president of Break Through Cancer and the David H. Koch Professor of Biology at the Massachusetts Institute of Technology; Alan Ashworth, Ph.D., the E. Dixon Heise Distinguished Professor in Oncology at the University of California San Francisco; and Simona Colla, Ph.D., associate professor of Leukemia at MD Anderson.

The event also will feature a panel discussion, “The Patient Is the Focus: Breakthroughs from Bench to Bedside, Clinical and Multiomics Integration and High Value Cancer Care.” Additional sessions will focus on the following topics:
- Clonal Expansion in Normal and Pathological Tissues: It’s All a Matter of Fitness
- Unleashing the Immune System to Develop Therapeutic Strategies
- Integrated Immune-Microbiome Biomarker Discovery
- Clinical Data Science
“In the spirit of cooperation, MD Anderson is excited to host the Leading Edge of Cancer Research Symposium, and we welcome cancer researchers to participate in sharing cutting-edge discoveries that enable fruitful scientific discussions and innovations in the field,” said Giulio Draetta, M.D., Ph.D., chief scientific officer. “This collaborative environment is accessible to everyone, and we encourage our peers to join our collective mission to end cancer as we strive to bring the best science to our patients.”

For more than 80 years, MD Anderson has advanced impactful research across the spectrum of cancer science. The institution has cultivated a unique environment that allows discoveries to be translated directly to the clinic and, simultaneously, insights from the clinic to inform studies in the lab. This seamless collaborative cycle enables significant breakthroughs at an unmatched pace.

The Leading Edge of Cancer Research Symposium brings together the global research community to engage in beneficial discussions and to stimulate innovative research that will improve patients’ lives. More information on the symposium, including a full agenda and links to register or submit posters, can be found at MDAnderson.org/ResearchSymposium.

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University of Texas M. D. Anderson Cancer Center

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October 13, 2022