Ricardo López‐Pérez

Instituto de Investigación Biomédica de Salamanca

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Jesús F. San Miguel

Clinica Universidad de Navarra

Ramón García‐Sánz

Universidad de Salamanca

Marcos González

Des Moines University

Ana Balanzategui

Centro de Investigación del Cáncer

Carmen Chillón

Centro de Investigación del Cáncer

Norma C. Gutiérrez

Centro de Investigación del Cáncer

David González

Universidad de Zaragoza

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Alberto Órfão

Centro de Investigación Biomédica en Red de Cáncer

I Alaejos

Universidad de Salamanca

Saber AlZahrani

King Fahad Specialist Hospital

Cooperative Institutions

Universidad de Salamanca

Centro de Investigación del Cáncer

Instituto de Investigación Biomédica de Salamanca

Complejo Hospitalario de Salamanca

Consejo Superior de Investigaciones Científicas

Centro de Investigación Biomédica en Red de Cáncer

King Fahad Specialist Hospital

Instituto de Salud Carlos III

Consejo Nacional de Investigaciones Científicas y Técnicas

Universidad Autónoma de Madrid

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Gene scanning of VDJH-amplified segments is a clinically relevant technique to detect contaminating tumor cells in the apheresis products of multiple myeloma patients undergoing autologous peripheral blood stem cell transplantation

Bone Marrow Transplantation (2001)

Ricardo López‐Pérez Ramón García‐Sánz David González Ana Balanzategui Carmen Chillón

Autologous stem-cell transplantation

10.1038/sj.bmt.1703219

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Citations (19)

49-P

Human Immunology (2012)

Rodney Scott Ricardo López‐Pérez Faisal Khan Noureddine Berka Dalal Abduladeem

Cut-off

Donor-Specific Antibodies

10.1016/j.humimm.2012.07.175

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Citations (1)

Cyclooxygenase 2-Regulated Genes an Alternative Avenue to the Development of New Therapeutic Drugs for Colorectal Cancer

Frontiers in Pharmacology (2020)

Alicia M. Hidalgo-Estévez Kostas Stamatakis Marta Jiménez-Martínez Ricardo López‐Pérez Manuel Fresno

Colorectal cancer (CRC) is one of the most common and recurrent types of cancer, with high mortality rates. Several clinical trials and meta-analyses have determined that the use of pharmacological inhibitors of cyclooxygenase 2 (COX-2), the enzyme that catalyses the rate-limiting step in the synthesis of prostaglandins (PG) from arachidonic acid, can reduce the incidence of CRC as well as the risk of recurrence of this disease, when used together with commonly used chemotherapeutic agents. These observations suggest that inhibition of COX-2 may be useful in the treatment of CRC, although the current drugs targeting COX-2 are not widely used since they increase the risk of health complications. To overcome this difficulty, a possibility is to identify genes regulated by COX-2 activity that could give an advantage to the cells to form tumours and/or metastasize. The modulation of those genes as effectors of COX-2 may cancel the beneficial effects of COX-2 in tumour transformation and metastasis. A review of the available databases and literature and our own data have identified some interesting molecules induced by prostaglandins or COX-2 that have been also described to play a role in colon cancer, being thus potential pharmacological targets in colon cancer. Among those mPGES-1, DUSP4 and 10, Programmed cell death 4, Trop2 and many from the TGFβ and p53 pathways have been identified as genes upregulated in response to COX-2 overexpression or PGs in colon carcinoma lines and overexpressed in colon tumour tissue. Here, we review the available evidence of the potential roles of those molecules in colon cancer in the context of PG/COX signalling pathways that could be critical mediators of some of the tumour growth and metastasis advantage induced by COX-2. At the end, this may allow defining new therapeutic targets/drugs against CRC that could act specifically against tumour cells and would be effective in the prevention and treatment of CRC, lacking the unwanted side effects of COX-2 pharmacological inhibitors, providing alternative approaches in colon cancer.

10.3389/fphar.2020.00533

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Citations (29)

Pitfall in the interpretation of DQ HLA-antibodies

Human Immunology (2015)

Rabab Alattas Dalal AlAbduladheem Adel Shawhatti Ricardo López‐Pérez Abdelhamid Liacini

HLA-DQ

10.1016/j.humimm.2015.07.077

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De novo methylation of tumor suppressor gene p16/INK4a is a frequent finding in multiple myeloma patients at diagnosis

Leukemia (2000)

Marcos González MV Mateos Ramón García‐Sánz Ana Balanzategui Ricardo López‐Pérez

Cyclin-dependent kinase 6

Plasma cell leukemia

CpG site

Southern blot

10.1038/sj.leu.2401617

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Citations (59)

The Histone Deacetylase Inhibitor LBH589 Is a Potent Antimyeloma Agent that Overcomes Drug Resistance

Cancer Research (2006)

Patricia Maiso Xonia Carvajal‐Vergara Enrique M. Ocio Ricardo López‐Pérez Gema Mateo

Multiple myeloma represents an incurable disease, for which development of new therapies is required. Here, we report the effect on myeloma cells of LBH589, a new hydroxamic acid-derived histone deacetylase inhibitor. LBH589 was a potent antimyeloma agent (IC(50) < 40 nmol/L) on both cell lines and fresh cells from multiple myeloma patients, including cells resistant to conventional chemotherapeutic agents. In addition, LBH589 potentiated the action of drugs, such as bortezomib, dexamethasone, or melphalan. Using gene array, quantitative PCR, and Western analyses, we observed that LBH589 affected a large number of genes involved in cell cycle and cell death pathways. LBH589 blocked cell cycle progression, and this was accompanied by p21, p53, and p57 up-regulation. LBH589 induced cell death through an increase in the mitochondrial outer membrane permeability. LBH589 favored apoptosome formation by inducing cytochrome c release, Apaf-1 up-regulation, and caspase-9 cleavage. In addition, LBH589 stimulated a caspase-independent pathway through the release of AIF from the mitochondria. LBH589 down-regulated Bcl-2 and particularly Bcl-X. Moreover, overexpression of Bcl-X in multiple myeloma cells prevented LBH589-induced cell death. All these data indicate that LBH589 could be a useful drug for the treatment of multiple myeloma patients.

Panobinostat

Histone deacetylase inhibitor

10.1158/0008-5472.can-05-4186

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Citations (243)

In silico whole-genome screening for cancer-related single-nucleotide polymorphisms located in human mRNA untranslated regions

HAL (Le Centre pour la Communication Scientifique Directe) (2007)

Abdel Aouacheria Vincent Navratil Ricardo López‐Pérez Norma C. Gutiérrez Alexander Churkin

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Molecular characteristics and gene segment usage in IGH gene rearrangements in multiple myeloma.

PubMed (2005)

David González Marcos González Ana Balanzategui María Eugenia Sarasquete Ricardo López‐Pérez

Analysis of IgH rearrangements in B-cell malignancies has provided clinical researchers with a wide range of information during the last few years. However, only a few studies have contributed to the characterization of these features in multiple myeloma (MM), and they have been focused on the analysis of the expressed IgH allele only. Comparison between the expressed and the non-functional IgH alleles allows further characterizion of the selection processes to which pre-myeloma cells are submitted.We analyzed a cohort of 84 untreated MM patients in order to characterize their functional VDJH and non-functional DJH rearrangements. The pattern of mutations and gene segment usage for both types of rearrangements was analyzed by polymerase chain reaction and sequencing.VH3 and VH1 family members were over- and under-represented, respectively. VH3-30 and VH3-15 segments were the most frequently used, whereas VH4-34 was found only in non-functional or heavily mutated VDJH rearrangements. DH2 and DH3 family members were over-represented in both VDJH and DJH repertoires, while the DH1 family was under-represented only in the productive VDJH rearrangements. Finally, DH3-22 and DH2-21 gene segments were found to be over-represented in the functional repertoire while segments commonly used by less mature B-cell malignancies, such as DH6-19 or DH3-3, were under-represented.Data reported here help to identify the clonogenic MM cell as a post-germinal center B cell that has undergone selection processes during the germinal center reaction.

Gene rearrangement

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Citations (29)

Debate Round-Table: Comments concerning chimerism studies

Leukemia (2001)

Marcos González Ricardo López‐Pérez Ramón García‐Sánz José Antonio Pérez‐Simón Jesús F. San Miguel

Table (database)

Round table

10.1038/sj.leu.2402310

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Citations (17)

Analysis of Methylation Pattern in Multiple Myeloma

Acta Haematologica (2005)

Jesús F. San Miguel Ramón García‐Sánz Ricardo López‐Pérez

DNA methylation is involved in malignancy and is seen, in progression, in more than 80% of all solid tumours. Methylation is one of the main physiological processes to induce silencing of gene expression. Much work has focused on the suppressor gene p16, which acts as a negative cell cycle regulator, while its inhibition (via methylation) will have a positive effect on the cell cycle advance. The methylation status of the p16 gene was analysed in a group of 159 patients. Methylation of the p16 gene was seen in 41/98 (42%) patients with multiple myeloma and 4/5 (80%) patients with primary plasma cell leukaemias. This data favours the importance of p16 methylation on cell cycle regulation in multiple myeloma. In a proposed mechanism, methylated CpG islands attract a protein, MeCP2, which recruits a transcriptional inhibitory complex that includes histone deacetylases. The deacetylated lysine tails of the histones closely interact with DNA, resulting in a transcriptionally repressed chromatin with inhibited gene transcription, providing potential synergy between demethylating drugs and histone deacetylase inhibitors. Based on the knowledge of epigenetic mechanisms, the potential application of demethylating agents should be further investigated. Multiple myeloma remains an incurable disease, so new treatment strategies are needed to improve the outcome of patients.

Epigenomics

Demethylating agent

Histone Methylation

10.1159/000087041

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Citations (14)