Survivors of adolescent, young adult cancers at double the risk of future cancers
Peer-Reviewed Publication
Updates every hour. Last Updated: 23-Jun-2026 02:15 ET (23-Jun-2026 06:15 GMT/UTC)
Relevance exists between tumorigenesis and embryonic development. Distinct clinical and molecular features, as well as the relationship between the pattern of lymphoma invasion and germ layer development remain largely unknown. Researchers identified a germ layer-dependent specification of extranodal invasion (ENI) in diffuse large B-cell lymphoma. Upon R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) treatment, mesoderm-originating ENI (ENI-mesoderm) was significantly associated with inferior progression-free survival and overall survival, as compared to ectoderm-originating ENI (ENI-ectoderm) and endoderm-originating ENI (ENI-endoderm). Representative oncogenic mutations were MYD88, PIM1, and TBL1XR1 in ENI-ectoderm, TP53 and TET2 in ENI-endoderm, and MYD88, PIM1, TBL1XR1, and CD79B in ENI-mesoderm. Notably, organotrophic migration exhibited temporal disparities corresponding to germ layer development, occurring from ectoderm- to endoderm- and mesoderm-originating organs, with a similar trajectory to the germ layer process. Single-cell RNA sequencing revealed that malignant B cells follow a developmental trajectory mirroring the germ layer process, differentiating from a progenitor state enriched with NF-κB and T-cell activation signaling into two distinct branches by either upregulated B-cell receptor signaling (Path I) or sustained T-cell activation (Path II). Regarding immune checkpoints, ENI-ectoderm, ENI-endoderm, and ENI-mesoderm exhibited significant upregulation of LGALS9, PD-L1, and B7-H3, respectively. Their findings thus contributed to a better understanding of crosstalk between lymphoma progression and embryonic development, providing new insights into targeted approaches against germ layer-dependent invasion in cancer treatment.
When in life we gain weight can have a significant impact on our health many years later. In a study involving over 600,000 people, researchers at Lund University in Sweden have investigated how changes in weight between the ages of 17 and 60 are linked to the risk of dying from various diseases. The results show a clear pattern: weight gain early in adulthood has the greatest impact.
Macrophages, much like Alice of “Alice in Wonderland,” recognize and consume tumor cells that display “eat me” surface markers. However, tumor cells can evade detection by macrophages if they successfully present “don’t eat me” signals. To counter this, researchers have developed drugs aimed at turning off these “don’t eat me” signals. However, such treatments haven’t been as effective as anticipated in patients with acute myeloid leukemia (AML) and other blood cancers. To better understand why, a team of researchers from Mass General Brigham, Dana-Farber Cancer Institute and the Broad Institute of MIT and Harvard looked at samples from patients treated for AML at Mass General Brigham. The team was led by Jooho Chung, MD, PhD, Mounica Vallurupalli, MD, Todd Golub, MD, and Robert Manguso, PhD.
Results from a phase 2 clinical trial designed and overseen by researchers at Mass General Brigham Cancer Institute show that the investigational medication mezagitamab can effectively boost platelet counts in patients with immune thrombocytopenia (ITP), an autoimmune disease characterized by elevated platelet destruction and reduced platelet production that increases bleeding risk and compromises quality of life.
Researchers at ITQB NOVA, in collaboration with IPO Lisboa, will seek new biomarkers to monitor the progression of the most aggressive types of breast cancer and help personalize treatment by studying how tumors “shut down” the immune system.
Researchers at Oregon Health & Science University have uncovered a key reason why immunotherapy has largely failed in pancreatic cancer — and identified a promising strategy to overcome that resistance.
The study, published in the journal Immunity, shows that pancreatic tumors actively reshape their immune environment by co‑opting regulatory immune cells that normally shut down tumor-killing cells. By reprogramming those cells, the research reveals a potential pathway to make immunotherapy effective against one of the deadliest and most treatment‑resistant cancers.