ÁE

Ángel Escamilla-Ramírez

Instituto Nacional de Neurología y Neurocirugía

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Cristina Trejo‐Solís

Instituto Nacional de Neurología y Neurocirugía

Juan Carlos López-Hernández

Instituto Nacional de Neurología y Neurocirugía

Rosa Angélica Castillo‐Rodríguez

Instituto Politécnico Nacional

Dolores Jiménez‐Farfán

Universidad Nacional Autónoma de México

Arturo Cruz-Salgado

Instituto Nacional de Salud Pública

Julio Sotelo

Instituto Nacional de Neurología y Neurocirugía

Edwin Steven Vargas-Cañas

Instituto Nacional de Neurología y Neurocirugía

Guadalupe Palencia

Instituto Nacional de Neurología y Neurocirugía

Javier Andrés Galnares‐Olalde

Instituto Nacional de Neurología y Neurocirugía

Bernardo Cacho‐Díaz

Instituto Nacional de Cancerología

Cooperative Institutions

Instituto Nacional de Neurología y Neurocirugía

Universidad Nacional Autónoma de México

Instituto Nacional de Cancerología

Secretaria de Salud

Universidad Autónoma Metropolitana

Asociación Mexicana de Psicología y Desarrollo Comunitario

Instituto Nacional de Cancerología

Weatherford College

Instituto Politécnico Nacional

Deleted Institution

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Miopatía inflamatoria de inicio tardío asociada con anticuerpos anti-Ro52 sin afectación pulmonar. Reporte de caso

Deleted Journal (2024)

Mitzi G. Márquez-Vargas Ángel Escamilla-Ramírez Gina González-Calderón Juan Carlos López-Hernández Javier Andrés Galnares‐Olalde

Las miopatías inflamatorias idiopáticas son un grupo heterogéneo de enfermedades autoinmunitarias, caracterizadas por debilidad muscular simétrica y, en ocasiones, compromiso sistémico. Presentan signos neurofisiológicos e histológicos de inflamación muscular crónica, así como elevación de enzimas musculares. Los autoanticuerpos específicos son biomarcadores útiles para el diagnóstico. Presentamos el caso de una paciente con miositis de superposición y anticuerpos anti-Ro52 positivos sin actividad sistémica al diagnóstico. Se trata de una mujer de 87 años, con antecedente de carcinoma basocelular en región malar izquierda e hipotiroidismo controlado. Presentó un cuadro progresivo que inició 6 meses previos a la valoración por nuestro servicio, caracterizado por fatiga, debilidad de la musculatura proximal en las cuatro extremidades, asociado a mialgias en la cintura pélvica. En el transcurso de 2 meses mostró dificultad para realizar actividades instrumentadas de la vida diaria. Al quinto mes manifestó disfagia. En la exploración física se documentó debilidad simétrica de predominio proximal, sin alteración de los reflejos de estiramiento muscular ni afectación sensitiva. Los análisis mostraron elevación de creatina fosfocinasa (2974 U/l). Se realizó panel de anticuerpos, encontrando anti-Ro52 +++. La PET corporal reveló discreto hipermetabolismo en la musculatura proximal de las cuatro extremidades, sin evidencia de actividad neoplásica. Se hizo biopsia muscular que reportó infiltrado inflamatorio intrafascicular y perivascular, y atrofia de fibras perifasciculares. Inició manejo con pulsos de metilprednisolona, presentando mejoría sintomática. La asociación de anticuerpos anti-Ro52 y dermatomiositis es infrecuente, presentándose hasta en un 26% en síndromes de superposición. Las presentaciones con enfermedad pulmonar intersticial y cáncer son de mal pronóstico.

10.24875/anc.m24000029

Cite

Citations (0)

The Cotard Delusion in a Patient With Neuropsychiatric Systemic Lupus Erythematosus: The Challenges of Autoimmune Psychosis

Cognitive and Behavioral Neurology (2024)

Alexis García-Sarreón Ángel Escamilla-Ramírez Yasmin Martínez-López Kevin Alan Garcia‐Esparza Nora E. Kerik-Rotenberg

The clinical features of neuropsychiatric systemic lupus erythematosus (NPSLE) are heterogeneous. Furthermore, therapeutic decision-making for NPSLE depends on the recognition of clinical syndromes that have not been sufficiently studied. This report describes the case of a 36-year-old woman with NPSLE who exhibited severe cognitive dysfunction and affective psychosis with persistent nihilistic delusions such as those described in the Cotard delusion. The patient insisted for several months that she was already dead. CSF analysis showed elevated levels of anti-ribosomal P antibodies and a positive determination of oligoclonal bands. Additionally, 18F -FDG PET/CT imaging revealed severe bilateral frontal hypermetabolism suggestive of brain inflammation and occipital hypometabolism. Results from the Systematic Lupus Erythematosus Disease Activity Index 2000 and the Systemic Lupus Erythematosus Disease Activity Score were consistent with an active state of the immunological disease. We then determined by an algorithm that this neuropsychiatric event could be attributed to the activity of the underlying immunological disease. Despite immunosuppressive and symptomatic treatment, only a partial improvement in cognition was achieved. The psychopathological features of the Cotard delusion remained unchanged 4 months after onset. However, we observed rapid remission of affective psychosis and significant improvement in cognition following electroconvulsive therapy. Subsequent follow-up examinations showed a sustained remission. This case describes a protracted form of the Cotard delusion, the diagnostic challenges that arise in the context of SLE, and treatment dilemmas that necessitate collaboration between neurology, psychiatry, and rheumatology.

10.1097/wnn.0000000000000375

Cite

Citations (1)

Patrones clínicos y neurofisiológicos de presentación temprana en la polirradiculoneuropatía inflamatoria desmielinizante crónica de inicio agudo

Revista de Neurología (2022)

Ángel Escamilla-Ramírez Juan Carlos López-Hernández R Díaz-Martínez Javier Andrés Galnares‐Olalde Edwin Steven Vargas-Cañas

The phenotypes of chronic inflammatory demyelinating polyneuropathy (CIDP) include an acute-onset phenotype (A-CIDP) with an evolution time of less than eight weeks from the onset of symptoms. This entity can be confused with Guillain-Barre syndrome of the acute inflammatory demyelinating variety (AIDP), delaying the start of treatment.To analyze the clinical and electrophysiological differences between A-CIDP, classic CIDP and AIDP, in order to identify factors that may help in the early differential diagnosis.A cross-sectional study was carried out with patients seen at the neuromuscular disease clinic of the National Institute of Neurology and Neurosurgery with a diagnosis of CIDP according to the criteria of the European Federation of Neurological Societies and Peripheral Nerve Society. Patients with CIDP <8 weeks were categorized as A-CIDP and were compared with patients diagnosed with classic CIDP and AIDP. Clinical, paraclinical and electrophysiological variables were obtained and analyzed.Significant differences in history of infection, cranial nerve involvement and dysautonomia were observed between A-CIDP and AIDP. Electrophysiological recordings reported significant differences in motor nerve conduction velocity and sural nerve recordings, being lower in the A-CIDP group.A history of infection, cranial nerve involvement and dysautonomia are important parameters to take into account for the differential diagnosis of these entities. Electrophysiological analysis is similar between A-CIDP and CIDP. The differential diagnosis between these types of demyelinating polyneuropathy must be based on clinical assessment.Patrones clínicos y neurofisiológicos de presentación temprana en la polirradiculoneuropatía inflamatoria desmielinizante crónica de inicio agudo.Introducción. Dentro de los fenotipos de polineuropatía desmielinizante inflamatoria crónica (CIDP) existe uno cuyo tiempo de evolución es menor de ocho semanas desde el inicio de los síntomas, denominado de inicio agudo (A-CIDP). Esta entidad puede confundirse con el síndrome de Guillain-Barré, variedad desmielinizante inflamatoria aguda (AIDP), lo que retrasa el inicio del tratamiento. Objetivo. Analizar las diferencias clínicas y electrofisiológicas entre A-CIDP, CIDP clásica y AIDP, con el fin de identificar factores que auxilien al diagnóstico diferencial de forma temprana. Pacientes y métodos. Se realizó un estudio transversal con pacientes atendidos en la clínica de enfermedades neuromusculares del Instituto Nacional de Neurología y Neurocirugía con diagnóstico de CIDP según criterios de la European Federation of Neurological Societies and Peripheral Nerve Society. Los pacientes con CIDP inferior a 8 semanas se catalogaron como A-CIDP y fueron comparados con pacientes diagnosticados con CIDP clásica y AIDP. Se obtuvieron y analizaron variables clínicas, paraclínicas y electrofisiológicas. Resultados. Se observaron diferencias significativas en antecedente de infección, afección de nervios del cráneo y disautonomías entre la A-CIDP y la AIDP. Los registros electrofisiológicos describieron diferencias significativas en velocidad de conducción de los nervios motores y en los registros del nervio sural, que fueron menores en el grupo de A-CIDP. Conclusión. El antecedente de infección, la afección de nervios del cráneo y las disautonomías son parámetros importantes que se debe tener en cuenta para el diagnóstico diferencial de estas entidades. El análisis electrofisiológico es similar entre la A-CIDP y la CIDP. El diagnóstico diferencial entre estos tipos de polineuropatía desmielinizante debe basarse en el juicio clínico.

10.33588/rn.7511.2022243

Cite

Citations (0)

URB597 and the Cannabinoid WIN55,212-2 Reduce Behavioral and Neurochemical Deficits Induced by MPTP in Mice: Possible Role of Redox Modulation and NMDA Receptors

Neurotoxicity Research (2017)

Ángel Escamilla-Ramírez Esperanza Garcı́a Guadalupe Palencia-Hernández Ana Laura Colín-González Sonia Galván‐Arzate

MPTP

Neurochemical

Anandamide

Palmitoylethanolamide

10.1007/s12640-016-9698-1

Cite

Citations (18)

The pentose phosphate pathway (PPP) in the glioma metabolism: a potent enhancer of malignancy

Biochimie (2025)

Cristina Trejo‐Solís Ángel Escamilla-Ramírez Saúl Gómez‐Manzo Rosa Angélica Castillo‐Rodríguez Francisca Palomares-Alonso

Warburg Effect

Metabolic pathway

10.1016/j.biochi.2025.01.013

Cite

Citations (0)

Autophagy as a Potential Therapy for Malignant Glioma

Pharmaceuticals (2020)

Ángel Escamilla-Ramírez Rosa Angélica Castillo‐Rodríguez Sergio Zavala-Vega Dolores Jiménez‐Farfán Isabel Anaya‐Rubio

Glioma is the most frequent and aggressive type of brain neoplasm, being anaplastic astrocytoma (AA) and glioblastoma multiforme (GBM), its most malignant forms. The survival rate in patients with these neoplasms is 15 months after diagnosis, despite a diversity of treatments, including surgery, radiation, chemotherapy, and immunotherapy. The resistance of GBM to various therapies is due to a highly mutated genome; these genetic changes induce a de-regulation of several signaling pathways and result in higher cell proliferation rates, angiogenesis, invasion, and a marked resistance to apoptosis; this latter trait is a hallmark of highly invasive tumor cells, such as glioma cells. Due to a defective apoptosis in gliomas, induced autophagic death can be an alternative to remove tumor cells. Paradoxically, however, autophagy in cancer can promote either a cell death or survival. Modulating the autophagic pathway as a death mechanism for cancer cells has prompted the use of both inhibitors and autophagy inducers. The autophagic process, either as a cancer suppressing or inducing mechanism in high-grade gliomas is discussed in this review, along with therapeutic approaches to inhibit or induce autophagy in pre-clinical and clinical studies, aiming to increase the efficiency of conventional treatments to remove glioma neoplastic cells.

Temozolomide

Anaplastic astrocytoma

10.3390/ph13070156

Cite

Citations (70)

Crosstalk of the Wnt/β-Catenin Signaling Pathway in the Induction of Apoptosis on Cancer Cells

Pharmaceuticals (2021)

Cristina Trejo‐Solís Ángel Escamilla-Ramírez Dolores Jiménez‐Farfán Rosa Angélica Castillo‐Rodríguez Athenea Flores‐Nájera

The Wnt/β-catenin signaling pathway plays a major role in cell survival and proliferation, as well as in angiogenesis, migration, invasion, metastasis, and stem cell renewal in various cancer types. However, the modulation (either up- or downregulation) of this pathway can inhibit cell proliferation and apoptosis both through β-catenin-dependent and independent mechanisms, and by crosstalk with other signaling pathways in a wide range of malignant tumors. Existing studies have reported conflicting results, indicating that the Wnt signaling can have both oncogenic and tumor-suppressing roles, depending on the cellular context. This review summarizes the available information on the role of the Wnt/β-catenin pathway and its crosstalk with other signaling pathways in apoptosis induction in cancer cells and presents a modified dual-signal model for the function of β-catenin. Understanding the proapoptotic mechanisms induced by the Wnt/β-catenin pathway could open new therapeutic opportunities.

Crosstalk

10.3390/ph14090871

Cite

Citations (48)

Real-World Experience in Hispanic Patients With Breast Cancer and Brain Metastases Using Different Prognostic Tools

International Journal of Radiation Oncology*Biology*Physics (2024)

Bernardo Cacho‐Díaz Debu Tripathy Víctor A. Arrieta Ángel Escamilla-Ramírez Alberto Alvarado‐Miranda

Akaike information criterion

10.1016/j.ijrobp.2024.01.222

Cite

Citations (0)

Anti-proliferative, pro-apoptotic and anti-invasive effect of the copper coordination compound Cas III-La through the induction of reactive oxygen species and regulation of Wnt/β-catenin pathway in glioma

Journal of Cancer (2021)

Rosa Angélica Castillo‐Rodríguez Guadalupe Palencia Isabel Anaya‐Rubio Juan Carlos Gallardo Pérez Dolores Jiménez‐Farfán

Gliomas are the most aggressive neoplasms that affect the central nervous system, being glioblastoma multiforme (GBM) the most malignant.The resistance of GBM to therapies is attributed to its high rate of cell proliferation, angiogenesis, invasion, and resistance to apoptosis; thus, finding alternative therapeutic approaches is vital.In this work, the anti-proliferative, pro-apoptotic, and anti-invasive effect of the copper coordination compound Casiopeina III-La (Cas III-La) on human U373 MG cells was determined in vitro and in vivo.Our results indicate that Cas III-La exerts an anti-proliferative effect, promoting apoptotic cell death and inactivating the invasive process by generating reactive oxygen species (ROS), inactivating GSK3β, activating JNK and ERK, and promoting the nuclear accumulation of β-catenin.The inhibition of ROS generation by N-acetyl-l-cysteine not only recovered cell migration and viability, but also reduced β-catenin accumulation and JNK and ERK activation.Additionally, Cas III-La significantly reduced tumor volume, cell proliferation and mitotic indices, and increased the apoptotic index in mice xenotransplanted with U373 glioma cells.Thus, Cas III-La is a promising agent to treat GBM.

Viability assay

10.7150/jca.59769

Cite

Citations (11)

Autophagic and Apoptotic Pathways as Targets for Chemotherapy in Glioblastoma

International Journal of Molecular Sciences (2018)

Cristina Trejo‐Solís Norma Serrano‐García Ángel Escamilla-Ramírez Rosa Angélica Castillo‐Rodríguez Dolores Jiménez‐Farfán

Glioblastoma multiforme is the most malignant and aggressive type of brain tumor, with a mean life expectancy of less than 15 months. This is due in part to the high resistance to apoptosis and moderate resistant to autophagic cell death in glioblastoma cells, and to the poor therapeutic response to conventional therapies. Autophagic cell death represents an alternative mechanism to overcome the resistance of glioblastoma to pro-apoptosis-related therapies. Nevertheless, apoptosis induction plays a major conceptual role in several experimental studies to develop novel therapies against brain tumors. In this review, we outline the different components of the apoptotic and autophagic pathways and explore the mechanisms of resistance to these cell death pathways in glioblastoma cells. Finally, we discuss drugs with clinical and preclinical use that interfere with the mechanisms of survival, proliferation, angiogenesis, migration, invasion, and cell death of malignant cells, favoring the induction of apoptosis and autophagy, or the inhibition of the latter leading to cell death, as well as their therapeutic potential in glioma, and examine new perspectives in this promising research field.

U87

Temozolomide

10.3390/ijms19123773

Cite

Citations (82)