Publications by authors named "Laura Broutier"

Background: Brain tumors are the deadliest solid tumors in children and adolescents. Most of these tumors are glial in origin and exhibit strong heterogeneity, hampering the development of effective therapeutic strategies. In the past decades, patient-derived tumor organoids (PDT-O) have emerged as powerful tools for modeling tumoral cell diversity and dynamics, and they could then help defining new therapeutic options for pediatric brain tumors.

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Article Synopsis
  • - Pediatric diffuse midline gliomas (pDMG) are aggressive childhood cancers characterized by fatal outcomes and linked to specific genetic mutations, particularly K27M in histone H3.
  • - About 20 to 30% of these tumors have alterations in the BMP signaling pathway, specifically involving mutations in the BMP type I receptor ALK2, but the effects of BMP in non-mutated cases are not fully understood.
  • - Recent research reveals that BMP2 and BMP7 are active in both wild-type and mutant tumors, and they work with the K27M mutation to alter cell behavior, indicating that the BMP pathway could be a target for treatment in pDMG.
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Rhabdomyosarcoma (RMS) is the main form of pediatric soft-tissue sarcoma. Its cure rate has not notably improved in the last 20 years following relapse, and the lack of reliable preclinical models has hampered the design of new therapies. This is particularly true for highly heterogeneous fusion-negative RMS (FNRMS).

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Toll-like receptor 3 (TLR3) is a pattern recognition receptor mainly known for its role in innate immune response to infection. Indeed, binding of double-stranded RNA (dsRNA) to TLR3 triggers a pro-inflammatory cascade leading to cytokine release and immune cell activation. Its anti-tumoral potential has emerged progressively, associated with a direct impact on tumor cell death induction and with an indirect action on immune system reactivation.

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Reliable establishment of tumor organoids is paramount to advance applications of organoid technology for personalized medicine. Here, we share our multi-center experience on initiation and tumorigenic confirmation of hepatobiliary cancer organoids. We discuss current concerns, propose potential solutions, and provide future perspectives for improvements in hepatobiliary cancer organoid establishment.

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Unlike adult cancers that frequently result from the accumulation in time of mutational "hits" often linked to lifestyle, childhood cancers are emerging as diseases of dysregulated development through massive epigenetic alterations. The ability to reconstruct these differences in cancer models is therefore crucial for better understanding the uniqueness of pediatric cancer biology. Cancer organoids (i.

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In vitro three-dimensional (3D) cell culture models, such as organoids and spheroids, are valuable tools for many applications including development and disease modeling, drug discovery, and regenerative medicine. To fully exploit these models, it is crucial to study them at cellular and subcellular levels. However, characterizing such in vitro 3D cell culture models can be technically challenging and requires specific expertise to perform effective analyses.

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The original version of this article contained an error in the name of one of the co-authors (Kayvan Mohkam). This has been corrected in the PDF and HTML versions.

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Pancreatic ductal adenocarcinoma (PDAC) is one of the solid tumors with the poorest prognosis. The stroma of this tumor is abundant and composed of extracellular matrix and stromal cells (including cancer-associated fibroblasts and immune cells). Nerve fibers invading this stroma represent a hallmark of PDAC, involved in neural remodeling, which participates in neuropathic pain, cancer cell dissemination and tumor relapse after surgery.

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Article Synopsis
  • Scientists are working on new ways to grow liver cancer cells in the lab to understand them better.
  • They created special mini-livers called organoids that behave like real liver tissue, keeping important features of the original cancer.
  • These organoids can help researchers find new treatments and better understand how liver cancer works.
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EphA4, an Ephrins tyrosine kinase receptor, behaves as a dependence receptor (DR) by triggering cell apoptosis in the absence of its ligand Ephrin-B3. DRs act as conditional tumor suppressors, engaging cell death based on ligand availability; this mechanism is bypassed by overexpression of DRs ligands in some aggressive cancers. The pair EphA4/Ephrin-B3 favors survival of neuronal progenitors of the brain subventricular zone, an area where glioblastoma multiform (GBM) are thought to originate.

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Adult somatic tissues have proven difficult to expand in vitro, largely because of the complexity of recreating appropriate environmental signals in culture. We have overcome this problem recently and developed culture conditions for adult stem cells that allow the long-term expansion of adult primary tissues from small intestine, stomach, liver and pancreas into self-assembling 3D structures that we have termed 'organoids'. We provide a detailed protocol that describes how to grow adult mouse and human liver and pancreas organoids, from cell isolation and long-term expansion to genetic manipulation in vitro.

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  • DCC is a protein that helps stop tumors from growing by making cancer cells die, but it can be turned off by a substance called netrin-1.
  • In some types of lymphoma, like diffuse large B-cell lymphoma, there seems to be a problem with the balance between DCC and netrin-1, which prevents cancer cells from dying.
  • Research shows that blocking netrin-1 could be a good way to treat certain lymphomas that have too much netrin-1, helping to get rid of the cancer.
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The role of deleted in colorectal carcinoma (DCC) as a tumour suppressor has been a matter of debate for the past 15 years. DCC gene expression is lost or markedly reduced in the majority of advanced colorectal cancers and, by functioning as a dependence receptor, DCC has been shown to induce apoptosis unless engaged by its ligand, netrin-1 (ref. 2).

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