Cancer

Hodgkin lymphoma (HL) is curable in most cases by modern chemotherapy with/without radiotherapy (CT"‰Â±"‰RT). Most treatment failures represent either primary refractory disease or early relapses within 1 year (PR/ER). Relapses >1 year from treatment completion are considered "late relapses" (LR) associated with better outcomes [1]. The relapse rate gradually drops after the first year [2] and patients with sustained complete remission (CR) for >5 years are generally considered "cured". However, relapses after >5 years (very late relapses (VLRs)) occasionally occur, and, until recently, VLRs after CT"‰Â±"‰RT had been evaluated in rather small patient series [3,4,5,6,7,8,9,10,11]. In 2005, we initially analyzed the incidence of VLRs-those occurring >5 years from initial treatment initiation-and searched for relevant prognostic factors. In 2017, the German Hodgkin Study Group (GHSG) analyzed the incidence of VLRs in 4935 patients mainly treated with CT"‰Â±"‰RT within the HD7-HD12 trials, reporting a linear pattern of continuous relapses up to 20 years [12]. However, it continuous to be unclear if this linear trend continues beyond 20 years without reaching a plateau and if baseline prognostic factors or treatment regimens or RT strategies affect the risk of VLR.

Leukemia is often the result of the disruption to the fine balance in blood cell production where new cells are manufactured and old blood cells die. As we age, mutations in blood stem cells can mean that the altered cells can have a growth benefit over other blood cells and outnumber them in what is referred to as fitness advantage.

More than 11,000 bowel cancer deaths could be prevented by simply sending an additional invitation to people who have not yet been screened, a new study by the University of Sheffield has found. The study, funded by Cancer Research UK, found that re-inviting those people who had not returned their...

Glioblastoma multiforme (GBM) is the most malignant brain tumor and is refractory to conventional therapies. Although previous studies have proposed that the interaction between gene mutations and the external environment leads to the occurrence of GBM, the pathogenesis of GBM is still unclear and much remains to be studied. Herein, we show an association between human glycoprotein stanniocalcin-2 (STC2) and aggressive GBM progression, and demonstrate the underlying mechanism. Elevated STC2 expression and secretion greatly increase GBM cell growth and invasive phenotypes. Mechanistically, both, conditioned media (CM) containing STC2 and recombinant STC2, can induce the transformation of GBM cells into more malignant phenotypes by upregulating the expression of the epithelial-mesenchymal transition transcription factor, snail family transcription repressor 2 (SNAI2) as well as matrix metalloproteinases (MMPs). Moreover, we further demonstrate that the oncogenic function of STC2 in GBM is mediated through the MAPK signaling pathway. Collectively, these results identify the mechanism of STC2 targeting SNAI2 and MMPs through the MAPK pathway in GBM, and provide insights into a potential therapeutic strategy for GBM.

The cure rate of children with Burkitt lymphoma (BL) and -leukemia (B-AL) reaches 90% with NHL-BFM-type chemotherapy. Only children with clinical high-risk disease (stage III or IV, LDH"‰>"‰500U/l and/or CNS-involvement, risk groups R3 and R4; supplementary table 1) have a relapse rate exceeding 15% and their survival at relapse is 20% [1,2,3,4]. Therefore, early identification of children with highest risk of relapse among clinical high-risk patients is essential for further therapy optimization. The goal of our study was to analyze the prognostic value of IG-MYC-breakpoints from the hallmark translocations t(8;14) (IGH-MYC), t(2;8) (IgK-MYC) and t(8;22) (IGL-MYC) and apply them to evaluate quantitative minimal disseminated disease (MDD, for BL) or minimal residual disease (MRD, for B-AL) as risk factors among children with high-risk disease.

One of the chief challenges cancer researchers face today is finding a way to outsmart the disease’s defense mechanisms. Because the cancer isn’t an infection but a mutation of the patient’s own cells, it has a unique ability to evade attack from the immune system, both by hiding from it and by suppressing it.

Seagen Inc SGEN announced full results from the phase 2 MOUNTAINEER trial, which showed Tukysa (tucatinib) combined with trastuzumab was well-tolerated with durable responses in patients with previously treated HER2-positive metastatic colorectal cancer (mCRC). Topline results were announced in May. At a median duration of follow-up of 20.7 months, the...

AstraZeneca Plc AZN has agreed to acquire TeneoTwo, Inc, including its Phase 1 clinical-stage CD19/CD3 T-cell engager, TNB-486, currently under evaluation in relapsed and refractory B-cell non-Hodgkin lymphoma. Deal consideration includes an upfront payment of $100 million. AstraZeneca will make additional contingent R&D-related milestone payments of up to $805 million...

Drew Laird was 18 when a fit stranger on a bicycle who appeared to be in his 60s changed Laird’s mindset forever. The encounter happened in April 2020 when out of pandemic boredom Laird decided to take a ride on his rarely used bicycle, setting out on the Farmington Canal trail, an easy, safe ride. He was “huffing and puffing” and surprised his baseline fitness wasn’t better at his age, when a ...