Dr. Javier Camacho

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Academic Career Length

21Years (2006-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

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20 December 2012 in International Journal of Molecular Sciences

Journal Article

Mechanisms of Resistance to Endocrine Therapy in Breast Cancer: Focus on Signaling Pathways, miRNAs and Genetically Based Resistance

Breast cancer is the most frequent malignancy diagnosed in women. Approximately 70% of breast tumors express the estrogen receptor (ER). Tamoxifen and aromatase inhibitors (AIs) are the most common and effective therapies for patients with ERα-positive breast cancer. Alone or combined with chemotherapy, tamoxifen significantly reduces disease progression and is associated with more favorable impact on survival in patients. Unfortunately, endocrine resistance occurs, either de novo or acquired during the course of the treatment. The mechanisms that contribute to hormonal resistance include loss or modification in the ERα expression, regulation of signal transduction pathways, altered expression of specific microRNAs, balance of co-regulatory proteins, and genetic polymorphisms involved in tamoxifen metabolic activity. Because of the clinical consequences of endocrine resistance, new treatment strategies are arising to make the cells sensitive to tamoxifen. Here, we will review the current knowledge on mechanisms of endocrine resistance in breast cancer cells. In addition, we will discuss novel therapeutic strategies to overcome such resistance. Undoubtedly, circumventing endocrine resistance should help to improve therapy for the benefit of breast cancer patients.

1 January 2016 in Oxidative Medicine and Cellular Longevity

Journal Article

Molecular and Cellular Effects of Hydrogen Peroxide on Human Lung Cancer Cells: Potential Therapeutic Implications

Gabriela Vilema-Enríquez

Aurora Arroyo

Marcelo Grijalva

Ricardo Israel Amador-Zafra

Javier Camacho

Lung cancer has a very high mortality‐to‐incidence ratio, representing one of the main causes of cancer mortality worldwide. Therefore, new treatment strategies are urgently needed. Several diseases including lung cancer have been associated with the action of reactive oxygen species (ROS) from which hydrogen peroxide (H₂O₂) is one of the most studied. Despite the fact that H₂O₂ may have opposite effects on cell proliferation depending on the concentration and cell type, it triggers several antiproliferative responses. H₂O₂ produces both nuclear and mitochondrial DNA lesions, increases the expression of cell adhesion molecules, and increases p53 activity and other transcription factors orchestrating cancer cell death. In addition, H₂O₂ facilitates the endocytosis of oligonucleotides, affects membrane proteins, induces calcium release, and decreases cancer cell migration and invasion. Furthermore, the MAPK pathway and the expression of genes related to inflammation including interleukins, TNF‐α, and NF‐κB are also affected by H₂O₂. Herein, we will summarize the main effects of hydrogen peroxide on human lung cancer leading to suggesting it as a potential therapeutic tool to fight this disease. Because of the multimechanistic nature of this molecule, novel therapeutic approaches for lung cancer based on the use of H₂O₂ may help to decrease the mortality from this malignancy.

1 February 2006 in Cancer Letters

Journal Article

Ether à go-go potassium channels and cancer

Javier Camacho

5 January 2016 in Oxidative Medicine and Cellular Longevity

Journal Article

Ion Channels and Oxidative Stress as a Potential Link for the Diagnosis or Treatment of Liver Diseases

Ana Ramírez

Alma Yolanda Vázquez-Sánchez

Natalia Carrión-Robalino

Javier Camacho

Oxidative stress results from a disturbed balance between oxidation and antioxidant systems. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) may be either harmful or beneficial to the cells. Ion channels are transmembrane proteins that participate in a large variety of cellular functions and have been implicated in the development of a variety of diseases. A significant amount of the available drugs in the market targets ion channels. These proteins have sulfhydryl groups of cysteine and methionine residues in their structure that can be targeted by ROS and RNS altering channel function including gating and conducting properties, as well as the corresponding signaling pathways associated. The regulation of ion channels by ROS has been suggested to be associated with some pathological conditions including liver diseases. This review focuses on understanding the role and the potential association of ion channels and oxidative stress in liver diseases including fibrosis, alcoholic liver disease, and cancer. The potential association between ion channels and oxidative stress conditions could be used to develop new treatments for major liver diseases.

24 August 2010 in Journal of Applied Toxicology

Journal Article

Ion channels in toxicology

Iván Restrepo‐Angulo

Andrea De Vizcaya-Ruiz

Javier Camacho

10 May 2012 in Sensors

Journal Article

Eag1 Channels as Potential Cancer Biomarkers

Jesús Adrián Rodríguez-Rasgado

Isabel Acuña-Macías

Javier Camacho

Cancer is a leading cause of death worldwide. New early tumor markers are needed to treat the disease at curable stages. In addition, new therapeutic targets are required to treat patients not responding to available treatments. Ion channels play major roles in health and disease, including cancer. Actually, several ion channels have been suggested as potential tumor markers and therapeutic targets for different types of malignancies. One of most studied ion channels in cancer is the voltage-gated potassium channel Eag1 (ether à go-go 1), which has a high potential to be used as a cancer biomarker. Eag1 is expressed in most human tumors, in contrast to its restricted distribution in healthy tissues. Several findings suggest Eag1 as a potential early marker for cervical, colon, and breast cancer. In addition, because Eag1 amplification/expression is associated with poor survival in leukemia, colon and ovarian cancer patients, it has also been proposed as a prognosis marker. Moreover, inhibition of either expression or activity of Eag1 leads to reduced proliferation of cancer cells, making Eag1 a potential anticancer target. Using Eag1 in cancer detection programs could help to reduce mortality from this disease.

About Me

Javier Camacho was born in Mexico City and studied Biology at U.N.A.M. He obtained his M. Sc. degree and Ph. D. in Physiology at CINVESTAV, I.P.N., and was a postdoctoral fellow at the Max-Planck Institute for experimental Medicine in Göttingen, Germany where he started to study ion channels involved in cancer in the group of Prof. Dr. Walter Stühmer. Then, he formed his own research group in the Pharmacology Department at CINVESTAV, Mexico focusing on ion channels in cervical, liver, prostate, lung and pancreatic cancer. Together with his group and collaborators he has published original results in very important journals in the cancer field. They have also published reviews and book chapters, and filed several patents. These patents are related to early diagnosis of cancer and novel therapeutic approaches especially for cervical, lung and liver cancer. He has served as invited reviewer in almost 100 different scientific journals. Some of his projects have been awarded in Mexico by the industry. He spent a sabbatical year at the University of British Columbia in Vancouver, Canada, collaborating with Prof. Dr. Terry Snutch. He has contributed in Ecuador to the development of basic cancer research at different universities. He has supervised more than 80 students in his lab from undergraduate to postdocs. Currently, he is the Head of the Pharmacology Department at CINVESTAV.

Dr. Javier Camacho

Dr. Javier Camacho

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