A5071862986- Cancer-related Molecular Pathways
- RNA modifications and cancer
- Retinoids in leukemia and cellular processes
- Ubiquitin and proteasome pathways
- Lymphoma Diagnosis and Treatment
- RNA Research and Splicing
- DNA Repair Mechanisms
- Vitamin C and Antioxidants Research
- CAR-T cell therapy research
- Cancer-related molecular mechanisms research
- Cancer-related gene regulation
- Pluripotent Stem Cells Research
- Cancer therapeutics and mechanisms
- Protein Degradation and Inhibitors
- CNS Lymphoma Diagnosis and Treatment
- Medical and Biological Ozone Research
- Cancer Research and Treatments
- Advanced Breast Cancer Therapies
- Immune Cell Function and Interaction
- Cancer, Hypoxia, and Metabolism
- Cerebrovascular and genetic disorders
- Microtubule and mitosis dynamics
- Bone health and treatments
- Coenzyme Q10 studies and effects
- Cancer Mechanisms and Therapy
European Institute of Oncology
2018-2023
Istituti di Ricovero e Cura a Carattere Scientifico
2021
University of Cincinnati
2013
Institut d'Investigació Biomédica de Bellvitge
2012-2013
Institut Català d'Oncologia
2013
Duran i Reynals Hospital
2013
University of Bologna
2007-2012
Manufacturas Serviplast (Spain)
2012
Recently, we demonstrated that RPL5 and RPL11 act in a mutually dependent manner to inhibit Hdm2 stabilize p53 following impaired ribosome biogenesis. Given form preribosomal complex with noncoding 5S ribosomal RNA (rRNA) the three have been implicated response, reasoned they may be part of an Hdm2-inhibitory complex. Here, show small interfering RNAs directed against rRNA no effect on total or nascent levels rRNA, though prevent reported Hdm4 inhibition p53. To achieve efficient synthesis,...
Abstract Cell growth is a prerequisite for cell proliferation, and ribosome biogenesis limiting factor growth. In mammalian cells, the tumor suppressor p53 has been shown to induce cell-cycle arrest in response impaired biogenesis. Recently, p53-independent mechanisms of alterations have described. These findings provide rational basis use drugs that specifically impact treatment cancers lacking active extend scenario involved relationship between proliferation. Cancer Res; 72(7); 1602–7. ©2012 AACR.
The tumour suppressor p53 negatively controls cell cycle progression in response to perturbed ribosome biogenesis mammalian cells, thus coordinating growth with proliferation. Unlike is not involved the control of proliferation yeasts and flies. We investigated whether a p53-independent mechanism inadequate rate also present cells. studied effect specific inhibition rRNA synthesis on human cancer lines using small-interfering RNA procedure silence POLR1A gene, which encodes catalytic subunit...
The antibiotic tigecycline and the BCL2 inhibitor venetoclax cooperate to treat MYC/BCL2 double-hit lymphomas in xenografted mice.
Abstract Purpose: The RB tumor-suppressor activity may influence the therapeutic response in human breast cancers. effect of adjuvant therapy on clinical outcome cancer patients was analyzed, and sensitivity to 5-fluorouracil (5-FU) methotrexate investigated MCF-7 HCT-116 cells, according their status. Experimental Design: protein (pRB) expression prospectively evaluated by immunocytochemistry 518 consecutive its predictive value determined treatments. cells silenced for RB1 were treated...
Abstract MYC is a key oncogenic driver in multiple tumor types, but concomitantly endows cancer cells with series of vulnerabilities that provide opportunities for targeted pharmacological intervention. For example, drugs suppress mitochondrial respiration selectively kill MYC‐overexpressing cells. Here, we unravel the mechanistic basis this synthetic lethal interaction and exploit it to improve anticancer effects respiratory complex I inhibitor IACS‐010759. In B‐lymphoid cell line, ectopic...
Abstract. Objectives : To evaluate the effects of rRNA synthesis inhibition on cell cycle progression and population growth according to RB p53 status. Material methods RB‐ p53‐proficient U2OS cells p53‐deficient SAOS‐2 were used, transcription hindered by actinomycin D, analysed flow cytometry. Results One hour D treatment induced in a block at checkpoints G 1 ‐S 2 ‐M, which was removed only after resumed. did not influence cells. No effect D‐induced also found silenced for expression. A...
Multiple molecular features, such as activation of specific oncogenes (e.g., MYC, BCL2) or a variety gene expression signatures, have been associated with disease course in diffuse large B-cell lymphoma (DLBCL), although their relationships and implications for targeted therapy remain to be fully unraveled. We report that MYC activity is closely correlated with-and most likely driver of-gene signatures related oxidative phosphorylation (OxPhos) DLBCL, pointing OxPhos enzymes, particular...
Abstract Despite the well‐established function of p53 in determining cell cycle arrest and/or apoptosis response to cytostatic/cytotoxic stresses, role status chemotherapeutic agents human cancers has been not clearly defined. We wondered whether this was due fact that p53‐mediated chemotherapy drugs might be conditioned by retinoblastoma protein (pRb), a downstream factor pathway activated stabilization, which is frequently disrupted cancer. The dependence chemosensitivity on pRb first...
Recent data challenge the relevance of RB pathway to cancer based on inactivation, at least in breast tumors. To obtain information actual role components tumor progression we decided investigate whether their quantitative changes were associated with variations level phosphorylation human cancer. A series 68 primary carcinomas was studied. Five cases excluded from study due lack expression. In remaining 63 expression cyclin D1, cdk4, E, and INK4a mRNA assessed by real-time RT-PCR. The...
Comment on: Morgado-Palacin L, et al. Cell Cycle 2012; 11:503–10
The tumour suppressor p53 negatively controls cell cycle progression in response to perturbed ribosome biogenesis mammalian cells, thus coordinating growth with proliferation. Unlike is not involved the control of proliferation yeasts and flies. We investigated whether a p53-independent mechanism inadequate rate also present cells. studied effect specific inhibition rRNA synthesis on human cancer lines using small-interfering RNA procedure silence POLR1A gene, which encodes catalytic subunit...
ABSTRACT MYC is a key oncogenic driver and an adverse prognostic factor in multiple types of cancer, including diffuse large B-cell lymphoma (DLBCL). Yet, activation also endows cancer cells with series metabolic dependencies, which can provide strategic points for targeted pharmacological intervention. We recently reported that targeting the mitochondrial electron transport chain (ETC) complex I small molecule inhibitor IACS-010759 selectively killed MYC-overexpressing lymphoid cells. Here,...
Abstract Multiple molecular features, such as activation of specific oncogenes (e. g. MYC , BCL2 ) or a variety gene expression signatures, have been associated with disease course in diffuse large B-cell lymphoma (DLBCL). Understanding the relationships between these features and their possible exploitation toward classification therapy remains major priority field. Here, we report that activity DLBCL is closely correlated – most likely driver signatures related to Oxidative Phosphorylation...