Latest news with #CancerCell
Bangkok Post
19-07-2025
- Health
- Bangkok Post
Chemotherapy can speed up cancer spread: study
HONG KONG — A team of Chinese scientists has found that the spread of cancer from original tumour sites to distant organs can be caused by chemotherapy triggering the awakening of dormant cancer cells. Their findings shed light on why breast cancer patients can experience cancer metastasis in organs like the lungs despite successful treatment of their primary tumours. The team also found that the use of specific drugs in combination with chemotherapy could be used to inhibit this process in mice, and a clinical trial is already under way in breast cancer patients. "We demonstrate that chemotherapeutic drugs, including doxorubicin and cisplatin, enhance proliferation and lung metastasis of dormant breast cancer cells," the team wrote in a paper published in the peer-reviewed journal Cancer Cell on July 3. "This study provides direct evidence of dormancy awakening and reveals a mechanism underlying [the] detrimental effect of chemotherapy on metastasis, highlighting potential strategies to improve cancer treatment." Researchers in the United States previously found that high doses of radiation therapy to treat cancer could paradoxically lead to the growth of metastatic tumours. Many patients who undergo chemotherapy to treat primary tumours, the original tumour site in the body where cancer cells first start to develop, can have cancer relapses in other organs even after complete primary tumour regression. This has led to research into whether chemotherapy can have a similar paradoxical effect, in which it both treats primary tumours and triggers cancer metastasis. "It is postulated that the reactivation, or awakening, of dormant disseminated tumour cells (DTCs) in distant organs results in metastatic relapse after the asymptomatic period," the team said. Studies have shown that disseminated cancer cells, which travel from primary tumours to sites in the body, can be found even during the early stages of primary cancer formation, according to a news release by the Chinese Academy of Sciences (CAS). These cells can stay in a dormant state for years, during which they do not grow and multiply, allowing them to evade chemotherapy. Researchers have previously identified molecular mechanisms that regulate metastatic relapse and disseminated cancer cell dormancy. However, it has not been clear whether metastasis results from the reactivation of dormant cells or the growth of rare, non-dormant disseminated cells. "Understanding the exogenous causes of DTC awakening will help disease management of cancer survivors, offering opportunities to prevent and interrupt metastatic relapse after initial therapies," the researchers said in their paper. To study this, the team led by Hu Guohong, a professor at CAS' Shanghai Institute of Nutrition and Health, along with researchers from Fudan University and Qilu Hospital of Shandong University, developed a cancer cell dormancy tracing approach. The team confirmed that chemotherapy-induced reactivation of dormant cells from breast cancer could lead to metastatic relapse in the lungs of mice. Their findings demonstrated that the "awakening of dormant DTCs, but not accumulation of pre-existing proliferative DTCs, is responsible for metastases induced by chemotherapy". Chemotherapy induces senescence - an accelerated state of ageing in which cells stop multiplying and release inflammation-causing chemicals - in specialised connective tissue called fibroblasts. The team found that senescent fibroblasts release proteins that cause immune cells called neutrophils to form weblike formations, called neutrophil extracellular traps, which change the environment in the lung into one that helps dormant cancer cells restart their growth. The remodelling of the extracellular matrix, a complex network of molecules that support and surround cells, also degrades tumour-suppressing factors. "We explored if chemotherapy-induced senescent fibroblasts could be a therapeutic target to improve the effect of chemotherapy on metastasis inhibition," the team said. The researchers discovered that combining senolytic drugs, which eliminate senescent cells, with the chemotherapy drug doxorubicin reduced senescent fibroblasts in the lungs of mice. "Since the senolytics have shown acceptable safety profiles and benefits in clinics, this could be a promising strategy and warrant further clinical investigation," they said. The team said that, based on these study results, a phase II clinical trial was under way to explore the safety of combining the senolytic drugs dasatinib and quercetin with chemotherapy to treat triple-negative breast cancer. Triple-negative breast cancer is an invasive and aggressive form of the disease that cannot be treated with the usual hormone therapy used to help treat such cancers.
South China Morning Post
19-07-2025
- Health
- South China Morning Post
Chemotherapy can speed up cancer spread, Chinese study finds
A team of Chinese scientists has found that the spread of cancer from original tumour sites to distant organs can be caused by chemotherapy triggering the awakening of dormant cancer cells Advertisement Their findings shed light on why breast cancer patients can experience cancer metastasis in organs like the lungs despite successful treatment of their primary tumours. The team also found that the use of specific drugs in combination with chemotherapy could be used to inhibit this process in mice, and a clinical trial is already under way in breast cancer patients. 'We demonstrate that chemotherapeutic drugs, including doxorubicin and cisplatin, enhance proliferation and lung metastasis of dormant breast cancer cells ,' the team wrote in a paper published in the peer-reviewed journal Cancer Cell on July 3. 'This study provides direct evidence of dormancy awakening and reveals a mechanism underlying [the] detrimental effect of chemotherapy on metastasis, highlighting potential strategies to improve cancer treatment.' Advertisement
Al Bawaba
18-05-2025
- Health
- Al Bawaba
WCM-Q researchers probe links between insulin resistance and colorectal cancer
Researchers at Weill Cornell Medicine-Qatar (WCM-Q) have explored the possible links between insulin resistance and early-onset colorectal cancer (EOCRC) in a new article published in Cancer Cell (Cell Press), a leading scientific journal. Cancer, regardless of type, is generally considered a disease that occurs later in life, typically after 50-60 years of age. Data from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute (NCI), USA, indicates that the median age of a cancer diagnosis is 66. However, more recently, younger individuals under the age of 45-50 have been diagnosed with cancers (early-onset cancers; EOCs). Although this shifting trend in cancer epidemiology has been reported previously, this occurrence gained significant attention in early 2024, with many major news outlets and research/medical institutions reporting a rise in EOCs. Among the various EOCs, gastrointestinal cancers, particularly colorectal cancer (CRC), seem to be rapidly increasing among the younger population. This trend appears similar for countries in the MENA region, including Qatar. "As cancer researchers, we were captivated by the question of 'why this is happening?'" said Prof. Dr. Dietrich Büsselberg, professor of physiology and biophysics, one of the co-corresponding authors of the article. "It is well known that genetic mutations that cause CRC and hereditary CRC-associated syndromes are highly penetrant and increase the risk of CRC. However, it is unlikely that this risk factor alone has changed so dramatically in successive generations of the population to account for the significant increase in EOCRC in recent years. Dr. Samson Mathews Samuel, research associate in physiology and biophysics and co-corresponding author of the article, said: 'Our in-depth review of existing literature led us to identify a possible culprit behind this occurrence, namely insulin resistance. Our study, therefore, examined the mechanisms through which insulin resistance may facilitate the development of colorectal cancer, particularly in younger populations.' A growing body of evidence points to insulin resistance, a hallmark of common metabolic diseases such as obesity, diabetes, and metabolic syndrome, as a possible key risk factor contributing to the incidence and progression of EOCRC. Insulin resistance, defined as the inability of cells to respond to normal insulin, results in hyperinsulinemia (an increase in circulating insulin levels in the blood) much earlier in life than is typically recognized. This is because the possible early signs of insulin resistance usually go unnoticed, and blood tests for insulin resistance are not commonly done as a routine screening measure unless obesity, pre-diabetes/diabetes, or metabolic syndrome have been diagnosed. While several studies link obesity, diabetes, and metabolic syndrome to the risk and progression of CRC, insulin resistance as a risk factor in its own right is often overlooked. Surprisingly, insulin resistance can drive metabolic changes very early in life and depends on several early-life external factors to which the individual is exposed. 'For example, the overuse of antibiotics or supplements disrupts the microbiome of a pregnant mother, leading to insulin resistance that could also affect the fetus,' said Prof. Busselberg. Environmental factors and minor dietary and lifestyle choices may contribute to insulin resistance, which can play a role in the occurrence of EOCRC. Ms. Elizabeth Varghese, a senior research specialist, is the other author of the paper, titled 'Complexity of insulin resistance in early-onset colorectal cancer'. The paper also infers that managing insulin resistance through dietary and/or lifestyle changes and therapeutic interventions is likely to be effective in reducing the incidence of colorectal cancer among young individuals. The study was made possible through funding from the Biomedical Research Program at Weill Cornell Medicine-Qatar and NPRP-Standard (NPRP-S) 14th Cycle grant NPRP14S-0311-210033 from Qatar National Research Fund (a member of Qatar Foundation).
