bims-tumhet Biomed News
on Tumor heterogeneity
Issue of 2026–02–01
five papers selected by
Sergio Marchini, Humanitas Research



  1. Curr Oncol. 2025 Dec 29. pii: 17. [Epub ahead of print]33(1):
      Advanced-stage epithelial ovarian cancer (EOC) is defined by biological heterogeneity and poor outcomes, and traditional survival metrics fail to reflect the evolving nature of prognosis as patients survive longer. This study aimed to evaluate conditional survival (CS) in advanced EOC using both overall survival (OS) and progression-free survival (PFS) metrics to provide a dynamic understanding of long-term outcomes. We retrospectively analyzed 808 patients with FIGO stage III-IV EOC who underwent surgery at Baskent University Ankara Hospital between 2004 and 2024. CS estimates were calculated for additional 1- and 5-year intervals among patients who had already survived 6 months, 1, 3, or 5 years after surgery. Median OS and PFS were 4.37 and 1.70 years, respectively. Peritoneal dissemination and platinum resistance were independent predictors of poor survival. Approximately 11% of patients achieved survival beyond ten years. The 1-year CS-OS increased from 87% at 6 months to 95% at 5 years, while the 5-year CS-OS rose from 49% to 66%; corresponding CS-PFS values increased from 89% to 95% and from 44% to 62%. Conditional survival analysis underscores that prognosis in advanced ovarian cancer is not static but continually improves with time survived and sustained disease control. These insights redefine long-term outcomes and provide a modern foundation for individualized patient counseling and survivorship planning.
    Keywords:  conditional survival; disease progression; long-term survival; ovarian carcinoma; prognosis
    DOI:  https://doi.org/10.3390/curroncol33010017
  2. Clin Cancer Res. 2026 Jan 27.
       PURPOSE: Cancers present significant DNA methylation changes, which arise in a stochastic manner, marked by extensive epigenetic variation, indicative of high epigenetic instability. We aimed to evaluate the utility of epigenetic instability for cell-free DNA (cfDNA)-based cancer detection.
    EXPERIMENTAL DESIGN: Through analysis of cancer DNA methylation datasets (n=2,084), we identified a set of 269 CGI regions that robustly captures this instability in a cancer-specific manner. We developed metrics to measure this epigenetic instability, termed the Epigenetic Instability Index (EII), for cancer screening via cfDNA methylation.
    RESULTS: Machine learning classifiers employing the EII of these 269 regions efficiently identified breast and lung cancer from cfDNA, differentiating even stage IA LUAD with ~81% sensitivity and early-stage breast cancer with ~68% sensitivity, both at 95% specificity.
    CONCLUSION: Our studies demonstrate that quantifying epigenetic instability is a novel, capable approach to distinguishing cancer from normal cases using cfDNA, performing better than standard approaches using absolute methylation changes. The epigenetic instability-based approaches for cancer detection developed here, along with their validation in independent datasets, support further development and the potential for future clinical application of these strategies in cancer screening.
    DOI:  https://doi.org/10.1158/1078-0432.CCR-25-3384
  3. NPJ Precis Oncol. 2026 Jan 24.
      Circulating tumor DNA (ctDNA)-based response assessment is appealing but limited by conventional analytical thresholds. We utilized a whole genome sequencing based, tumor-informed ultrasensitive ctDNA assay which tracked ~1800 somatic mutations to analyze 227 longitudinal plasma samples from 39 patients with advanced/metastatic cancers receiving immune checkpoint inhibitors (ICIs). ctDNA was detected from 2.0-239,315 PPM (median limit of detection: 1.77 PPM), with 33% of positive detections below 100 PPM. Early molecular response, defined as >50% ctDNA reduction or sustained ctDNA negativity from baseline to first follow-up, strongly predicted improved progression-free survival (PFS) (hazard ratio (HR) = 0.09, 95% CI: 0.02-0.39, p = 0.001) and was independently prognostic of PFS. Molecular complete response (mCR), defined as any ctDNA clearance, predicted overall survival and PFS, with 1-year PFS of 87% in mCR patients versus 16% in non-mCR patients (HR = 0.14, 95% CI: 0.04-0.50, p = 0.003). The high-sensitivity ctDNA monitoring may enable precise, real-time evaluation of ICI response to guide clinical decision-making.
    DOI:  https://doi.org/10.1038/s41698-026-01287-3
  4. Cancer. 2026 Feb 01. 132(3): e70286
      Minimal residual disease (MRD) refers to the presence of residual cancer cells or tumor-derived fragments that persist after treatment and remain undetectable by conventional imaging or protein-based assays. Circulating tumor DNA (ctDNA) has emerged as a dynamic biomarker for MRD detection. It enables real-time disease monitoring, prognostication, and often therapeutic decision-making. Two major ctDNA approaches exist, tumor-informed and tumor-agnostic, and they differ in sensitivity, specificity, and clinical feasibility. Recent clinical trials have supported a prognostic and predictive utility of ctDNA MRD in gastrointestinal, lung, breast, and other malignancies, with positive postoperative or post-treatment MRD status correlating with higher recurrence risk and inferior survival outcomes. However, integration into clinical practice remains limited by challenges, including tumor heterogeneity, variable ctDNA shedding across tumor stage, location and timing, lack of standardized assay interpretation, and cost-effectiveness concerns. Emerging technologies such as methylation-based sequencing, ultra-deep next-generation sequencing, and machine learning-driven risk models hold promise for improving detection accuracy and clinical applicability. Ongoing clinical trials are expected to determine the impact of earlier MRD detection and intervention on patient outcomes, potentially supporting the broader adoption of ctDNA MRD. In this article, the authors reviewed the recent clinical applications, limitations and future directions of MRD in solid tumors.
    Keywords:  cancer monitoring; circulating tumor DNA; clinical applications; minimal residual disease; prognostic and predictive biomarker; solid tumors
    DOI:  https://doi.org/10.1002/cncr.70286
  5. Clin Cancer Res. 2026 Jan 29.
       PURPOSE: This study aimed to evaluate the efficacy and safety of poly(ADP-ribose) polymerase inhibitor (PARPi) rechallenge combined with bevacizumab as maintenance therapy in patients with platinum-sensitive recurrent ovarian cancer previously treated with a PARPi.
    EXPERIMENTAL DESIGN: KGOG 3056/NIRVANA-R is a multicenter, single-arm, phase II trial that enrolled 44 patients with platinum-sensitive recurrent ovarian cancer who had received ≥2 prior lines of platinum-based chemotherapy and prior PARPi maintenance. Eligible patients achieving a response to the most recent platinum therapy received daily niraparib and triweekly bevacizumab until disease progression or unacceptable toxicity. The primary endpoint was the 6-month progression-free survival (PFS) rate, analyzed using Simon's two-stage design with adaptive statistical inference.
    RESULTS: The primary endpoint was met, with 26 of 44 patients (59.1%) remaining progression-free at 6 months. The estimated 6-month PFS rate was 68% [95% confidence interval (CI), 55%-85%], and the median PFS was 11.5 months [95% CI, 7.9-not reached]. Subgroup analyses suggested greater benefit in patients with a longer treatment-free interval after the penultimate chemotherapy and in those who achieved a complete response to the most recent chemotherapy. Grade ≥3 treatment-related adverse events occurred in 27.3% of patients, with no treatment-related deaths or new safety signals observed.
    CONCLUSIONS: This is the first report of PARPi rechallenge with bevacizumab as maintenance therapy in this setting. The combination demonstrated promising efficacy, particularly in patients with favorable platinum responsiveness, and warrants further investigation in biomarker-driven studies.
    DOI:  https://doi.org/10.1158/1078-0432.CCR-25-2916