Clinical Trials

This phase III trial compares the effect of adding tivozanib to standard therapy pembrolizumab versus pembrolizumab alone for the treatment of patients with high-risk renal cell carcinoma (RCC). Immunotherapy with monoclonal antibodies, such as pembrolizumab, may help the body's immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Tivozanib is in a class of medications called kinase inhibitors. It works by blocking the action of the abnormal protein that signals tumor cells to multiply. This helps stop the spread of tumor cells. Giving pembrolizumab and tivozanib together may work better than pembrolizumab alone in treating patients with RCC.

This phase III trial compares perioperative chemotherapy (given before and after surgery) versus adjuvant chemotherapy (given after surgery) for the treatment of pancreatic cancer that can be removed by surgery (removable/resectable). Chemotherapy drugs, such as fluorouracil, irinotecan, leucovorin, and oxaliplatin, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Giving chemotherapy before and after surgery (perioperatively) may work better in treating patients with pancreatic cancer compared to giving chemotherapy after surgery (adjuvantly).

NRG-GI008, also known as the “CIRCULATE-NORTH AMERICA” trial, is a clinical study for people with stage III and high-risk stage II colon cancer. The study will be seeking to determine whether chemotherapy is needed for all or only some patients in this population, and, if chemotherapy is needed, what kind of chemotherapy to recommend to patients based on the presence or absence of circulating tumor DNA (ctDNA) following surgery for colon cancer. The study aims to both spare patients who may not need chemotherapy from its side effects and, for patients who do need chemotherapy, to better determine the most effective form of chemotherapy for them.

This partially randomized phase III trial studies the side effects of different combinations of risk-adapted chemotherapy regimens and how well they work in treating younger patients with newly diagnosed standard-risk acute lymphoblastic leukemia or B-lineage lymphoblastic lymphoma that is found only in the tissue or organ where it began (localized). Drugs used in chemotherapy work in different ways to stop the growth of cancer cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Giving more than one drug (combination chemotherapy), giving the drugs in different doses, and giving the drugs in different combinations may kill more cancer cells.

This research trial studies kidney tumors in younger patients. Collecting and storing samples of tumor tissue, blood, and urine from patients with cancer to study in the laboratory may help doctors learn more about changes that occur in deoxyribonucleic acid (DNA) and identify biomarkers related to cancer.

RAS mutations result in upregulation of the mitogen-activated protein kinase (MAPK) pathway and are thought to be key driver mutations in many malignancies. . The importance of RAS mutations is underscored by its high prevalence in human malignancies. Data from the COSMIC database indicates that RAS, which has three highly homologous isoforms KRAS, N-RAS, and HRAS, is mutated in approximately 30% of human malignancies. Mutations in NRAS are found in approximately 8% of human cancers. While most frequently seen in melanomas, NRAS mutations are seen in many other solid malignancies including colorectal, gastric, thyroid, uterine endometrial, lung, among others. Despite enormous efforts from both academia and industry, successful targeting of RAS mutated malignancies has been an elusive goal. Clinical trials testing numerous strategies, including farnesyl transferase inhibitors and combined MEK/PI3K inhibition, have failed to produce widespread, clinically meaningful results. Interestingly, preclinical testing demonstrates that NRAS mutated cell lines are more sensitive to MEK inhibitor than KRAS mutated cell lines. For example, a study of lung cancer cell lines demonstrated that five of six NRAS mutant cell lines were sensitive to the MEK inhibitors. Consistent with in vitro observations, the most successful effort in targeting RAS mutations has been seen in NRAS mutated melanoma. In an open label phase 2 study, treatment of 117 patients with NRAS mutated melanoma with the MEK inhibitor binimetinib resulted in an overall response rate of 14.5% with PFS of 3.6 months and OS of 12.2 months14. In a smaller phase 2 trial of binimetinib, six (20%; 95% CI 8-39%) of 30 patients with NRAS-mutated melanoma had a partial response.

This study gathers health information for the Project: Every Child for younger patients with cancer. Gathering health information over time from younger patients with cancer may help doctors find better methods of treatment and on-going care.

This randomized phase III trial studies how well crizotinib works and compares it to placebo in treating patients with stage IB-IIIA non-small cell lung cancer that has been removed by surgery and has a mutation in a protein called ALK. Mutations, or changes, in ALK can make it very active and important for tumor cell growth and progression. Tumors with this mutation may respond to treatments that target the mutation, such as crizotinib. Crizotinib may stop the growth of tumor cells by blocking the ALK protein from working. It is not yet known if crizotinib may be an effective treatment for treating non-small cell lung cancer with an ALK fusion mutation. Study Arms: 1) Experimental: Arm A (crizotinib) Patients receive crizotinib on days 1-21. Treatment repeats every 21 days for up to 2 years in the absence of disease progression or unacceptable toxicity. 2) Placebo Comparator: Arm B (placebo) Patients receive placebo on days 1-21. Treatment repeats every 21 days for up to 2 years in the absence of disease progression or unacceptable toxicity.

The purpose of this study is to compare the effect on your cancer of using either olaparib by itself or the combination of cediranib and olaparib to the usual chemotherapy given for your cancer (carboplatin and paclitaxel; carboplatin and gemcitabine; or carboplatin and pegylated liposomal doxorubicin [PLD]). Any of these different approaches could shrink your cancer but could also cause side effects. This study will allow the researchers to learn whether giving olaparib by itself or giving the combination of cediranib and olaparib is better, the same, or worse than the usual chemotherapy by observing both the effect of these treatments on your cancer as well as any side effects that may be experienced. Both olaparib and cediranib have already been tested for safety; however, they are not part of the standard approach. Olaparib by itself has been approved by the Food and Drug Administration (FDA) for women with advanced ovarian cancer and a mutation in either BRCA1 or BRCA2 (these are genes in which mutations can be inherited that have been linked to a higher risk of developing cancers, including breast and ovarian cancer) who have received three or more prior treatments for their cancer. The use of olaparib in the setting of platinum-sensitive recurrent ovarian cancer like yours is still being studied and is not FDA-approved. The combination of olaparib and cediranib is still being studied and is not yet FDA-approved. There will be about 450 people taking part in this study. About 5-10 people will be put on this study at this site.

PRIMARY OBJECTIVES: I. To evaluate the disease-free survival (DFS) of patients with stage III-IV squamous cell carcinoma of the head and neck (SCCHN) and disruptive p53 mutations after primary surgical resection followed by postoperative radiotherapy (PORT) alone or PORT with concurrent cisplatin. SECONDARY OBJECTIVES: I. To evaluate the DFS of patients with stage III-IV SCCHN and non-disruptive p53 mutations after primary surgical resection followed by PORT alone or PORT with concurrent cisplatin. II. To evaluate the DFS of patients with stage III-IV SCCHN and p53 wild type after primary surgical resection followed by PORT alone or PORT with concurrent cisplatin. III. To evaluate toxicities of PORT alone or PORT with concurrent cisplatin. IV. To evaluate p53 mutation as a predictive biomarker of survival benefit given post-operative concurrent radiation and cisplatin. V. To identify potential genomic alterations in addition to TP53 mutations that may be developed to a novel treatment approach. OUTLINE: Patients are randomized to 1 of 2 treatment arms. ARM A: Patients undergo intensity-modulated radiation therapy (IMRT) once daily (QD) 5 days a week for 6 weeks in the absence of disease progression or unacceptable toxicity. ARM B: Patients undergo IMRT QD 5 days a week and receive cisplatin intravenously (IV) over 1-2 hours weekly for 6 weeks in the absence of disease progression or unacceptable toxicity. After completion of study treatment, patients are followed up every 6 months for 3 years and then every 12 months for 7 years.