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Brain Tumor

A New Path Forward: Unlocking Brain Cell Activity with Potassium Channels to Treat Depression

A mechanism involving potassium channels in the brain that control brain cell activity could provide a new and fundamentally different way of treating depression symptoms in adults with major depressive disorder.
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The groundbreaking research by scientists at the Icahn School of Medicine at Mount Sinai has shed new light on a promising approach to treating major depressive disorder in adults. A mechanism involving potassium channels in the brain that control brain cell activity could provide a fundamentally different way of addressing depression symptoms.

The study, published in two papers in Biological Psychiatry and Molecular Psychiatry, provides new insights into how the drug ezogabine may impact the brain to improve depression. Ezogabine was approved by the U.S. Food and Drug Administration in 2011 as an anticonvulsant medication for partial-onset seizures in adults with epilepsy.

Researchers found that increasing KCNQ channel activity could represent a new approach to treating depression, building on previous neuroscience research in mice conducted at The Friedman Brain Institute at Mount Sinai. Dr. Murrough’s research team was the first to test this hypothesis in humans with depression.

Their study revealed that ezogabine was associated with significant improvements in depression symptoms and the ability to experience pleasure (anhedonia) in patients who were treated with the drug compared to those who received placebo. The two new papers provide details from new analyses of the human brain imaging data collected from that initial clinical trial.

The first paper, published in Molecular Psychiatry, sheds light on the effects of ezogabine on a specific brain pathway. This study examined the impact of ezogabine on the ventral tegmental area (VTA) of the brain, which is involved in the release of dopamine, a neurotransmitter essential for motivation, pleasure, and reinforcement of behaviors.

The results showed an important role for KCNQ channel openers like ezogabine in normalizing hyperactivity of the VTA in people with both depression and anhedonia. “Up to half of people with depression do not respond to first-line treatment, which may be due to the lack of interventions that directly affect the neurobiology underlying symptoms like anhedonia,” says Laurel S. Morris, PhD, Adjunct Professor of Psychiatry at the Icahn School of Medicine.

By specifically targeting VTA activity and connectivity, ezogabine could open the door to decidedly improved outcomes for people who struggle daily with depression and anhedonia.

In a second paper, published in Biological Psychiatry, research revealed that ezogabine was able to normalize connectivity between the brain’s key reward regions and larger-scale brain networks including the posterior cingulate cortex, which plays a key role in internally directed thought and negative emotions.

Patients who experienced greater improvement in their depression and anhedonia when treated with ezogabine showed decreased connectivity between brain reward regions and the cingulate cortex. Together, these two complementary studies suggest that KCNQ channel openers can potentially alleviate the specific known neurobiological changes that occur in animal models of depression as well as change the function of larger brain networks that might be uniquely used in humans to regulate thought processes such as rumination.

“These findings suggested to us that drugs targeting the KCNQ channel may trigger antidepressant effects by reducing interactions between the reward centers in the brain and those related to negative thinking and emotion,” Dr. Murrough explains. “This hypothesis will require confirmation in larger clinical trials.”

Dr. Murrough is a named inventor on a pending patent application for the use of ezogabine and other KCNQ channel openers to treat depression and related disorders.

Source:The Mount Sinai Hospital / Mount Sinai School of Medicine
Original Link:https://www.sciencedaily.com/releases/2025/05/250521124629.htm
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Brain Tumor

Uncovering the Key to Pancreatic Cancer Spread: The Role of PCSK9

Scientists have discovered how pancreatic cancer cells thrive in the lungs or liver, environments that are as distinct to cells as the ocean and desert are to animals. The spread of cancer cells to organs like these often produces the very first symptoms of pancreatic cancer. But by that time, the pancreatic cancer has spread out of control.
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June 4, 2025

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Pancreatic cancer is one of the most aggressive forms of cancer, often diagnosed at an advanced stage when it has already spread to other parts of the body. Scientists at the University of California San Francisco (UCSF) have made a groundbreaking discovery that could change the way we understand and treat this disease. They found that a protein called PCSK9 plays a crucial role in determining how pancreatic cancer cells metastasize to different organs, such as the liver or lungs.

The researchers analyzed data from a project called MetMap, which contains information on pancreatic cancer cell lines with a tendency to colonize either the lung or the liver. They identified genetic differences that could explain why these cells prefer one organ over the other. To their surprise, they discovered that PCSK9 is the key factor in this process.

PCSK9 controls how cells obtain cholesterol. When PCSK9 levels are low, pancreatic cancer cells consume nearby cholesterol, which is abundant in the liver. However, when PCSK9 levels are high, the cancer cells produce their own cholesterol and make molecules that protect them from damage by oxygen, a perfect adaptation to survival in the lungs.

The team’s findings open up new avenues for treating pancreatic cancer. By manipulating how cells acquire cholesterol, it may be possible to prevent or slow down metastasis. The study was funded by reputable organizations such as the National Institutes of Health (NIH), the National Science Foundation (NSF), and the American Association for Cancer Research.

As Dr. Rushika Perera, PhD, senior author of the paper, explained, “Cancers persist by adapting to live in new tissues and organs, and we found that pancreatic tumors use PCSK9 to adapt as they spread.” This discovery has significant implications for cancer research and treatment, offering hope for a better understanding and management of this deadly disease.

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Brain Tumor

Unlocking the Key to Aggressive Prostate Cancer: Researchers Discover a Promising Treatment Strategy

Researchers have identified a gene that plays a key role in prostate cancer cells that have transitioned to a more aggressive, treatment-resistant form. The gene can be indirectly targeted with an existing class of drugs, suggesting a potential treatment strategy for patients with aggressive subtypes of prostate cancer.
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June 3, 2025

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The University of Michigan Rogel Cancer Center has made a groundbreaking discovery that may lead to a new treatment strategy for aggressive prostate cancer. Researchers have identified a gene, PROX1, which plays a key role in the transition of prostate cancer cells from a less aggressive to a more aggressive form. This transformation is known as lineage plasticity, and it’s associated with a poor prognosis.

The study, led by Zhi Duan, Ph.D., found that PROX1 becomes highly expressed as prostate cancer cells undergo lineage plasticity. By examining patient tumor biopsies and cell lines, the team confirmed that PROX1 is an early marker of this process. They also discovered that tumors with low activity of the androgen receptor (double-negative prostate cancer) and those that completely lose expression of the androgen receptor (neuroendocrine prostate cancer) turn on PROX1.

The researchers showed that adding PROX1 to prostate cancer cells turned off the androgen receptor, suggesting that PROX1 may be regulating the androgen receptor. They also found that eliminating PROX1 expression with genetic methods in both double-negative prostate cancer and neuroendocrine prostate cancer cells stopped their growth and led to cell death.

One of the challenges in targeting PROX1 is that it’s a transcription factor, making it difficult to target with drugs. However, the team identified histone deacetylases (HDACs) as potential partners that cooperate with PROX1. HDAC inhibitors are already approved for other cancers, and the researchers found that they can block PROX1 expression in prostate cancer cells.

The study’s lead author, Joshi J. Alumkal, M.D., noted that their work implicates PROX1 as an important early driver away from androgen receptor dependence. He suggested that HDAC inhibitors could be a promising treatment strategy for patients with aggressive subtypes of prostate cancer.

This research has significant implications for the development of new treatments for prostate cancer. The discovery of PROX1 as a key player in lineage plasticity provides a potential target for therapy, and the use of HDAC inhibitors may offer a new approach for treating patients with aggressive forms of this disease.

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Brain Tumor

A New Biomarker for Skin Cancer: Unlocking the Secrets of Metastasis Risk and Treatment Opportunities

Researchers have identified C5aR1 as a novel biomarker for metastasis risk and poor prognosis in patients with cutaneous squamous cell carcinoma (cSCC), the most common type of metastatic skin cancer. The new study’s findings in The American Journal of Pathology, published by Elsevier, found that C5aR1 promotes the invasion of cSCC tumor cells. Its elevated presence suggests that C5aR1 might serve as a useful prognostic marker for metastatic disease and, potentially, a target for future therapies in advanced cSCC.
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June 1, 2025

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A New Biomarker for Skin Cancer: Unlocking the Secrets of Metastasis Risk and Treatment Opportunities

Cutaneous squamous cell carcinoma (cSCC), the most common type of metastatic skin cancer, affects a significant number of people worldwide. Despite its relatively low incidence rate compared to other types of cancers, cSCC is responsible for nearly 25% of annual skin cancer deaths. The prognosis for patients with metastatic cSCC is poor, with limited treatment options available.

Researchers have identified C5aR1 as a potential biomarker for metastasis risk and poor prognosis in patients with cSCC. This novel finding, published in The American Journal of Pathology, has significant implications for the diagnosis and treatment of this aggressive form of skin cancer.

The complement system, a part of the human innate immune system, plays a crucial role in tumor suppression by inducing inflammation or causing immunosuppression. However, studies have shown that the complement system can also contribute to tumor progression and metastasis. This complex interplay between the complement system and cancer cells has prompted researchers to investigate the interaction between C5a (a signaling molecule) and its protein receptor C5aR1.

The study’s findings reveal that C5a binds to C5aR1, activating signaling pathways within the cell, leading to changes in cell behavior. The investigators examined C5aR1 in the context of cSCC progression and metastasis by combining in vitro 3D spheroid co-culture of cSCC cells and skin fibroblasts, human cSCC xenograft tumors grown in SCID mice, and a large panel of patient-derived tumor samples.

The results showed that C5aR1 expression is linked to metastasis risk and poor survival in patients with cSCC. High C5aR1 expression was observed in both tumor cells and stromal fibroblasts, suggesting that the interplay between tumor cells and their surroundings plays a crucial role in cancer progression.

The researchers concluded that C5aR1 is a potential metastatic risk marker, a novel prognostic biomarker, and promising therapeutic target for cSCC. This discovery has significant implications for the diagnosis and treatment of this aggressive form of skin cancer, offering new hope for patients and their families.

In conclusion, the identification of C5aR1 as a potential biomarker for metastasis risk and poor prognosis in patients with cSCC is a significant breakthrough in the field of skin cancer research. Further studies are needed to fully understand the role of C5aR1 in cSCC progression and metastasis, but this discovery has the potential to unlock new treatment opportunities and improve patient outcomes.

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