Primary objectives:
Evaluate the feasibility of rapidly accruing 30 participants with recurrent metastatic head and neck squamous cell carcinoma for the development of patient derived xenographs (PDX) from fresh, real time biopsies in which sensitivity to < 4 Ontario funded chemotherapeutic regimen will be tested. Written feedback to the primary oncologist will be provided.
There is also a curative intent cohort of 30 participants undergoing surgical resection with curative intent. These PDX models will undergo exome sequencing with written feedback.
Feasibility in both surgical and recurrent cohorts will be a measure of i) engraftment rate, ii) patient status at the time of drug testing completion and iii) rate of accrual.

Start Date01 Nov 2015

Sponsor / Collaborator

Lawson Health Research Institute

[+1]

NCT02720796 / TerminatedNot Applicable

A Prospective Correlative Trial of Personalized Patient-Derived Xenograft (PDX or TumorGraft) Modeling in Adult Patients With Metastatic or Recurrent Sarcoma

Patients with recurrent or metastatic sarcoma will be consented to develop a patient derived xenograft (PDX or TumorGraft) model of their tumor to perform drug sensitivity testing. The purpose of the study is to evaluate the accuracy of the patient derived xenograft (PDX) model in predicting patient clinical response to the same drug treatment.

Start Date01 Nov 2015

Sponsor / Collaborator

Champions Oncology, Inc.

[+1]

NCT02247037 / CompletedNot ApplicableIIT

Patient-derived Xenograft (PDX) Modeling of Treatment Response for Triple Negative Breast Cancer

This study will determine if patient-derived tumor xenograft (PDX) mouse models can serve as a reliable model for treatment response for individual patients with triple negative breast cancer. The collection of patient tumor tissue will also provide insight into the mechanisms of therapeutic resistance for those individuals. Ultimately, this study will enhance our understanding of the genomic basis for treatment response for triple negative cancer on an individual basis, while having the potential to suggest new therapeutic options for high-risk triple negative breast cancer patients with residual disease post neoadjuvant.

Start Date01 Jul 2014

Sponsor / Collaborator

Icahn School of Medicine at Mount Sinai

[+1]

100 Clinical Results associated with Champions Oncology, Inc.

0 Patents (Medical) associated with Champions Oncology, Inc.

Literatures (Medical) associated with Champions Oncology, Inc.

02 May 2024·Cancer Research

Abstract PO5-24-12: IRX5010, a Highly Selective RARγ Nuclear Receptor Agonist Compound Inhibits In Vivo Growth of Murine EMT-6 Triple Negative Breast Cancer and Human JIMT-1Her2+ Breast Cancer By Induction of Tumor-Infiltrating Effector Memory T-cells

Author: Vuligonda, Vidyasagar ; Sanders, Martin ; Topalovski, Mary

AbstractResearch Objectives and Rationale: Previously, RARγ agonism has been shown to play an essential role in CD8 T-cell-mediated immunity to infectious pathogens. However, we found no previous reports on effects of RARγ agonists on in vivo tumor growth of triple negative or Her2+ breast cancers. Here we explored whether RARγ could play a critical role in T-cell-mediated immunity in these breast cancers, using potent highly selective novel RARγ agonist compounds.Experimental methods and results: We synthesized and screened compounds for selective transactivation of RAR γ in reporter assays. Three highly potent compounds, demonstrating highly selective RARγ transactivation at less than one nanomolar concentrations, were selected for further evaluation of potential anti-cancer activities in vitro. None of the three evaluated compounds demonstrated significant inhibitory effects on in vitro growth of EMT-6 triple negative breast cancer cells at concentrations of 20-100 millimolar, indicating that the three compounds have insignificant direct inhibitory effects on EMT-6 cancer cell growth in vitro. We then examined the effects of one of the compounds in vivo in a syngeneic mouse model of EMT-6 triple negative breast cancer. Treatment with the most potent of the three compounds, IRX5010, demonstrated dose response inhibition of in vivo growth of EMT-6 tumors. Inhibition of tumor growth at day 17 relative to vehicle was 59% and 69% respectively in mice treated with IRX5010 at 10 or 25 mg/kg/day. A cohort treated with 50 mg/kg/day was sacrificed early on day 12 due to excessive weight loss and deaths of some of the animals. This cohort experienced a 73% inhibition of tumor growth relative to vehicle. Gross necropsies of animals in the 25 and 50 mg/kg/day dose groups did not show observable pathologic findings in any major organ. Flow cytometry was performed on freshly excised tumors on the day of termination of the in-life portion of the study in the 10 and 25 mg/kg/day dose groups. Tumors from mice treated with IRX5010 had increased intratumoral numbers of Total CD45+ cells; Total CD3+, Total CD4+, and Total CD8+ T-cells per mg of tumor tissue, relative to vehicle controls. IRX5010 treated mice also had increased intratumoral CD4+IL-17+ T-helper cells; and increased CD4+CD62L- and CD8+CD62L- T-effector memory T-cells per mg of tumor tissue relative to vehicle-treated control mice.We also conducted an experiment of treatment with IRX5010 in mice transplanted with human immune cells (to provide a human immune system) to examine its effects on xenografted human Her2+ JIMT-1 cancer cells. In this model, treatment with IRX5010 at 10 mg/kg/day resulted in a 17% inhibition of tumor growth relative to vehicle control over 26 days of treatment. Flow cytometric analysis showed that tumors from the IRX5010 treated mice contained increased numbers per mg of tumor tissue of intratumoral human CD8+ T-cells, most of which were CD8+ CD7- CD45RA+ terminally differentiated effector memory phenotype T-cells.Conclusions: Treatment with IRX5010, a potent and highly selective RARγ nuclear receptor agonist compound demonstrated substantial treatment effects relative to vehicle control on inhibition of growth of murine triple negative breast cancer in vivo, despite having essentially no growth inhibitory effect on these cells in vitro. Treatment of xenografted human Her2+ tumors in mice with humanized immune systems resulted in a moderate inhibition of Her2+ breast cancer growth relative to vehicle controls. In both models, treatment with IRX5010 induced tumor infiltrating T-lymphocytes of largely effector memory phenotypes, demonstrating an effect on the tumor immune microenvironment. These data identify RARγ and RARγ agonists as a new treatment target and novel treatment modality for breast cancers, especially for the highly unmet need for new and better treatments for triple negative breast cancer.Citation Format: Martin Sanders, Mary Topalovski, Vidyasagar Vuligonda. IRX5010, a Highly Selective RARγ Nuclear Receptor Agonist Compound Inhibits In Vivo Growth of Murine EMT-6 Triple Negative Breast Cancer and Human JIMT-1Her2+ Breast Cancer By Induction of Tumor-Infiltrating Effector Memory T-cells [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-24-12.

02 May 2024·Cancer Research

Abstract PO4-23-08: Estrogen therapy induces receptor-dependent DNA damage enhanced by PARP inhibition in ER+ breast cancer

Author: Heverly, Paul ; Duffy, Emily ; Johnson, Anneka ; Mosesson, Yaron ; Kolling, Fred ; Marotti, Jonathan ; Demidenko, Eugene ; Schwartz, Gary ; Miller, Todd ; Soucy, Shannon ; Goen, Abigail ; Hosford, Sarah ; Tau, Steven ; Romo, Bianca ; Roberts, Alyssa ; Jiang, Amanda ; Traphagen, Nicole

AbstractAlthough clinical evidence indicates that treatment with estrogens elicits anti-cancer effects in ~30% of patients with advanced endocrine-resistant ER+ breast cancer, the underlying mechanism of action is unclear and this treatment remains under-utilized. ER+ breast cancer cells with acquired resistance to long-term estrogen deprivation (LTED) were used to model resistance to aromatase inhibitors (AIs) seen clinically. Genome-wide CRISPR/Cas9 knockout screening and transcriptomic profiling of LTED cells highlighted DNA Damage Response as a required pathway for therapeutic response to the estrogen 17b-estradiol. Tumor specimens from 2 patients with advanced ER+ breast cancer showed increased DNA damage response upon treatment with 17b-estradiol therapy compared to baseline. LTED cells treated with 17b-estradiol exhibited replication-dependent markers of DNA damage and the DNA damage response prior to apoptosis, while parental cells did not. Such DNA damage was partially driven by the formation of DNA:RNA hybrids (R-loops), and RNase H1-mediated prevention of R-loop formation abrogated 17b-estradiol-induced DNA damage. Pharmacological suppression of the DNA damage response via poly(ADP-ribose) polymerase (PARP) inhibition with olaparib enhanced 17b-estradiol-induced DNA damage. PARP inhibition synergized with 17b-estradiol to suppress growth and prevent tumor recurrence in both BRCA1/2-mutant and BRCA1/2-wild-type cell line and patient-derived xenograft models. We therefore conclude that 17b-estradiol-induced ER activity drives DNA damage and growth inhibition in endocrine-resistant breast cancer cells, and inhibition of the DNA damage response using drugs such as PARP inhibitors can exacerbate transcriptional stress and enhance therapeutic response to 17b-estradiol. This concept is being explored clinically in the PHOEBE trial testing the combination of 17b-estradiol and olaparib (NCT05900895). These findings also warrant further study of other DNA damage response inhibitors in advanced ER+ breast cancer. Moreover, these data indicate that PARP inhibitors may have applications beyond homologous recombination-deficient tumors.Citation Format: Nicole Traphagen, Gary Schwartz, Steven Tau, Alyssa Roberts, Amanda Jiang, Sarah Hosford, Jonathan Marotti, Abigail Goen, Bianca Romo, Anneka Johnson, Emily Duffy, Eugene Demidenko, Paul Heverly, Yaron Mosesson, Shannon Soucy, Fred Kolling, Todd Miller. Estrogen therapy induces receptor-dependent DNA damage enhanced by PARP inhibition in ER+ breast cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO4-23-08.

01 Apr 2024·Lung Cancer

Ex vivo drug testing of patient-derived lung organoids to predict treatment responses for personalized medicine

Review

Author: Chen, Chun-Liang ; Sambandam, Vaishnavi ; Williams, Ryan ; Williams, Madison ; Hsiang-Ling Chiu, Cheryl ; Schiavini, Paolo ; Gaczynska, Maria E ; Gaspard, Christine ; Osmulski, Pawel A ; Kamali, Samaneh ; Song, Lina ; Hung, Chia-Nung ; DeArmond, Daniel T ; Jin, Lingtao ; Kusi, Meena ; Chen, Meizhen ; Mancini, Maria ; Pandya, Abhishek N ; Taverna, Josephine A

Lung cancer is the leading cause of global cancer-related mortality resulting in ∼ 1.8 million deaths annually. Systemic, molecular targeted, and immune therapies have provided significant improvements of survival outcomes for patients. However, drug resistance usually arises and there is an urgent need for novel therapy screening and personalized medicine. 3D patient-derived organoid (PDO) models have emerged as a more effective and efficient alternative for ex vivo drug screening than 2D cell culture and patient-derived xenograft (PDX) models. In this review, we performed an extensive search of lung cancer PDO-based ex vivo drug screening studies. Lung cancer PDOs were successfully established from fresh or bio-banked sections and/or biopsies, pleural effusions and PDX mouse models. PDOs were subject to ex vivo drug screening with chemotherapy, targeted therapy and/or immunotherapy. PDOs consistently recapitulated the genomic alterations and drug sensitivity of primary tumors. Although sample sizes of the previous studies were limited and some technical challenges remain, PDOs showed great promise in the screening of novel therapy drugs. With the technical advances of high throughput, tumor-on-chip, and combined microenvironment, the drug screening process using PDOs will enhance precision care of lung cancer patients.

News (Medical) associated with Champions Oncology, Inc.

04 Dec 2023

·www.biospace.com

Champions Oncology to Announce Second Quarter Financial Results on Tuesday, December 12, 2023

HACKENSACK, NJ / ACCESSWIRE / December 4, 2023 / Champions Oncology, Inc. (CSBR), a global preclinical and clinical research services provider that offers end-to-end oncology solutions, will report its financial and operational results for the second quarter ended October 31, 2023, on Tuesday, December 12, 2023, after market close. The company will host a conference call to discuss the results that day at 4:30 P.M. EST (1:30 P.M. PST). To join the call dial 888-506-0062 (Domestic) or 973-528-0011 (International) and enter the access code 589886. A replay of the call will be available by dialing 877-481-4010 (Domestic) or 919-882-2331 (International) and entering passcode: 49578, or by accessing the investors section of the company's website within 72 hours. About Champions Oncology, Inc. Champions Oncology is a global preclinical and clinical research services provider that offers end-to-end oncology R&D solutions to biopharma organizations. With the largest and most annotated bank of clinically relevant patient-derived xenograft (PDX) and primary hematological malignancy models, Champions delivers innovative highest-quality data through proprietary in vivo and ex vivo platforms. Through its large portfolio of cutting-edge bioanalytical platforms, groundbreaking data platform and analytics, and scientific excellence, Champions enables the advancement of preclinical and clinical oncology drug discovery and development programs worldwide. For more information, please visit . SOURCE: Champions Oncology, Inc. View source version on accesswire.com:

Financial Statement

02 Nov 2023

·www.biospace.com

Champions Oncology's European Research Operations Site Receives ISO-9001:2015 Accreditation and ATS Certification

HACKENSACK, NJ / ACCESSWIRE / November 2, 2023 / Champions Oncology, Inc. (NASDAQ:CSBR), a global preclinical and clinical research services provider that offers end-to-end oncology solutions, announced its European research operations site in Bresso, Italy, received ISO-9001:2015 laboratory accreditation from the Bureau Veritas S.p.A. and ATS certification from the Lombardy Region. These two achievements together continue to strengthen Champions Oncology's reputation as a global clinical specialty testing provider within Europe. These standards demonstrate that Champions is qualified to design assays, deliver analysis, and manage data effectively for clinical trials using flow cytometry or pathology techniques. Obtaining ISO-9001:2015 accreditation and ATS certification validates the quality of clinical testing services that Champions Oncology's European research team can provide and will enable specialty testing of clinical patient sample across all phases for our global biopharma partners in Europe. Ronnie Morris, CEO of Champions Oncology stated, "We are extremely proud of our talented scientists. With these achievements, we can continue to grow our customer base in Europe, while continuing to provide clinical expertise and fostering relationships with our existing clients." About Champions Oncology Champions Oncology is a global preclinical and clinical research services provider that offers end-to-end oncology R&D solutions to biopharma organizations. With the largest and most annotated bank of clinically relevant patient-derived xenograft (PDX) and primary hematological malignancy models, Champions delivers innovative highest-quality data through proprietary in vivo and ex vivo platforms. Through its large portfolio of cutting-edge bioanalytical platforms, groundbreaking data platform and analytics, and scientific excellence, Champions enables the advancement of preclinical and clinical oncology drug discovery and development programs worldwide. For more information, please visit . Media Inquiries: Rachel Bunting, MS, MBA VP, Global Marketing Marketing@ChampionsOncology.com Website: Facebook: LinkedIn: Twitter: Instagram: SOURCE: Champions Oncology, Inc. View source version on accesswire.com:

17 Oct 2023

·www.biospace.com

Champions Oncology Announces the Addition of Brady Davis as President

HACKENSACK, NJ / ACCESSWIRE / October 17, 2023 / Champions Oncology, Inc. (Nasdaq:CSBR), a global preclinical and clinical research services provider that offers end-to-end oncology solutions, has appointed Brady Davis as President to continue to develop new strategic initiatives to drive accelerated growth. "We are thrilled to have Brady join the already incredibly talented team here at Champions Oncology. Brady has deep healthcare, data and oncology-specific experience and has a proven track record of building products and solutions that align with customer needs," stated Ronnie Morris, CEO of Champions Oncology. Mr. Davis brings more than 25 years of international experience leading medical instrument, software, data, and services companies in the healthcare space. As an executive leader, he has advanced commercial, product/market development, marketing, and bioinformatics teams in both established (Hewlett Packard, Oracle, Illumina) and developing (DNAnexus, Canexia Health) companies. Mr. Davis will be collaborating with the executive team including the commercial and scientific teams to explore strategies to accelerate growth, both organically and in-organically. "At a time of great advancements in cancer multi-omics research and bioinformatics, I am honored to join Champions Oncology at this juncture, in the efforts to help accelerate growth through our proprietary data and platforms," said Mr. Davis. "I am confident that we will further solidify the company's leadership position as the premier tech-enabled clinical and preclinical research partner, advancing precision oncology around the world." About Champions Oncology Champions Oncology is a global preclinical and clinical research services provider that offers end-to-end oncology R&D solutions to biopharma organizations. With the largest and most annotated bank of clinically relevant patient-derived xenograft (PDX) and primary hematological malignancy models, Champions delivers innovative highest-quality data through proprietary in vivo and ex vivo platforms. Through its large portfolio of cutting-edge bioanalytical platforms, groundbreaking data platform and analytics, and scientific excellence, Champions enables the advancement of preclinical and clinical oncology drug discovery and development programs worldwide. For more information, please visit . Media Contact: Rachel Bunting, MS, MBA VP, Global Marketing Marketing@ChampionsOncology.com Website: Facebook: LinkedIn: Twitter: Instagram: SOURCE: Champions Oncology, Inc. View source version on accesswire.com:

Executive Change

100 Deals associated with Champions Oncology, Inc.

100 Translational Medicine associated with Champions Oncology, Inc.

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The statistics for drugs in the Pipeline is the current organization and its subsidiaries are counted as organizations,Early Phase 1 is incorporated into Phase 1, Phase 1/2 is incorporated into phase 2, and phase 2/3 is incorporated into phase 3

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Drug(Targets)	Indications	Global Highest Phase

CO-1024	Solid tumor More	Preclinical
CO-1008	Acute Myeloid Leukemia More	Preclinical
Anti-COF-01 Raptamer-drug conjugates	Neoplasms More	Preclinical
CO-1002	Solid tumor More	Preclinical
CO-1023	Solid tumor More	Discovery

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