Latest news with #ctDNA
Associated Press
2 hours ago
- Business
- Associated Press
ChiMei Medical Center adopts Inocras MRDVision and WGS bioinformatics platform for precision oncology in Taiwan
SAN DIEGO & TAINAN CITY, Taiwan--(BUSINESS WIRE)--Jul 7, 2025-- Inocras Inc., a global leader in whole-genome sequencing (WGS) and bioinformatics, today announced the signing of a Memorandum of Understanding (MOU) with ChiMei Medical Center (CMMC), a premier medical institution in Taiwan, and Trivator Biomedical Limited, a biomedical advisory firm in Taiwan. This expansion agreement aims to introduce Inocras's MRDVision tumor-informed minimal residual disease (MRD) test, utilizing circulating tumor DNA (ctDNA) blood samples, and CancerVision, its AI-powered bioinformatics cloud solution, to support WGS at CMMC, advancing Taiwan's precision oncology landscape. This initiative brings together CMMC's in-house WGS laboratory infrastructure with Inocras's advanced bioinformatics and ctDNA analysis platforms, creating a synergistic ecosystem for both research and clinical-grade genomics. The integration of MRDVision's ultra-sensitive ctDNA monitoring with CancerVision's scalable cloud analytics enables an end-to-end workflow—from sequencing to interpretation—within CMMC's existing clinical operations. CancerVision, Inocras's whole-genome tumor profiling test, forms the foundation for tumor-informed MRD analysis by first characterizing each patient's tumor genome. This enables the application of MRDVision, which monitors circulating tumor DNA (ctDNA) across the entire genome with a simulated limit of detection of 1 part per million (ppm), without requiring patient-specific panels. Powered by Ultima Genomics' ppmSeq technology and Inocras's bioinformatics platform, MRDVision identified tumor signals in 6% of cases missed by a leading MRD assay in a head-to-head clinical study of post-surgical ovarian and lung cancer patients. Integrated into CMMC's sequencing and clinical workflows, CancerVision and MRDVision together provide an end-to-end solution for genome-informed cancer monitoring and personalized treatment assessment. 'We are excited to partner with ChiMei Medical Center and Trivator to bring MRDVision and our CancerVision bioinformatics cloud solution to Taiwan,' said Jehee Suh, CEO of Inocras Inc. 'MRDVision's unmatched sensitivity, combined with CancerVision's robust cloud-based analytics, will empower CMMC to deliver cutting-edge cancer monitoring and precision medicine to patients.' Chi Mei Medical Center, renowned for its leadership in innovative healthcare, will leverage its clinical expertise and advanced infrastructure to implement the MRDVision and CancerVision platforms, further enhancing its whole-genome sequencing (WGS) capabilities. Trivator Biomedical Limited will provide local advisory and logistical support to ensure seamless integration into Taiwan's routine medical practice. 'We are proud to be a regional pioneer in integrating genomic technologies into routine oncology practice,' said Dr. Chein-Feng Li, Director of the Core Laboratory for Precision Medicine at Chi Mei Medical Center. 'By incorporating Inocras's MRDVision and CancerVision platforms, we are strengthening our capabilities in personalized cancer diagnostics and advancing Taiwan's leadership in translational genomic medicine.' 'This collaboration is a transformative step for precision medicine in Taiwan,' said Wen-Tsao Lee, founder of Trivator Biomedical Limited. 'By introducing MRDVision and CancerVision, we are combining Inocras's innovative technologies with CMMC's clinical excellence to redefine cancer care and genomic research.' The MOU serves as a framework for future definitive agreements to scope collaborative projects. The parties are committed to assessing market feasibility, engaging key opinion leaders, and establishing Taiwan as a hub for WGS-based precision medicine, with a focus on MRDVision and CancerVision. For more information about Inocras and its precision medicine solutions, visit View source version on CONTACT: Media Contact Inocras Inc. Gordon Cheung Email:[email protected] Phone: +852-3511-6347ChiMei Medical Center Chein Feng Li Email:[email protected] Phone: +886-6-281-2811 Ext 53680Trivator Biomedical Limited Wen-Tsao Lee Email:[email protected] Phone: +886-955-817-357 KEYWORD: NORTH AMERICA UNITED STATES SOUTH KOREA ASIA PACIFIC TAIWAN CALIFORNIA INDUSTRY KEYWORD: ONCOLOGY HEALTH HEALTH TECHNOLOGY GENETICS RESEARCH SCIENCE BIOTECHNOLOGY SOURCE: Inocras Inc. Copyright Business Wire 2025. PUB: 07/07/2025 10:31 AM/DISC: 07/07/2025 10:32 AM
Medscape
6 days ago
- Health
- Medscape
Emerging Themes in GI Oncology from ASCO 2025
This transcript has been edited for clarity. Hello. I'm Dr Mark Lewis, director of gastrointestinal (GI) oncology at Intermountain Health in Utah. I'm speaking from the 2025 ASCO Annual Meeting in Chicago, where we've seen some interesting new data in GI cancers. I always enjoy doing this kind of on-the-ground reporting, and the real reason I love coming to these meetings is, while it's wonderful to network with colleagues, there is true progress in our field that we can take back almost immediately to our clinics to help our patients. There are three themes in GI oncology that I've seen emerge at this meeting. One is the utility or not of circulating tumor DNA (ctDNA) in affecting treatment decisions. The second is the role of immunotherapy in GI oncology, and the third is, I think, a real triumph for targeted therapy in oncology. Addressing the first, and to be honest, most controversial point: Where are we with ctDNA in GI oncology, and most importantly, where are we with these assays in terms of how we counsel our patients? Sometimes what's most important about ASCO is trials that are arguably negative in their findings. This year, it really caught my attention that DYNAMIC-III sort of turned over the apple carton terms of ctDNA-informed approaches to colon cancer. The design of this study was looking at patients with stage III colon cancer and using a ctDNA-informed approach in a randomized fashion to see if we should be escalating chemotherapy in patients who have a positive ctDNA signal. The randomization was against the standard of care. For years, I think there has been a false binary between using modern ctDNA technology and our traditional clinicopathologic criteria. After all, the whole way we classify stage III colon cancer is based on TNM staging, so that remains the foundation. What we are trying to discern together, and especially together with our patients, is when it is appropriate for this technology to be layered on top of traditional clinicopathologic criteria and thus affect treatment decision-making. The takeaway from this trial for me, especially since recurrence-free survival was worse for the ctDNA-informed cohort vs the standard of care, was that this is a prognostic assay, but not necessarily predictive. Patients who have a ctDNA signal that is positive who had escalation of their adjuvant therapy did not seem to benefit from the addition of, say, irinotecan to a traditional fluoropyrimidine and platinum doublet. Interestingly, also, I think this study validated that roughly one third — maybe no more than 30% — of stage III colon cancer patients have a positive ctDNA signal. My takeaway, again, is we're sort of going back to the future. It was the MOSAIC trial that was published in June 2004 that established the current standard of care for how we approach adjuvant therapy in stage III colon cancer. Now, slightly over two decades later, we really have not made vast improvements in the field, and ctDNA is wonderful, but it is not entirely supplanting the understanding we've had since MOSAIC and since IDEA. Without getting too into the weeds, I'll also point out that I think the statistical design here was ambitious. The hazard ratio in this particular trial, DYNAMIC-III, was frankly suggestive of the fact the study might have been underpowered, enrolling just over 200 patients, whereas MOSAIC had over 2000 to reach its practice-changing conclusions. Watch out for upcoming studies such as CIRCULATE-US and NRG-GI008, which will again use ctDNA negativity to look at de-escalation and ctDNA positivity to look at escalation. Until that trial matures, I don't think this assay is actually going to change the standard-of-care approach to stage III colon cancer in the United States. The second point I'd like to make is about immunotherapy. I love the fact that when patients come to me, and I've been described before our first visit as a chemotherapy doctor, I can tell them that there's more to medical oncology than indiscriminate cytotoxicity. We are truly in the era where immunotherapy has a role to play in a variety of GI cancers. We heard at the ASCO plenary session that immunotherapy has a major role to play now in adjuvant therapy for stage III colon cancer with mismatch repair deficiency. The ATOMIC trial showed a significant 3-year disease-free survival benefit using atezolizumab along with traditional FOLFOX chemotherapy to help patients in the adjuvant setting. The MATTERHORN study showed the advantage of using durvalumab atop FLOT in the perioperative setting in gastric cancer. So two different GI histologies, but a huge role now for immunotherapy in this space. Finally, dealing with metastatic colorectal cancer, the maturation of CheckMate-8HW shows that the ipilimumab-nivolumab (ipi-nivo) doublet definitely has a role to play in the metastatic setting. This has been interesting because when I think about immunotherapy trials that have changed my practice, the one I keep coming back to is KEYNOTE-177. It was such a triumph at the time of its publication and remains so. What's sobering to realize, though, is that as more time has elapsed since KEYNOTE-177 matured, the 5-year survival rate of the pembrolizumab arm remains about 60%. Also, you might remember that the initial survival curve dipped below the chemotherapy arm before it plateaued and improved for immunotherapy. There are certainly some patients who need an earlier, more aggressive response. Enter ipi-nivo. What I like about this trial is that the ipilimumab dosing seems quite conservative, at 1 mg/kg, with four exposures to that agent before nivolumab continues by itself. That's appealing to those of us who have always had some reservations about using an anti-CTLA-4 approach. The very first time I ever used immunotherapy in any setting was during fellowship. It was 2011, and it was ipilimumab in the setting of metastatic melanoma. I watched in amazement as this patient's disease melted away, but at a dose then of 10 mg/kg, the endocrinopathy was significant. I also watched as my patient suffered from pan-hypopituitarism. For medical oncologists who are understandably tentative about anti-CTLA-4 as a mechanism, the question is always, is the juice worth the squeeze? Here, you do get a higher response rate from ipi-nivo than you would with nivolumab alone for patients who, say, might be on the verge of visceral crisis and need a faster initial response. Finally, I want to talk about targeted therapy. I think what was incredible about ASCO this year is realizing just how much progress we're making with BRAF -mutant colon cancer. We have known for a very long time that this mutation confers a worse prognosis, and we've often wondered whether it's appropriate to treat these patients sequentially or should we take the BREAKWATER-informed approach of giving them encorafenib, cetuximab, a fluoropyrimidine, and a platinum upfront — arguably a quadruplet. I think the answer from this meeting is a resounding yes— a doubling of median overall survival from 15 to 30 months by essentially frontloading all of the effective treatment and not trying to do it in sequential lines of therapy. You never get a second chance to make a first impression. Really, what this means is we have to know as soon as possible that we're dealing with a BRAF mutation. There are certain clinical phenotypes that we look for — more aggressive disease, carcinoembryonic antigen rising in the right colon — but this is proof, once again, that the oncologist without the pathologist is blind. I cannot take proper care of my patients without a fully biomarker informed approach, and I can't wait for these test results to come back. This study allowed for at least early exposure to FOLFOX alone while BRAF mutation results were maturing, but we really need to partner with a pathologist and understand metastatic disease in GI the same way we would understand it in metastatic breast cancer. There is not a single breast cancer oncologist I know who would try treating their patients without knowing estrogen receptor, progesterone receptor, and HER2 status. I think we are absolutely at the point in GI oncology where it should be unacceptable to treat our patients without knowing KRAS , NRAS , BRAF , and arguably HER2 status, and certainly mismatch repair or microsatellite instability status. The final targeted therapy triumph at this ASCO looked at DESTINY-Gastric04. DESTINY has been an interesting suite of trials looking at the role of trastuzumab deruxtecan in a variety of HER2-positive cancers. I vividly remember the plenary session several years ago where the data for DESTINY-Breast04 earned a standing ovation. I was one of those people who stood up as a GI oncologist because I could see how this was going to help patients with HER2-positive disease across various primary sites. What we learned at this meeting with the maturation of DESTINY-Gastric04 is this drug particularly seems to outperform traditional second-line therapies such as ramucirumab-paclitaxel. There are downsides. This drug famously (or infamously) causes interstitial lung disease in about 1 in 7 patients. It's also absolutely vital to re-biopsy at time of progression to ensure that the HER2 target for this antibody-drug conjugate is still there. HER2 heterogeneity remains something we haven't fully grappled with, but I find that my patients, when I explain the role of a targeted therapy, are generally willing to undergo another liver biopsy —if they understand the lock and key hypothesis between the HER2 mutation and a drug such as trastuzumab deruxtecan. To sum up, from ASCO 2025 for GI oncology, the three main areas I see of progress, at least in our understanding, are number one, circulating tumor DNA remaining prognostic, but likely not predictive at this point; number two, immunotherapy having a major role to play now in the adjuvant colon cancer setting as well as in perioperative gastric cancer management; and number three, targeted therapy with BREAKWATER really becoming, I think, the standard of care in the first line for BRAF V600E-mutant colon cancer and trastuzumab deruxtecan making a strong play for second-line therapy in HER2-positive gastric cancer. This has been Mark Lewis, the director of medical oncology for gastrointestinal oncology at Intermountain Healthcare, reporting for Medscape from ASCO 2025. Thank you.
Yahoo
6 days ago
- Business
- Yahoo
Natera to Present Clinical and Economic Utility of Signatera at ESMO GI, Highlights Innovations in MRD
AUSTIN, Texas, July 01, 2025--(BUSINESS WIRE)--Natera, Inc. (NASDAQ: NTRA), a global leader in cell-free DNA and precision medicine, announced new data that will be presented at the 2025 European Society for Medical Oncology GI Congress (ESMO GI) in Barcelona, Spain. These presentations reinforce the strong clinical and economic utility of Signatera™ monitoring across colon and rectal cancers (CRC), as well as new clinical validation data on its tissue-free MRD assay. Signatera in CRC surveillance Data on >3,000 CRC patients will be shared in an oral presentation, concluding that adding Signatera ctDNA* monitoring to the current standard of care in surveillance can better identify patients who are candidates for metastasis-directed therapy (MDT). Results indicated that Signatera-positive patients were up to 20x more likely to receive curative-intent MDT than Signatera-negative patients. By comparison, CEA positivity led to only a 2x increase, with no added value in stage IV. Signatera Genome in rectal cancer An analysis will be presented from the MD Anderson INTERCEPT study (n=31) that used serial Signatera Genome testing in patients with locally advanced rectal cancer after neoadjuvant therapy. Results demonstrated 100% specificity/PPV, with surveillance sensitivity of 100% in the surgical cohort and 88% (7/8) overall. Economic utility of Signatera-guided therapy in adjuvant CRC A budget impact model from BUPA, a multinational health insurance provider with over 60 million customers, will outline a 43% expected reduction in healthcare costs using Signatera-guided adjuvant treatment versus standard of care in stage II-III CRC. "We're excited to present these new findings that continue to support the utility of Natera's products across GI cancers," said Adham Jurdi, M.D., senior medical director of oncology at Natera. "These data highlight our commitment to improving outcomes and driving innovation in MRD detection." Full list of data featuring Natera's technology at ESMO GI: July 4, 16:40-16:50 CET | FPN: 20 | Signatera (Oral Presentation)Presenter: Arvind Dasari, M.D., MSClinical utility of including circulating tumor DNA (ctDNA) monitoring in standard of care (SoC) colorectal cancer (CRC) surveillance July 4, 16:50-17:00 CET | FPN: 30 | Signatera (Oral Presentation)Presenter: Hideaki Bando, of ctDNA Clearance with Disease-Free Survival and Safety and Quality of Life from ctDNA-Directed Therapy: Findings from the ALTAIR Study July 4, 15:30-16:30 CET | FPN: 102P | Signatera (Poster Presentation)Presenter: Christos Mikropoulos, MBBS, MSc, M.D. (Res), MRCP, FRCRDirect cost of healthcare analysis of Signatera ctDNA testing in the adjuvant setting for a hypothetical cohort of stage II and stage III colorectal cancer (CRC) patients: a UK private payer perspective July 4, 15:30-16:30 CET | FPN: 243P | Signatera Genome (Poster Presentation)Presenter: Arvind Dasari, M.D., MSClinical performance of Signatera Genome assay in a sub-cohort of locally advanced rectal cancer (LARC) patients (pts) in the MD Anderson INTERCEPT program July 4, 15:30-16:30 CET | FPN: 93P | Tissue-free MRD (Poster Presentation)Presenter: Yoshiaki Nakamura, M.D., validation of a methylation-based, tissue-free colorectal cancer test for the detection of molecular residual disease by circulating tumor DNA July 4, 15:30-16:30 CET | FPN: 89P | Early Cancer Detection (Poster Presentation)Presenter: John P.Y. Shen, of methylation-based biomarkers to predict metastases, treatment effect, and microsatellite status in colorectal cancer Notes*Circulating tumor DNA About Natera Natera™ is a global leader in cell-free DNA and genetic testing, dedicated to oncology, women's health, and organ health. We aim to make personalized genetic testing and diagnostics part of the standard-of-care to protect health and inform earlier, more targeted interventions that help lead to longer, healthier lives. Natera's tests are supported by more than 300 peer-reviewed publications that demonstrate excellent performance. Natera operates ISO 13485-certified and CAP-accredited laboratories certified under the Clinical Laboratory Improvement Amendments (CLIA) in Austin, Texas, and San Carlos, California. For more information, visit Forward-Looking Statements All statements other than statements of historical facts contained in this press release are forward-looking statements and are not a representation that Natera's plans, estimates, or expectations will be achieved. These forward-looking statements represent Natera's expectations as of the date of this press release, and Natera disclaims any obligation to update the forward-looking statements. These forward-looking statements are subject to known and unknown risks and uncertainties that may cause actual results to differ materially, including with respect to whether the results of clinical or other studies will support the use of our product offerings, the impact of results of such studies, our expectations of the reliability, accuracy and performance of our tests, or of the benefits of our tests and product offerings to patients, providers and payers. Additional risks and uncertainties are discussed in greater detail in "Risk Factors" in Natera's recent filings on Forms 10-K and 10-Q and in other filings Natera makes with the SEC from time to time. These documents are available at and View source version on Contacts Investor Relations: Mike Brophy, CFO, Natera, Inc., investor@ Media: Lesley Bogdanow, VP of Corporate Communications, Natera, Inc., pr@ Sign in to access your portfolio
Medscape
24-06-2025
- Health
- Medscape
Blood-Based KRAS Testing Fails in Ovarian Cancer
Blood-based circulating tumor DNA (ctDNA) testing has proven to be insufficient for detecting KRAS mutations in patients with low-grade serous ovarian cancer (LGSOC), according to a study. The findings of the new research suggest that treatment decisions should continue to rely on traditional tumor tissue analysis rather than liquid biopsies for this rare cancer subtype, said study author Els Van Nieuwenhuysen, MD, at the European Society for Medical Oncology Gynecological Cancers Congress 2025. Van Nieuwenhuysen, University Hospitals Leuven, Belgium, presented her analysis of samples from 65 patients enrolled in the RAMP-201 trial at the meeting. She found that blood-based testing missed KRAS mutations in 56% of patients who had detectable mutations in their tumor tissue. The Potential of Liquid Biopsies LGSOC represents less than 10% of all epithelial ovarian cancers but poses unique treatment challenges, Van Nieuwenhuysen said. 'Unlike its high-grade counterpart, LGSOC is driven by alterations in the RAS/MAPK pathway, with KRAS mutations present in approximately 30% of patients,' she said. These tumors show remarkable resistance to conventional chemotherapy, with response rates ranging between 0% and 13%, she added. Based on the RAMP-201 results, the FDA granted accelerated approval in May 2024 for the combination of avutometinib (a RAF/MEK inhibitor) and defactinib (a FAK inhibitor) for patients with KRAS -mutated recurrent LGSOC who failed prior systemic therapy. The combination showed response rates of 44% in patients with KRAS mutations , compared with 17% in those with wild-type KRAS . Van Nieuwenhuysen explained that the indication for patients with KRAS -mutated tumors makes accurate KRAS mutation detection crucial for selecting the most effective treatment. 'We can detect ctDNA because tumor cells can release or shed DNA into the bloodstream by either apoptosis or necrosis,' said Van Nieuwenhuysen during her presentation. However, she noted that ctDNA is only present in small amounts, ranging from approximately 0.1% to 10% of the total circulating DNA. The potential for blood-based testing has generated significant interest as molecular profiling has become a standard practice for ovarian cancer patients. A previous small series of 13 KRAS -mutated patients had detected mutations in blood samples from six patients, which — according to Van Nieuwenhuysen — suggests promise for this less invasive approach. Liquid Biopsy Falls Short in Detecting KRAS mutations The RAMP-201 analysis examined blood samples from 65 patients with confirmed LGSOC; 50 patients had KRAS mutations detected in tumor tissue, and 15 had KRAS wild-type tumors. Using the Tempus xF panel, which tests 105 cancer-related genes, including KRAS , researchers found that only 32% of patients had detectable ctDNA levels above the 0.25% limit of detection. Van Nieuwenhuysen emphasized that the most concerning was the high false-negative rate. Among the 50 patients with tumor tissue-confirmed KRAS mutations, blood-based testing detected mutations in only 22 patients (44%), while 28 patients (56%) showed false-negative results. Patients with wild-type KRAS in tumor samples also tested negative in the blood, indicating no false-positive results. 'These findings suggest that ctDNA screening is not a sufficiently robust method for detecting KRAS mutations in patients with LGSOC,' Van Nieuwenhuysen said, emphasizing that 'treatment decisions should not be made based on the lack of KRAS mutation detection in the blood.' Technical Considerations Kristina Lindemann, MD, of Oslo University Hospital, Norway, who served as discussant during the session, said that technical factors, including the choice of testing panel and timing of sample collection, might have influenced the study's findings. Lindemann noted that the panel used, Tempus, includes 105 genes, explaining that 'the broader the panel, the less sensitivity you get in terms of the limit of detection.' She suggested that a more targeted approach focusing specifically on KRAS mutations 'would potentially have brought down the level limit of detection.' Lindemann also raised questions about sample timing, noting the 'median of 2 years between tissue accessibility and entering the trial.' She emphasized that KRAS mutations typically arise very early in the development of cancer, and they 'may even be lost during the disease trajectory due to treatment pressure.' Tumor Biology May Explain Poor Detection According to Van Nieuwenhuysen, the amount of ctDNA in the blood varies by cancer type, and the low rate of detection of KRAS mutations in ctDNA may reflect the unique biology of LGSOC, suggesting that LGSOC may be a 'low-shedding tumor' compared with other ovarian cancer subtypes. Lindemann provided additional perspective on tumor heterogeneity, citing data from lung cancer showing high discordance rates (primary tumor vs metastasis) in KRAS mutations in lymph node and lung metastases. She added that the location of metastasis might influence ctDNA shedding, as 'metastases with high accessibility of blood cells or sites potentially would be more likely to shed ctDNA.' Looking Ahead Lindemann noted that, despite the limited ability of liquid biopsy to detect KRAS mutations in LGSOC, the study confirms that when KRAS mutations are detected in blood, they correlate with tumor tissue findings. This conclusion was based on no false positives having been observed, she said. However, she emphasized that the high false-negative rate means that negative blood tests cannot rule out the presence of actionable mutations. For now, clinicians treating patients with LGSOC should continue to rely on tumor tissue-based molecular profiling to guide treatment decisions, she concluded. The ongoing RAMP-301 phase 3 confirmatory trial will provide additional data on the clinical utility of KRAS mutation testing in LGSOC. Van Nieuwenhuysen reports financial relationships with AstraZeneca, GSK, MSD, Oncoinvent, Regeneron, Bioncotech Therapeutics, Merck, Novartis, Roche, Seagen, and Verastem Oncology. Lindemann reports financial relationships with GSK, MSD, AstraZeneca, Karyopharm, Eisai, and Genmab.
Yahoo
23-06-2025
- Business
- Yahoo
Exact Sciences Expands Oncodetect Validation, Unveils MRD Innovation Roadmap.
Exact Sciences Corporation (NASDAQ:EXAS) is among the 11 Best Genomics Stocks to Buy According to Hedge Funds. It has released fresh data from the Beta-CORRECT study that validates the clinical efficacy of its tumor-informed Oncodetect™ test for recurrence monitoring in stage II-IV colorectal cancer. A research team in a laboratory discussing the results of a lab screening test for biomarkers. The findings, presented at ASCO 2025, revealed that patients with ctDNA-positive results after therapy and during surveillance had a 24- and 37-fold greater risk of recurrence, respectively. The business also disclosed plans to introduce a next-generation test in 2026 that will use Broad Institute's MAESTRO technology, which can track up to 5,000 patient-specific variations and identify ctDNA levels below 1 part per million. Oncodetect, which was created for molecular residual disease identification, has improved prognosis prediction over standard-of-care approaches in stage III colorectal cancer, as proven by both Alpha- and Beta-CORRECT trials. The revised version uses whole-genome sequencing that is solely licensed from the Broad Institute to improve sensitivity and scalability. This is Exact Sciences Corporation (NASDAQ:EXAS)'s largest MRD clinical research to date, with over 400 patients enrolled, and it reflects the company's ambition to enhance precision oncology through advances based on ctDNA. While we acknowledge the potential of EXAS as an investment, we believe certain AI stocks offer greater upside potential and carry less downside risk. If you're looking for an extremely undervalued AI stock that also stands to benefit significantly from Trump-era tariffs and the onshoring trend, see our free report on the best short-term AI stock. READ NEXT: 10 High-Growth EV Stocks to Invest In and 13 Best Car Stocks to Buy in 2025. Disclosure. None. Error in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
