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Geha, S.

Publications and source records attributed to Geha, S..

2 recordsLinked to original sources

Development of metastases in mice induced by plasma sample collected during radiotherapy in patient with triple-negative breast cancer: Role of Rab4A

The relapse rate in early-stage triple-negative breast cancer (TNBC) is significantly higher than in other breast cancer subtypes. This study assessed the relevance to target RAB4A to prevent the development of metastases that occur after treatment. The ability of cancer cells to invade peritumoral tissue is associated with the expression of membrane-type matrix metalloproteinase-1 on their surface, which is regulated by RAB4A. When RAB4A was downregulated using shRNA in the TNBC cells D2A1 and MDA-MB-231, a significant reduction in the proteolytic activity of MT1-MMP and the invasion capacity of these TNBC cells were measured. Plasma samples from an early-stage TNBC patient, who developed metastases six months after treatment, were collected before radiotherapy and after the fourth radiation dose. Compared to the plasma collected before radiotherapy, the plasma collected during the treatment significantly enhanced the invasiveness of the TNBC cells, as assessed with Boyden chambers. The development of lung metastases was also stimulated when the D2A1 cells were preincubated with this plasma before their i.v. injection in female Balb/c mice. Importantly, these adverse effects of plasma collected during radiotherapy were significantly blocked by downregulating RAB4A. These results highlight the relevance of developing RAB4A inhibitors to prevent the development of metastases occurring after treatment in TNBC patients.

cancer biology↗

Proof-of-principle of NF1 Gene Therapy in plexiform neurofibroma mice models

Neurofibromatosis type I is a rare neurocutaneous syndrome characterized by the development of disfiguring neurofibroma tumors with unmet clinical needs. As Neurofibromatosis Type I is a monogenic disease, the development of gene therapy is highly attractive, but it is currently unknown if rescuing the NF1 gene in established neurofibroma is sufficient for tumor regression. Here, we test this hypothesis by building two novel NF1 mouse models with reversible NF1 expression. In the first model, the human NF1 -/- Schwann cells named ipNF95.11b were genetically modified with a doxycycline-inducible full-length mouse Nf1 gene. One month after cells implantation in the sciatic nerve, mice were split into 2 groups. Strikingly, all sciatic nerves from mice allowed to drink doxycycline water for one month display complete normalization of the sciatic nerve histologically (n=6 sciatic nerves) whereas 83% (5 out of 6 sciatic nerves) develop or maintain a neurofibroma when drinking regular water. In the second model, the human NF1 +/- Schwann cells named ipNF95.11c were genetically modified with a doxycycline-inducible potent shRNA against the NF1 mRNA transcript. Strikingly, doxycycline withdrawal after neurofibroma establishment allowed complete normalization (n=4 sciatic nerves), whereas all sciatic nerves showed evidence of neurofibroma when kept on doxycycline (n=4 sciatic nerves). Thus, we proof-of-principle NF1 Gene Therapy in plexiform neurofibroma mice models.

cancer biology↗