When a patient is diagnosed with cancer, we often rely on a single snapshot. A biopsy is taken, the tumor is analyzed, and a treatment plan is created based on that information. This approach has guided clinical care for many years, but it has a limitation. It assumes that cancer is stable.

In reality, cancer is constantly changing. It evolves under pressure from treatment, the immune system, and its surrounding environment. A tumor that looks one way at diagnosis may behave very differently months or years later.

This is why I believe we must begin to think about cancer not as a fixed condition, but as a process that unfolds over time.

What Epigenetics Reveals About Change

Epigenetics offers a powerful way to study this process. While genetic mutations are relatively stable, epigenetic changes are dynamic. They can shift in response to therapy, stress, and environmental signals.

These changes include DNA methylation, histone modification, and chromatin remodeling. Together, they control which genes are active and which are silent. In breast cancer, for example, epigenetic regulation determines whether a tumor expresses the estrogen receptor and remains sensitive to hormone therapy.

In my research, I have seen how epigenetic silencing of key genes like ESR1 can develop over time, especially under the pressure of endocrine treatment. This does not happen all at once. It is a gradual shift, often invisible at the beginning but significant in its long-term impact.

By tracking these changes over time, we can begin to understand how tumors adapt and why they become resistant.

The Value of Longitudinal Profiling

Longitudinal profiling means collecting and analyzing biological data from the same patient at multiple time points. Instead of relying on a single biopsy, we follow the tumor as it evolves.

This approach can reveal patterns that would otherwise be missed. For example:

• A tumor may start as hormone receptor-positive but gradually lose receptor expression
• Epigenetic markers associated with drug resistance may appear before clinical relapse
• Different subpopulations of cells may emerge and compete within the tumor

By observing these changes, we can identify early warning signs of treatment failure and adjust our strategy before the disease progresses.

Learning From Treatment Pressure

Every therapy we use creates pressure on cancer cells. Some cells die, while others survive and adapt. This process is similar to natural selection. The strongest or most adaptable cells become dominant over time.

Epigenetic changes play a key role in this adaptation. They allow cancer cells to switch gene programs without needing new mutations. This makes the process faster and more flexible.

For example, under hormone therapy, some breast cancer cells may reduce their dependence on estrogen signaling by silencing ESR1. Others may activate alternative survival pathways. These changes can be subtle at first, but they can lead to full resistance if not addressed.

Longitudinal profiling helps us see these shifts as they happen, rather than after resistance is already established.

Moving Toward Adaptive Treatment

If we can track how tumors evolve, we can begin to design adaptive treatment strategies. Instead of following a fixed treatment plan, we adjust therapy based on how the tumor is responding in real time.

This might include:

• Switching therapies when early signs of resistance appear
• Combining treatments to prevent the emergence of resistant cell populations
• Introducing epigenetic therapies to restore sensitivity to existing treatments

This approach requires close monitoring and strong collaboration between researchers and clinicians. It also requires tools that can measure epigenetic changes quickly and accurately.

New Tools for Real-Time Monitoring

Advances in technology are making longitudinal profiling more practical. Techniques such as liquid biopsy allow us to analyze tumor-derived DNA in the blood, reducing the need for repeated tissue biopsies.

We can now measure changes in DNA methylation patterns, track circulating tumor cells, and analyze gene expression profiles over time. These tools provide a more complete picture of how the disease is evolving.

In the future, I believe we will integrate these data into predictive models that help guide clinical decisions. Instead of reacting to visible disease progression, we will anticipate it.

Challenges We Must Address

While the potential of longitudinal epigenetic profiling is exciting, there are still challenges to overcome.

First, we need standardized methods for collecting and analyzing epigenetic data. Variability in techniques can make it difficult to compare results across studies.

Second, we must ensure that these approaches are accessible and cost-effective. Advanced profiling should not be limited to a small number of research centers.

Third, we need to train clinicians and scientists to interpret complex data. Understanding how epigenetic changes relate to treatment decisions requires both technical knowledge and clinical insight.

These challenges are real, but they are not insurmountable. With collaboration and investment, we can build systems that support this new approach.

Teaching a New Way of Thinking

As an educator, I encourage my students to think about cancer in terms of time and change. I ask them to consider not just what a tumor is, but what it might become.

This perspective changes how we design experiments and how we interpret results. It also prepares the next generation of scientists to work in a field that is becoming increasingly dynamic and data-driven.

When students understand that cancer is evolving, they begin to ask deeper questions. They look for patterns, transitions, and interactions. This is the kind of thinking we need to move the field forward.

Seeing the Full Story

A single snapshot of cancer can tell us a great deal, but it cannot tell us everything. To truly understand the disease, we must follow it over time. We must observe how it responds, adapts, and sometimes escapes our best efforts.

Longitudinal epigenetic profiling gives us a way to do this. It allows us to see the full story of cancer, not just one chapter.

By mapping these changes, we can move toward a future where treatment is not only personalized, but also responsive and adaptive. This is how we improve outcomes and give patients the best possible chance for long-term success.

The post Mapping Cancer Over Time: The Role of Longitudinal Epigenetic Profiling in Predicting Treatment Outcomes appeared first on Chun Ju Chang.

Real impact in academic medicine reaches far beyond citations or budgets. It can be seen in the growth of a young scientist, the development of a new clinical tool, the change in how a patient is treated, or the strength of the institution we leave behind for the next generation. These are harder to measure but no less meaningful.

Mentorship as a Legacy

When I think about the most rewarding parts of my career, I don’t think of my highest-impact papers. I think of the students and postdocs I’ve mentored, the ones who were unsure of themselves when they first joined my lab and who have now gone on to lead projects, publish independently, and mentor others.

Mentorship is one of the most powerful ways to create lasting influence. When we teach young scientists how to think critically, how to ask good questions, and how to uphold ethical standards, we shape the future of science itself. The skills and confidence they gain will continue to multiply long after they leave our lab.

At China Medical University, we take mentorship seriously. We track how many of our students go on to advanced graduate programs, how many publish their first papers, and how many secure academic positions at reputable institutions. These are not formal metrics in most evaluations, but I believe they should be.

Translating Research Into Practice

As a cancer biologist, I spend much of my time studying how genes like TET2 influence breast cancer behavior. But my goal is not only to publish those findings. I want them to reach the clinic.

This is where translational impact becomes important. If our research leads to a new way to predict treatment resistance or guide therapy choices to help real patients, that is when I feel our work has made a difference.

We need better ways to recognize and reward this kind of impact. If a faculty member contributes to the development of a diagnostic tool, leads a clinical guideline update, or trains clinicians in a new approach, these contributions should be counted alongside publications and grants.

Patient Outcomes as a True Measure

It can be easy to forget in academic environments, but the ultimate goal of medical research is to improve patient lives. Whether we are studying molecular mechanisms, drug responses, or health systems, the end result should be better care.

At CMU, we are working on ways to measure how research influences patient outcomes. This may include new treatments introduced at our affiliated hospitals, improvements in screening or follow-up care, or even reductions in treatment side effects. These are slow, cumulative changes, but they are the most meaningful signs of impact.

I often remind my students that behind every data point is a person. If our work helps one woman avoid unnecessary chemotherapy or helps one doctor make a more informed decision, we have done something important.

Building Institutional Strength

Another form of impact I care deeply about is institutional capacity building. This includes helping CMU develop stronger research programs, attracting international collaborations, creating bilingual educational materials, and supporting new faculty members as they grow.

When I mentor junior faculty on how to design a curriculum, apply for a grant, or balance research and teaching, I am investing in the long-term success of our university. This kind of leadership does not come with an impact factor, but it strengthens the entire system.

We should create space in academic evaluations for recognizing service, curriculum innovation, cross-departmental teamwork, and other forms of academic citizenship. These contributions are the glue that holds our institutions together.

Redefining What We Celebrate

I believe it is time to shift the culture in academic medicine. Instead of celebrating only the biggest grants or most cited papers, we should also highlight mentorship stories, translational milestones, and contributions to public health.

We can start by including these elements in faculty reviews, award nominations, and annual reports. We can create platforms where researchers can share the broader effects of their work, not just the results, but the people and systems it touched.

We can also encourage young scientists to define their own success more broadly. It is good to aim for publications and funding, but it is even better to ask, “Who did I help? What did I change? 

Finding Meaning in the Work

At this stage in my career, I find the most meaning not in accumulation, but in connection. I feel fulfilled when a former student writes to say they are mentoring others. I feel proud when a research idea becomes part of a clinical discussion. I feel hopeful when our institution grows stronger, more inclusive, and more collaborative.

Grants and papers are part of our professional path, and I will continue to pursue both. But I will also continue to advocate for a more holistic view of academic success, one that honors the quiet victories, the long-term investments, and the many ways we can make a difference.

The post Success Is More Than a Number appeared first on Chun Ju Chang.

We are not just contributors of data or collaborators on large studies. We are leading teams, writing papers, organizing conferences, reviewing grants, and setting research agendas. And we must continue to expand that influence, especially in fields like cancer biology, where innovation and diversity of thought are critical.

From Regional Research to Global Impact

At China Medical University, I have worked closely with our faculty to encourage greater participation in international scientific platforms. Our researchers publish in high-impact journals and regularly present at major international conferences. But more importantly, we are helping them take on leadership roles, serving as journal reviewers, editor board, scientific association members, and research advisors in global networks.

This transition is important. Publishing results is only one part of the equation. Shaping scientific discourse means being involved in how research is framed, how questions are asked, how funding is allocated, and how policy is guided. Asian scientists must be more visible and vocal across all these areas.

Building Faculty Capacity Through Development

One way we foster this kind of leadership at CMU is through strong faculty development systems. Our Teacher Development Center offers a range of support tools, from teaching workshops to mentorship programs.

We hold lectures and symposiums that promote international collaborations and encourage faculty speak at global forums.

International Collaboration as a Starting Point

For many faculty in Asia, international collaboration is often the first entry point into global research. At CMU, we have active partnerships with institutions in the United States, Japan, South Korea, and Europe. These partnerships range from student exchanges to dual-degree programs and joint research projects. Faculty involved in these initiatives often find themselves invited to join editorial boards, speak at symposia, or help plan future research agendas.

I personally encourage early-career faculty to build genuine relationships with their peers abroad. It is through these connections that opportunities to co-author, co-lead, and co-host events begin to emerge. Science is not just about individual excellence. It is about connection, credibility, and contribution.

Representation in Editorial and Review Roles

One area where I hope to see more Asian faculty step forward is in scientific publishing and peer review. Serving on editorial boards or as peer reviewers allows us to shape what gets published and how scientific standards are upheld. It also provides insight into the review process, which helps improve our own writing and mentorship.

At CMU, I help mentor faculty who have the expertise and experience to take on these roles and encourage them to engage with journals that align with their research focus. I also advocate for international editorial opportunities that allow Taiwanese researchers to contribute to both regional and global literature.

Positioning Institutions for Visibility

It is not only individual researchers who must step up. Our institutions must also position themselves as global contributors. This includes improving the visibility of university research through high-quality websites, English-language content, accessible publication databases, and active participation in international academic networks.

We must also support faculty who attend international conferences, not only by funding their travel but also by preparing them to present their work clearly and effectively. At CMU, we offer guidance on communicating impactful science, writing compelling abstracts, and connecting with potential collaborators.

Mentoring the Next Generation to Lead Globally

As a mentor, I believe we must also prepare students and young researchers to think globally from the beginning. I regularly talk to my students about scientific communications, applying for international fellowships, and thinking about how their work can make a broader impact. We create opportunities for them to present to international audiences, even if virtually, so they can grow comfortable with cross-cultural scientific dialogue.

It is a joy to watch a student go from hesitantly presenting their research to confidently answering questions from international experts. That transformation is the first step toward global leadership.

A Shared Responsibility

Asian faculty have both the expertise and the responsibility to help guide the future of science. We bring cultural diversity, clinical insights, and research questions that are deeply relevant to populations often underrepresented in global studies. When we take our place in the broader scientific conversation, we enrich it.

We must move beyond simply contributing data and move toward shaping how knowledge is created, shared, and applied. That requires stepping outside the lab and into the lecture halls, conference rooms, editorial boards, and policy discussions that influence science worldwide.

At CMU and across Asia, I see a growing generation of researchers ready to take on that role. My job is to help them find their voice and use it, not only in Taiwan but across the world.

The post Science Needs More Voices at the Table appeared first on Chun Ju Chang.

This distinction between luminal and basal is more than just a label. It determines how a tumor behaves, how it responds to treatment, and ultimately, how likely it is to come back. Understanding what controls this cellular identity is critical for designing more effective therapies and helping patients live longer and better lives.

The Epigenetic Code Behind Cell Fate

While much of cancer research focuses on mutations in DNA, we now know that epigenetic changes play an equally powerful role. Epigenetics refers to chemical modifications that turn genes on or off without changing the DNA sequence itself. One of the most important of these modifications is DNA methylation, which acts like a switch. When a gene is highly methylated, it usually gets turned off. When methylation is removed, the gene can be turned back on.

In our recent research at China Medical University, we discovered that epigenetic regulation helps control whether a breast cell becomes a luminal cell or a basal-like cell, and this regulation is especially relevant in the development of hormone receptor-positive breast cancer.

The Role of TET2 in Cell Differentiation

Our work focused on a gene called TET2, which helps remove DNA methylation and therefore supports the activation of key genes that drive luminal cell identity. TET2 plays the role of an epigenetic editor. It removes the chemical tags that silence important genes and allows the cell to become what it was meant to be.

In our mouse models, when we deleted TET2 in mammary epithelial cells, the result was dramatic. The cells failed to express key luminal markers like ESR1, the gene that produces the estrogen receptor, along with GATA3 and FOXA1. Without TET2, the cells began to shift away from a luminal fate and started developing into basal-like tumors, which are typically ER-negative and much more difficult to treat.

This shift was not caused by a mutation in ESR1 or other genes. Instead, the machinery that normally keeps these genes active was no longer functioning, all because TET2 was missing. This finding gave us a powerful insight into how the loss of epigenetic regulation can push cells in a completely different direction.

The FOXP1 Connection

We also found that TET2 does not work alone. It partners with another molecule called FOXP1, a transcription factor that binds to specific regions of DNA and helps regulate gene expression. Together, TET2 and FOXP1 form a molecular complex that activates the genes necessary for luminal identity.

When this partnership breaks down, the consequences are serious. Without FOXP1 or TET2, the genes that support luminal cell development cannot be properly activated. The cells lose their identity and the resulting tumors behave more like basal cells. These tumors do not respond to hormone therapy and often carry a worse prognosis.

This mechanism helped us better understand a frustrating clinical problem. Some patients with ER-positive breast cancer begin treatment with tamoxifen or aromatase inhibitors but eventually relapse with tumors that no longer express ER. It turns out that in some cases, this may be linked to the epigenetic silencing of ESR1, driven by the loss of TET2.

What This Means for Treatment

Understanding the molecular switches that control cell fate gives us new tools for developing better therapies. If a tumor has lost TET2 function and become resistant to endocrine therapy, we may be able to reactivate those pathways by targeting the epigenetic changes directly.

There are already drugs being tested that affect DNA methylation. Some of these are used in blood cancers and may hold promise in solid tumors like breast cancer. By restoring TET2 activity or mimicking its effects, we could potentially reprogram basal-like tumors to behave more like luminal tumors, making them sensitive to hormone therapy once again.

Another possibility is using TET2 expression as a biomarker. If we know a patient’s tumor has low TET2, we can predict that hormone therapy may not be effective and consider alternative or combination treatments from the beginning. This is the kind of personalized medicine that improves outcomes and reduces unnecessary side effects.

A New Lens for Breast Cancer Research

These discoveries offer a new lens for how we think about breast cancer. Instead of viewing it purely through genetic mutations, we can now appreciate the dynamic and reversible nature of cell identity. By targeting the epigenetic regulators like TET2 and FOXP1, we may be able to shift the course of the disease.

As a researcher and educator, I am excited about the possibilities this opens up, not just for science, but for the patients and families who face this disease every day. Cell fate may be determined by small molecular switches, but by understanding and targeting them, we can make a big difference in people’s lives.

The post Why Cell Identity Matters in Breast Cancer appeared first on Chun Ju Chang.

However, about 15 to 20 percent of patients who initially respond to endocrine therapy will eventually develop resistance. Their tumors stop responding to medication, begin growing again, and become much more difficult to treat. For many years, we have asked the same question in labs and clinics around the world: Why does this happen, and how can we stop it?

This question has been at the heart of my research at China Medical University in Taiwan. Our team discovered an important gene called TET2 that may help answer this question and point us toward a new strategy for treatment.

What We Found About TET2 and Breast Cancer

Our study, published in Nature Communications, looked at how epigenetic regulation affects breast cancer development. Epigenetics refers to changes in gene expression that do not involve altering the DNA sequence itself. One important way this happens is through a process called DNA methylation, which can “silence” genes that are normally active.

In ER+ breast cancer, the ESR1 gene, which encodes the estrogen receptor, must be active for hormone therapy to work. However, we discovered that in some cases of endocrine-resistant cancer, ESR1 is silenced by DNA methylation, making the estrogen receptor disappear and rendering hormone therapy ineffective.

This is where TET2 comes in. TET2 is a gene that produces an enzyme responsible for removing DNA methylation. It helps maintain the normal expression of critical genes, including ESR1, GATA3, and FOXA1, all essential for what we call luminal cell differentiation, the process that gives rise to estrogen receptor-positive cells.

Losing TET2 Changes Everything

Using a specially designed mouse model, we knocked out TET2 in mammary gland cells to see what would happen. The results were striking. Without TET2, the cells lost their luminal identity and instead began developing into a different type of cell known as basal-like cells. These basal-like tumors were ER-negative, highly aggressive, and resistant to tamoxifen.

Further investigation revealed that TET2 forms a functional complex with FOXP1, a transcription factor, and this complex drives the expression of ESR1 and other luminal markers. Without TET2, this machinery breaks down. The estrogen receptor is no longer expressed, and endocrine therapy becomes ineffective.

This discovery offers a clear mechanistic explanation for how some ER+ tumors become resistant to hormone therapy. It also provides a possible biomarker, TET2 expression levels, that could help doctors identify patients who may not respond well to standard hormone treatments.

From Lab Bench to New Hope for Patients

Understanding how TET2 functions opens the door to new therapeutic possibilities. If we can find ways to restore TET2 activity, we might be able to reprogram resistant tumors back into a hormone-sensitive state. This could make them responsive to tamoxifen or other endocrine therapies again.

We are now exploring ways to develop TET2-based treatment strategies. These could include small molecules that activate TET2 pathways, epigenetic drugs that reverse methylation in the ESR1 promoter region, or gene therapy techniques to restore normal TET2 expression.

The beauty of this approach is that it’s targeted. Instead of giving stronger doses of existing therapies, which often lead to toxic side effects, we could intervene at the molecular root of the resistance and help patients regain their ability to respond to standard treatment.

TET2 as a Biomarker for Personalized Medicine

Another important aspect of our work is using TET2 as a predictive biomarker. If we can test tumors for TET2 expression at the time of diagnosis or during treatment, we could better personalize therapy plans. Patients with low or absent TET2 may be steered toward combination therapies that include epigenetic modulators, while those with strong TET2 expression may continue with endocrine therapy alone.

This kind of approach is at the heart of precision oncology, where treatments are tailored to the specific genetic and epigenetic makeup of each patient’s tumor. It’s the future of cancer care and TET2 may play a major role in that future.

A Collaborative Journey

This research is just the beginning. We are now working with collaborators in Taiwan and the United States to validate our findings in human clinical samples and explore potential drug development pathways. The transition from lab discovery to clinical application takes time, funding, and a multidisciplinary team, but we are committed to seeing it through.

I am deeply proud of our team at China Medical University for their dedication and insight. Our work reflects the growing contributions of Taiwanese scientists to global cancer research, and I believe we have an important voice in the international conversation.

TET2 may seem like just another gene in the vast landscape of cancer biology, but in the context of hormone-resistant breast cancer, it could make all the difference. For the patients who are told their treatment has stopped working, this research represents something rare and powerful, a second chance.

The post Why Endocrine Therapy Doesn’t Always Work appeared first on Chun Ju Chang.

Cancer does not recognize borders. It touches lives everywhere — in small villages and big cities, across every continent and culture. Because of this, the search for better cancer treatments and cures must also be global.

As a cancer researcher who grew up in Taiwan, studied in the United States, and now teaches and conducts research at China Medical University in Taiwan, I have seen firsthand how different countries bring unique strengths to the fight against cancer. And I believe it’s time we shine a brighter light on the growing contributions coming from Asia, especially from Taiwan.

Too often, global cancer research is viewed through a Western lens. But in recent years, Taiwanese scientists, clinicians, and institutions have been quietly — and steadily — making major strides that deserve recognition and celebration.

Taiwan: Small Island, Big Impact

Taiwan may be small in size, but it punches well above its weight in scientific innovation. With a strong national healthcare system, high rates of education, and advanced technology infrastructure, Taiwan is uniquely positioned to conduct world-class research — particularly in the biomedical and life sciences.

When it comes to cancer, Taiwan has been investing heavily in prevention, diagnosis, and treatment. Our National Health Insurance system provides a rich source of population data for research, allowing scientists to track trends, outcomes, and new therapies across large groups of patients.

In addition, Taiwan’s government and academic institutions have created strong research partnerships — which help us stay connected to global advancements while contributing our own insights.

China Medical University: A Rising Research Powerhouse

As a professor at China Medical University (CMU), I’ve witnessed the university’s transformation into a leader in cancer research. Founded in 1958, CMU has grown rapidly, and now includes a large teaching hospital, research institutes, and collaborations with international medical centers.

CMU is particularly active in:

• Translational research that Bruges basic science to drug discovery
  
• Integrative approaches combining Western and traditional Chinese medicine
  

One of our proudest achievements is the establishment of the Translational Cancer Research Center, which brings together laboratory scientists, clinicians, and data analysts to move discoveries from the lab directly into patient care. We’re also involved in joint publications with top-tier institutions in the U.S. and Japan.

For me, this kind of integrated, cross-disciplinary environment is exactly what cancer research needs. It’s not just about the science — it’s about connection, collaboration, and care.

Innovations Coming Out of Taiwan

Here are just a few areas where Taiwan is making real contributions to global cancer research:

1. Genomic Medicine and Big Data

Taiwan is home to some of the most comprehensive national health databases in the world. These resources are helping researchers identify cancer risk factors, develop early detection methods, and personalize treatments based on genetic information. Our work in bioinformatics and AI-powered diagnosis tools is attracting international attention.

2. Early Detection Through Screening Programs

Taiwan’s national screening programs for breast, cervical, and colorectal cancer have been remarkably effective. These efforts have led to earlier diagnoses, improved survival rates, and valuable lessons for other countries building their own screening systems.

3. Herbal and Natural Product Research

Many labs, including those at CMU, are exploring how traditional Chinese medicine and herbal compounds can complement modern cancer therapies. Some compounds are being tested for their ability to reduce side effects from chemotherapy or boost immune response — an exciting area of integrative oncology.

4. Global Collaboration Networks

Taiwanese scientists are not working in isolation. Through exchange programs, dual-degree partnerships, and co-authored research, we are contributing to the international conversation around cancer care. This includes joint studies on cancer disparity and novel drug resistance mechanisms.

Women in Research: A Growing Force in Taiwan

As a female scientist, I’m also proud to see more Taiwanese women entering leadership roles in medicine and research. The culture is shifting. At CMU and other institutions, young women are taking up space in labs, giving keynote talks at international conferences, and receiving recognition for their work.

In the US, organizations like Women in Cancer Research (WICR) are helping foster that momentum, but we still have a long way to go — especially in ensuring women have equal opportunities in publishing, grant funding, and institutional leadership.

The Road Ahead: Challenges and Opportunities

Of course, we still face challenges. Like many Asian countries, Taiwan must balance innovation with funding limitations, keep up with fast-changing technologies, and ensure that research findings are quickly translated into clinical practice.

But with our strong foundation, talented researchers, and increasing global engagement, I believe the future is bright. Taiwan is no longer just contributing to global cancer research — we are helping shape its future.

Taiwan Roots, Global Reach

As a Taiwanese researcher, I carry a pride in our culture, our resilience, and our scientific contributions. But I also see myself as part of a much larger story — the global fight against cancer.

When we share our findings, work across borders, and lift each other up, we all win. Taiwan’s role in this movement is growing, and I’m honored to be part of it.

To every student, colleague, and collaborator: let’s keep pushing forward, together. Cancer doesn’t stand a chance when we stand united.

The post Asian Contributions to Global Cancer Research: Spotlight on Taiwanese Institutions appeared first on Chun Ju Chang.

This mitochondrial fusion supports asymmetrical cell division and promotes stem cell expansion both in vitro and in vivo. Notably, inhibition of the fission regulator DRP1 mimicked this effect, while MFN1 knockdown prevented it. In mouse models, deletion of Mir-200c triggered Pgc1a–Mfn1 expression, leading to mammary gland hyperplasia with expanded stem cell populations exhibiting increased self-renewal capacity.

Mechanistically, fused mitochondria were preferentially inherited by stem cell progeny during asymmetrical division, a process dependent on MFN1 interaction with the polarity protein PKCζ. This interaction enabled phosphorylation and exclusion of the differentiation factor NUMB from the stem cell progeny. Furthermore, mitochondrial fusion enhanced production of glutathione (GSH), a key antioxidant. Blocking GSH impaired stem cell expansion, while EMT was associated with reduced mitochondrial ROS levels.

Overall, this work highlights mitochondrial fusion as a key regulator of stem cell fate through modulation of polarity cues and oxidative stress. These findings provide valuable insights for developing stem cell–based regenerative therapies and targeting cancer progression. (Cited Source: Nature Reviews Molecular Cell Biology volume 20, page65, 2019)

About Dr. Chun Ju Chang
Dr. Chun Ju Chang is a leading expert in cancer metabolism and epigenetics, currently serving as a full professor at China Medical University in Taiwan. Formerly the dean of the College of Life Sciences, her research has significantly advanced our understanding of breast cancer development and holds promise for novel cancer therapeutic strategies.

The post Mitochondrial Dynamics in EMT-Driven Stem Cell Expansion appeared first on Chun Ju Chang.

In the world of biomedical research, it often feels like your worth is measured in citations and impact factors. From the moment we step into academia, we are taught a simple equation: more papers equals to more success. But is that really the full picture?

As someone who has spent years working in cancer research — from my time as a Ph.D. student at UCLA and now as a professor in Taiwan — I’ve felt both the pride of publication and the pressure of keeping up.

This is the reality for many scientists today. We’re passionate about discovery, about helping patients, about advancing knowledge. But we’re also navigating a system that can reward speed over substance, quantity over quality.

The Pressure Starts Early

Graduate students are now told that publishing is the ticket to everything — a good postdoc, a grant, a job, even self-worth. I’ve had students come to my office with frustrations and self-doubt because of a failed experiment or unsatisfactory progress reports.

As researchers, we’re expected to publish often, in high-impact journals, with novel findings. If your paper doesn’t land in a top-tier publication, it may feel like it doesn’t count. This culture creates an invisible, constant pressure that can affect not just your work, but your health.

What Are We Measuring, Really?

The current system of academic success often relies on a few key metrics:

• Number of publications
  
• Journal impact factor/ Citation
• Grant funding support
  
• Excellence in teaching and mentorship
  
• Reputation among peers
  

While these indicators have value, they are not the whole story. They don’t always reflect the depth of your work, the integrity of your process, or the hours spent mentoring others, refining experiments, or dealing with failed hypotheses.

Some of the most meaningful work I’ve done — including training students, building collaborations, and initiating team projects— may never be reflected in a citation count, but it has shaped careers and science all the same.

The Cost of the Publish-or-Perish Model

The constant drive to publish can have side effects:

• Rushed science: When deadlines loom, there’s pressure to “get a result” even if the study could benefit from more time or data.
  
• Repetitive studies: To maintain output, researchers may focus on low-risk, incremental findings rather than big, bold questions.
  
• Burnout: Constant pressure can lead to stress, exhaustion, and a loss of joy in discovery.
  

Redefining Productivity in Research

What if we reimagined productivity in science? What if we expanded how we measure success?

Here are a few things I believe we should value more:

1. Quality over quantity: A few well-designed, meaningful studies can be more impactful than many superficial ones.
   
2. Collaboration: Team-based science that crosses borders and disciplines is essential for tackling complex diseases like cancer.
   
3. Mentorship and teaching: Training the next generation is as important as any publication.
   
4. Responsibility and transparency: Science should be reproducible, sharing, and open for evaluation. 

Staying Grounded Amid the Pressure

So how do we survive — and thrive — in this environment?

• Stay connected to your purpose: For me, it’s the hope of improving cancer care. When I feel overwhelmed, I remind myself that every experiment, even the ones that “fail,” is part of that mission.
  
• Seek mentors who value the whole person: I was fortunate to have mentors who embraced curiosity and understanding. Be that mentor to others.
  
• Celebrate small wins: Not every success comes with a DOI number. A good discussion, a new technique mastered, or a breakthrough in a student’s confidence is worth celebrating.
  
• Speak openly about pressure: Normalize conversations about mental health, stress, and the need for reform in academic systems.
  

A Call to Institutions and Journals

Finally, I believe change must also come from the top. Academic institutions and journals should:

• Reward mentorship, collaboration, and community engagement in tenure decisions
  
• Support researchers who take risks or explore topics based on curiosity, not trendiness
  
• Create space for longer, more in-depth studies
  
• Publish replication studies and negative results
  
• Encourage a culture of care, not just competition
  

Because the cure for cancer won’t come from rushing. It will come from doing science the right way — together.

The post Publication Pressure and Productivity: Navigating the High-Stakes World of Medical Research appeared first on Chun Ju Chang.

Cancer is a global problem. It affects people in every country, across all age groups, and in every community. So why should the research to fight it be confined to national borders?

As a cancer researcher who has worked in both the United States and Taiwan — and who collaborates regularly with scientists from Europe, Asia, and North America — I’ve seen firsthand how powerful international partnerships can be. When we work together across cultures and continents, we share knowledge faster, avoid duplication, and ultimately accelerate the breakthroughs that save lives.

From Local Lab to Global Network

My career continues in Taiwan, but it truly blossomed when I pursued my Ph.D. at University of California and later completed postdoctoral training at MD Anderson Cancer Center. These experiences didn’t just expand my scientific knowledge — they opened my eyes to how differently cancer is approached around the world.

Some countries prioritize early screening and public health strategies. Others invest heavily in immunotherapy and precision medicine. Some researchers are experts in lab techniques I had never encountered before. By connecting with people from other countries, I didn’t just gain knowledge — I gained perspective.

Now, as a professor at China Medical University in Taiwan, I actively seek out cross-border collaborations. Whether it’s co-authoring papers, co-hosting workshops, or mentoring international students, I believe that the future of cancer research lies in a globally connected community.

Success Story #1: Pan-Asian Genomic Study

One recent project I’m proud to have supported involved a regional collaboration between researchers in Taiwan, South Korea, and Singapore. The goal was to understand how genetic mutations in cancer patients differ across Asian populations — something that had been underrepresented in Western-centric studies.

By pooling data from thousands of patients across borders, we were able to identify region-specific genetic patterns that could help refine diagnostic tools and treatment plans. No single country could have gathered that much data alone. But together, we created a powerful research engine — and we’re now publishing findings that could influence global cancer care.

Success Story #2: Shared Clinical Trials

Another major win came through a shared clinical trial between institutions in the U.S. and Taiwan, focused on a promising new therapy for liver cancer — a disease particularly prevalent in many parts of Asia. By opening the trial to patients in both countries, we not only sped up recruitment, but also collected more diverse clinical data.

This diversity is critical. Drugs tested only on one ethnic or genetic population may not work the same way for others. International trials help ensure that treatments are safe and effective for everyone — not just a small segment of the world’s population.

Why Collaboration Works

There are three key reasons international collaboration is so effective in cancer research:

1. Diverse Perspectives Spark Innovation
   When researchers from different backgrounds come together, they approach problems in unique ways. A scientist in Germany might think differently than one in Japan or Brazil. That diversity of thought is a goldmine for innovation.
   
2. Shared Resources, Faster Progress
   Scientific equipment, funding, and patient populations are often limited in any one institution. When we pool our resources — data, tools, technologies — we move faster. Collaboration allows us to do in two years what might have taken ten.
   
3. Training the Next Generation
   Through international exchanges, students and early-career scientists gain exposure to new methods and cultures. This prepares them to be more adaptable, creative, and globally-minded researchers.
   

How to Build Effective Global Partnerships

Of course, collaboration doesn’t happen automatically. It takes intention and effort. Here are a few lessons I’ve learned about making it work:

• Start with Shared Goals
  Before partnering with another lab or institution, clarify your mutual interests. Are you working toward the same scientific questions? Do your teams complement each other’s strengths?
  
• Build Trust Over Time
  Strong collaborations come from relationships — not just contracts. Take time to understand your partners, their culture, their values. Trust is what allows collaboration to survive when things get hard.
  
• Communicate Clearly and Often
  With time zones, language barriers, and different scientific traditions, clear communication is key. Use regular meetings, shared digital platforms, and be mindful of cultural differences.
  
• Include Institutions in Low- and Middle-Income Countries
  Some of the most exciting innovations are happening in places with fewer resources. By including diverse institutions, we not only help strengthen global health equity, but we also uncover perspectives that can lead to unexpected breakthroughs.
  

The Future is Global

If the past two decades have taught us anything, it’s that no single country — no matter how advanced — can solve cancer alone. The future of cancer research will be written by international teams, speaking different languages, working in different time zones, but united by a single mission: to cure cancer and improve lives.

I’m proud to be a small part of that global community. And I encourage every researcher — whether you’re just starting your career or leading a lab — to reach out, connect, and collaborate. The world is full of brilliant minds. Let’s put them to work — together.

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