Category: Cancer

Categories : Cancer DermatologyTags :

Albinism Awareness Month Puts Overlooked Skin Cancer Risks in Focus

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Plastic surgeon urges South Africans not to ignore the small skin changes that could eventually require major treatment and reconstruction

Photo by LekePOV

A sore that refuses to heal. A mole that starts changing. A small patch of skin that repeatedly bleeds or crusts. These changes can be easy to dismiss, but skin cancer is a potentially serious and life-threatening disease, and delaying assessment can allow even a small lesion to become considerably more difficult to treat.

In September, South Africa observes Albinism Awareness Month, raising awareness of the health and social challenges faced by people living with albinism. Albinism is a genetic condition impacting the production of melanin, the pigment responsible for colour in the skin, hair, and eyes. Melanin also provides some natural protection against ultraviolet radiation, meaning people with albinism, who produce very little or no melanin, face a particularly high risk of sun damage and skin cancer.

Professor Chrysis Sofianos, a triple board-certified plastic surgeon and Academic Head of the Division of Plastic and Reconstructive Surgery at the University of the Witwatersrand, says this makes ongoing sun protection and vigilance especially important.

“Albinism Awareness Month rightly draws attention to the greater vulnerability of people with albinism when it comes to sun exposure and skin cancer. The important message is to protect your skin and know what is normal for you so that you can have any concerning changes assessed early.”

Early recognition can, however, be more challenging in people with albinism. Some skin cancers may lack the pigmentation people commonly associate with suspicious lesions, making it especially important not to rely on colour alone when deciding whether a change needs medical attention.

He says the month can also challenge the broader assumption that skin cancer is exclusively a disease of fairer skin. While darker skin and higher levels of melanin offer greater natural protection, this does not mean immunity. Certain forms of skin cancer can further occur in areas not typically exposed to the sun, including the soles of the feet, palms, and underneath the nails.

“Everyone should be familiar with their skin and pay attention when something changes, including in less obvious areas. If something doesn’t seem right, have it checked rather than dismissing it or trying to diagnose it yourself.”

Nearly 27 000 skin cancer cases recorded

Demonstrating just how common skin cancers are, South Africa’s National Cancer Registry recorded 26,967 cases across three major skin cancer categories in 2024. These included basal cell carcinoma (BCC), squamous cell carcinoma (SCC) of the skin, and melanoma.

Additionally, the NCR ranked BCC as the second most common cancer among men and third among women, while SCC of the skin ranked third among men and fourth among women.

“The numbers matter because skin cancer can still be perceived as relatively uncommon or as something that will always be obvious when it develops. In reality, many lesions begin as something very small and seemingly insignificant. People may watch a lesion for months because it’s small, painless, or seems like an ordinary mole, sore, or sign of ageing. But the absence of pain doesn’t mean there’s nothing to worry about,” explains Sofianos.

Warning signs can include a new growth, a sore that repeatedly fails to heal, a lesion that bleeds or crusts, and changes in the size, shape or colour of an existing mole.

When removing the cancer is only part of the treatment

Skin cancers affecting the nose, eyelids, ears, scalp and other areas of the face may require the removal of enough tissue to treat the disease. Depending on the size and position of the resulting defect, reconstructive surgery may then be required to preserve function and appearance.

“People often think of plastic surgery purely in aesthetic terms, but reconstruction after cancer treatment is a significant part of the speciality. When cancer is removed from somewhere such as the nose, eyelid, or ear, we are not only considering how the wound closes. We have to think about restoring form and function, and achieving the best possible outcome for that patient.”

For people with albinism, their ongoing vulnerability to UV damage can compound their treatment burden. Some patients may develop more than one cancerous or precancerous lesion over time, and treatment is not always a once-off event. Careful follow-up, continued skin protection, and early assessment of new lesions remain important even after one cancer has been successfully treated.

As a plastic and reconstructive surgeon, Sofianos regularly manages patients requiring reconstruction after cancer removal, and he notes that the consequences of delayed diagnosis are clearly visible. Larger lesions may require wider removal and reconstruction, with greater potential for visible scarring or prolonged wound healing. This is another reason why fear of a scar should never deter someone from seeking assessment early.

“The earlier we can identify and appropriately treat a cancer, the better our chance of limiting how much tissue needs to be removed and how extensive the reconstruction may need to be.”

Albinism Awareness Month should therefore reinforce the special protection required by people with albinism while reminding all South Africans of the importance of identifying any suspicious skin changes early.

“For people with albinism, careful sun protection and regular attention to the skin are critically important. More broadly, if a lesion is changing, bleeding, repeatedly crusting, or failing to heal, don’t ignore it. Have it assessed.”

Categories : CancerTags :

First-line Trastuzumab Deruxtecan Extends Progression-free Survival in HER2-mutant Lung Cancer

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Photo by Ivan S

First-line treatment with trastuzumab deruxtecan (T-DXd) significantly improved progression-free survival compared with pembrolizumab plus platinum-based chemotherapy in patients with advanced or metastatic HER2-mutant non-small cell lung cancer (NSCLC), according to primary results from the phase 3 DESTINY-Lung04 trial presented at the International Association for the Study of Lung Cancer (IASLC) 2026 World Conference on Lung Cancer (WCLC).

DESTINY-Lung04 is the first global phase 3 trial to demonstrate a statistically significant and clinically meaningful improvement in progression-free survival with first-line single-agent T-DXd compared with standard-of-care pembrolizumab plus platinum doublet chemotherapy in this patient population. Median progression-free survival by blinded independent central review was 14.3 months with T-DXd versus 8.3 months with pembrolizumab plus chemotherapy, representing a 6-month improvement (HR 0.63; 95% CI, 0.50–0.79; P<0.0001).

HER2-mutant NSCLC is an aggressive form of lung cancer associated with a poor prognosis. According to the study investigators, many patients do not respond to first-line standard-of-care immunotherapy plus chemotherapy, underscoring the need for effective HER2-directed treatment options.

The global, open-label, randomised phase 3 DESTINY-Lung04 trial enrolled treatment-naïve patients with unresectable locally advanced or metastatic NSCLC harbouring HER2 exon 19 or exon 20 mutations. A total of 454 patients were randomised 1:1 to receive T-DXd 5.4mg/kg intravenously every three weeks or pembrolizumab plus platinum chemotherapy and pemetrexed. The primary endpoint was progression-free survival by blinded independent central review, with secondary endpoints including overall survival, objective response rate, progression-free survival 2, duration of response and safety.

T-DXd also produced a higher objective response rate than pembrolizumab plus chemotherapy. The objective response rate was 70.0% with T-DXd compared with 44.5% with pembrolizumab plus chemotherapy. Median duration of response was 13.4 months and 9.7 months, respectively.

“These results demonstrate substantial improvements in progression-free survival and response with first-line trastuzumab deruxtecan for patients with advanced or metastatic HER2-mutant NSCLC,” said Julia Rotow, MD, of the Dana-Farber Cancer Institute, Boston, Mass. “The findings support T-DXd as a new first-line treatment option for this patient population, for whom more effective HER2-directed approaches are needed.”

Median overall survival was 29.3 months with T-DXd and 33.1 months with pembrolizumab plus chemotherapy (HR 1.15; 95% CI, 0.88–1.52). Investigators noted that subsequent therapies were imbalanced between the treatment groups, primarily involving HER2-directed and immunotherapy-based treatments, which confounded interpretation of the overall survival results.

The safety profile of T-DXd was generally consistent with its known profile. Adjudicated drug-related interstitial lung disease (ILD)/pneumonitis occurred in 20.8% of patients treated with T-DXd, with most events classified as grade 1 or 2 (78.7%), compared with 2.3% of patients receiving pembrolizumab plus chemotherapy. The study’s safety analysis also reported grade 3 or higher drug-related adverse events in 34.1% of patients receiving T-DXd and 33.6% receiving pembrolizumab plus chemotherapy.

The investigators concluded that T-DXd improved progression-free survival, response rates and durability of response compared with pembrolizumab plus chemotherapy, supporting T-DXd as a new first-line option for patients with advanced or metastatic HER2-mutant NSCLC.

Source: International Association for the Study of Lung Cancer

Categories : CancerTags :

Novel Immunotherapy Leads to Complete Regression of Liver Cancer in a Child

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Photo by CDC on Unsplash

A new report in the New England Journal of Medicine by researchers at Baylor College of Medicine, Texas Children’s Hospital and Seattle Children’s describes a complete regression of hepatoblastoma, the most common paediatric liver cancer, in a 3-year-old treated with a novel immunotherapy. The patient is enrolled in the CARE study (NCT04715191), a first-in-human, Phase 1 trial evaluating glypican-3-specific chimeric antigen receptor (GPC3-CAR) T cells armed with interleukin-15 and -21 (IL15 and IL21).

The child initially presented with a large primary liver tumour and metastases in the lungs. Prior to enrolment in the CARE study, the patient was treated with three lines of chemotherapy and underwent complete resection of the primary liver tumour and two lung metastases. His cancer was no longer responsive to chemotherapy, and a new lung metastasis recurred after surgery when he was enrolled on the CARE study.

The immunotherapy was engineered from the patient’s own cells at the Good Manufacturing Practices laboratories at the Center for Cell and Gene Therapy using two vectors: one encoding the second-generation GPC3-CAR and the second encoding IL15, IL21 and the inducible caspase 9 safety switch, which Center for Cell and Gene Therapy investigators previously showed controlled CAR T expansion.

Two infusions were administered eight weeks apart in the outpatient setting. A partial response was observed after the first infusion, and imaging showed complete resolution of the metastatic disease after the second infusion. No dose-limiting toxicities or cytokine release syndrome occurred. Complete regression continues one year after treatment.

“This case demonstrates that a durable complete response in a chemotherapy-resistant solid tumour can be achieved entirely in the outpatient setting without systemic toxicity,” said first author Dr David Steffin, associate chief of cellular therapy and bone marrow transplant at Texas Children’s and associate professor of paediatrics – haematology and oncology in the Center for Cell and Gene Therapy at Baylor.

“This study provides evidence that these novel CAR T cells may be a safe and effective modality for hepatoblastoma and highlights the need for further assessment in patients with GPC3+ solid tumors,” said corresponding author Dr Andras Heczey, principal investigator at Seattle Children’s and professor of pediatrics in hematology-oncology at the University of Washington School of Medicine. Heczey was at Baylor and Texas Children’s at the time of research.

Source: Baylor College of Medicine

Categories : CancerTags :

A Less-intensive Drug Combination is More Effective in Treating AML, Trial Shows

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Acute myeloid leukaemia patients receiving azacitidine plus venetoclax tolerated treatment better, spent less time in the hospital and were more likely to reach stem cell transplantation

Photo by Ivan S

Investigators from the Mass General Brigham Cancer Institute have found that adults with newly diagnosed acute myeloid leukaemia (AML) receiving a less-intensive combination of azacitidine and venetoclax had more than twice as much time before treatment failed, the leukemia returned or worsened, or they died, compared with patients receiving intensive chemotherapy. Published in The New England Journal of Medicine, the findings could change the initial treatment approach for many patients with AML.

“Less-intensive treatment does not necessarily mean less-effective treatment,” said lead author Amir T. Fathi, MD, director of the Leukemia Program at the Mass General Brigham Cancer Institute. “Our goal is to optimally treat acute myeloid leukemia while reducing serious complications and the amount of time patients spend in the hospital.”

The less-intensive combination is already used in older patients or those unable to tolerate intensive chemotherapy. The PARADIGM trial tested whether it could work as well – or better – for patients who could receive intensive chemotherapy, including younger patients.

The phase 2 clinical trial randomly assigned 172 adults eligible for intensive chemotherapy at nine U.S. centres to azacitidine plus venetoclax or intensive chemotherapy. Nearly three-quarters had harder-to-treat forms of AML.

Patients receiving the combination went 14.5 months before treatment failed, the leukaemia returned or worsened, or they died, compared with 6.2 months for those receiving intensive chemotherapy.

Treatment brought leukaemia into a remission state in 78% of patients receiving the combination and 53% of those receiving intensive chemotherapy. Patients receiving the combination also had fewer serious infections and bleeding problems. In the first 30 days, patients spent 12.5 days in the hospital with the combination versus 27.3 days with intensive chemotherapy. More patients receiving the gentler combination then proceeded to stem cell transplantation: 60%, compared with 40% of those receiving intensive chemotherapy.

“For decades, intensive chemotherapy has been the standard upfront treatment for patients considered able to tolerate it,” Fathi said. “Our findings suggest that some of these patients may do better with a less-intensive approach.”

The trial was not designed to show whether either treatment helped patients live longer. Future studies should test less-intensive treatments in excluded groups, including patients younger than 60 with NPM1-mutated AML and those with FLT3-mutated AML.

Source: Mass General Brigham

Categories : Cancer Cardiovascular DiseaseTags :

Cancer Drug Reduces Atherosclerosis Inflammation and Plaque

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Source: Wikimedia CC0

A new Yale study has identified a promising therapeutic avenue for atherosclerosis, a condition caused by inflammation and plaque buildup in arteries.

Martin Schwartz, PhD, Robert W. Berliner Professor of Medicine (Cardiology) and the study’s principal investigator, investigates how the mechanical forces from blood flow and pressure affect the cells lining the arteries and how cell responses to forces contribute to cardiovascular disease. Atherosclerosis predominantly impacts regions of the arteries that bend or branch, creating disturbances in blood flow dynamics that activate cells’ inflammatory pathways and eventually lead to plaque buildup.

In a study published August 31 in Proceedings of the National Academy of Sciences, Schwartz’s team, led by associate research scientist Divyesh Joshi, PhD, has now found that a protein complex called Polycomb Repressive Complex 2 (PRC2) is associated with disturbed blood flow, and that it inhibits anti-inflammatory mechanisms in the arteries that mitigate atherosclerosis.

By blocking PRC2, the team successfully reduced harmful plaque in animal models of the disease.

“By inhibiting PRC2, we boost protective pathways that reduce inflammation and could protect people from plaque rupture in atherosclerosis,” Schwartz says.

What causes atherosclerosis?

Atherosclerotic plaques are present in nearly all adults in developed countries. They are usually asymptomatic because a protective fibrous cap forms over the plaques. But if the cap weakens and ruptures, it triggers the formation of a blood clot that can lead to a heart attack or stroke. Plaques vulnerable to rupture tend to have a thinner cap or exhibit heightened inflammation.

Scientists believe there are three types of factors driving atherosclerosis. The first are metabolic risk factors, including elevated cholesterol and blood sugar. Inflammation is another – individuals with autoimmune or other inflammatory diseases are at a higher risk for the disease.

An important but overlooked third factor, Schwartz says, is the biomechanics of blood flow through the arteries. In places where the arteries are straight tubes, the blood flow activates protective, anti-inflammatory genes. Where arteries curve sharply, disturbing blood flow, there are fewer of these protective factors and increased inflammation.

Protein complex suppresses protective genes

The cells lining the arteries, called vascular endothelial cells, have receptors that detect blood flow. Previous research in Schwartz’s laboratory has shown that blocking those receptors can inhibit inflammatory processes and enhance protective ones. In the new study, the researchers investigated the underlying mechanisms of the inflammation associated with disturbed blood flow.

First, they used previously published datasets to investigate genes that interact with anti-inflammatory genes in endothelial cells, and then identified those that promote disease. These analyses revealed that genes associated with PRC2, a protein complex that inhibits gene expression, were strongly associated with suppression of certain anti-inflammatory genes.

“PCR2 is understood to be pro-inflammatory in vascular endothelial cells,” Joshi says.

The researchers also studied gene expression in human endothelial cells exposed to normal and disturbed blood flow. These experiments confirmed that genes associated with PRC2 are upregulated during disturbed blood flow where inflammation tends to be higher.

However, when the researchers treated endothelial cells with tazemetostat, a drug that inhibits PRC2 and was previously used to treat cancer, they found that inflammatory signals were reduced. The findings suggest targeting PRC2 could be a treatment for atherosclerosis.

A new avenue for treating atherosclerosis

To explore PRC2 inhibition as a therapeutic avenue, the researchers developed animal models of the disease and tested the effects of tazemetostat. They found that the drug slowed plaque growth and reduced the amount of vulnerable plaque.

“It takes an unstable plaque and turns it into a more stable form that is no longer at risk of rupture,” Schwartz says.

Since conducting the study, the manufacturers of tazemetostat have withdrawn it from the market due to emerging evidence that patients who take the drug have a slightly increased risk of secondary cancers. But there are other PRC2-inhibiting drugs that may be similarly useful for treating atherosclerosis, the researchers note.

“This is a potential path forward to treating patients,” Schwartz says.

By Isabella Backman

Source: Yale School of Medicine

Categories : Cancer Cardiovascular DiseaseTags :

Survivors of HER2+ Breast Cancer Could Avoid Lifelong Heart Medication

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Many breast cancer survivors whose treatment caused problems with their heart function can safely stop medication after their heart recovers, finds a new study led by researchers at University College London.

The trial, which was funded by the British Heart Foundation, involved 90 women who had recovered from heart problems caused by a specific type of breast cancer treatment. Most were in their 40s and 50s and would previously have been advised to stay on heart medication for life, due to fears their heart function would decline once the drugs were stopped. 

Researchers found that 98% of the group who stopped taking their heart medication had no change in their heart function after one year, with only one woman experiencing a decline in her heart’s pumping ability.

Women who came off their medication also reported a slightly better quality of life at 12 months than those who continued, based on their scores on questionnaires designed to measure quality of life in people with heart failure. The study is published in the European Heart Journal and was presented at the European Society of Cardiology Congress in Munich.

The women in the trial will continue to be followed up over the next five years to monitor their heart health. But the researchers suggest their findings can start important conversations between survivors and their doctors about whether they need to continue treatment long-term.

Professor Charlotte Manisty (UCL Institute of Cardiovascular Science), who is also a consultant cardiologist at Barts Heart Centre and UCLH, said: “Modern breast cancer treatment is a remarkable success story. But the damaging effects of these drugs on the heart leave survivors and their doctors with difficult questions about ongoing treatment to maintain their heart health. 

“Our study provides the first evidence that heart failure therapies can be safely stopped in survivors whose hearts have recovered, with the support of ongoing close monitoring. We hope these findings will be encouraging for survivors and their doctors, giving hope for a future free from treatment.” 

These patients are usually offered targeted biological treatments such as Trastuzumab (better known as Herceptin), which attach to HER2 receptors to help block the growth and spread of cancer. But in around 10% of patients, this treatment causes problems with heart function, leaving them in need of treatment with multiple medications – such as beta-blockers and ACE inhibitors – to help recovery. Survivors are currently advised to stay on these drugs for life, even after their cancer treatment ends and their heart recovers. 

The trial involved 90 breast cancer survivors at four hospitals in the UK who started taking heart failure medication after a diagnosis of HER2-targeted therapy-related cardiac dysfunction, but whose hearts later recovered following treatment. All study volunteers were women, with an average age of 50.

Everyone in the study was randomly assigned to either gradually withdraw from their heart failure medication (46 women) or to continue taking it (44 women). They were followed closely for one year with blood tests, quality-of-life questionnaires and cardiac MRI scans to check whether their heart function had worsened.

One woman in the group that stopped their medication experienced a decline in her left ventricular ejection fraction (a measure of the heart’s pumping ability). She didn’t report any symptoms, but the decrease was picked up on an MRI scan at 12 months. Her heart function improved when she started taking their heart failure medication again. 

None of the group that continued to take their heart failure treatment saw a decline in their heart function. 

Overall, left ventricular ejection fraction remained stable in both groups (minus one per cent in the withdrawal group and minus 0.2% in the continuation group) with no significant differences between the two groups after one year (withdrawal group 55.2 per cent compared to 55.6% in continuation group). 

None of the women in the trial reported any heart failure symptoms, required hospital treatment or experienced any other heart problems during the trial.

Dr Sonya Babu-Narayan, clinical director at the British Heart Foundation and consultant cardiologist, said: “These findings will be hugely encouraging for the thousands of breast cancer survivors whose heart health has been affected by lifesaving cancer treatment. 

“The study results give hope that many women will be able to safely stop medicines once their heart has recovered. The importance of ongoing monitoring is highlighted by the one study participant whose heart scan showed her heart function deteriorated but then bounced back when her heart treatment was restarted. More research is needed and the women will be followed up for longer, but in the meantime the good news for this group of breast cancer survivors is lifelong medications after heart complications need not be the default.”

Source: University College London

Categories : CancerTags :

Targeted Therapy for Metastatic Pancreatic Cancer Receives Approval in US

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Pancreatic cancer. Credit: Scientific Animations CC BY-SA 4.0

The US Food and Drug Administration has approved daraxonrasib, to be sold under the brand name Rasonque, for the treatment of adults with metastatic pancreatic adenocarcinoma who have received at least one prior systemic therapy or who are not candidates for multiagent systemic therapy. The approval follows results from an international phase 3 study co-led by UCLA that showed the targeted therapy significantly extended overall survival and reduced the risk of death by 60% compared with standard chemotherapy.

In the study, patients who received daraxonrasib, an oral RAS(ON) multi-selective inhibitor designed to block active RAS signaling, one of the primary drivers of pancreatic cancer, lived a median of 13.2 months compared with 6.7 months for those who received investigator’s choice chemotherapy.

The FDA approval provides a new treatment option for patients with metastatic pancreatic cancer, a disease that remains among the most lethal cancers and has historically had limited effective therapies.

The results were published in the New England Journal of Medicine and presented earlier this year at the annual meeting of the American Society of Clinical Oncology in Chicago.

“This FDA approval represents an important milestone for patients with metastatic pancreatic cancer, who have needed new and more effective treatment options,” said Dr. Zev Wainberg, professor of medicine and investigator at the UCLA Health Jonsson Comprehensive Cancer Center and co-first author of the study. “The results of this trial demonstrate that targeting RAS can meaningfully extend survival and improve disease control, and it is exciting to see these findings translated into an approved treatment for patients.”

More than 90% of tumours are driven by alterations in the RAS signalling pathway, particularly mutations in KRAS, a gene that helps regulate cell growth. When mutated, the gene can lock cells into a constant growth state, fuelling tumour development. Despite decades of research, RAS proteins have proved notoriously difficult to target with drugs.

Unlike earlier targeted therapies that focused on a single mutation subtype, daraxonrasib is part of a new class of therapies designed to inhibit multiple RAS mutations, including G12, G13 and Q61 alterations that dominate pancreatic cancer.

The study involved 500 patients with metastatic pancreatic cancer whose disease had already progressed after one previous treatment from 60 clinical sites across six countries. Participants were randomly assigned to receive either daraxonrasib orally once daily (248 patients) or standard chemotherapy chosen by their doctor (252 patients). About 92% of patients had RAS G12 mutations.

In addition to improved overall survival, patients treated with daraxonrasib experienced significantly longer disease control. Median progression-free survival was 7.2 months compared with 3.6 months for chemotherapy, effectively doubling the time before cancer progression, in the overall study population.

Tumour shrinkage was also more frequent in the daraxonrasib group, with approximately 30% of patients achieving an objective response in the overall study population compared with about 11% in the chemotherapy group. Patients receiving the targeted therapy also experienced slower worsening of pain and better preservation of quality of life over time.

“While most patients had RAS G12 mutations, the benefit appeared generally consistent across different patient groups and mutation types,” said Wainberg, who is also the co-director of the UCLA GI Oncology Program. “These findings support the idea that blocking active RAS signaling will become an important treatment strategy for pancreatic cancer.”

The most common side effects of daraxonrasib include rash, diarrhoea, stomatitis, nausea, fatigue, vomiting, abdominal pain, enema, decreased appetite and haemorrhage. The prescribing information also includes warnings and precautions for dermatologic and soft tissue toxicity, stomatitis and oral disorders, diarrhoea, gastrointestinal perforation, interstitial lung disease or pneumonitis and embryo-foetal toxicity.

Rasonque is manufactured by Revolution Medicines.

Source: UCLA Health

Categories : CancerTags :

Cancer Biosimilars Associated with Lower Costs for Insurers and Patients

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Analysis of more than 14 000 patient-drug pairs found biosimilar use was associated with lower costs and declining use of original branded biologic drugs

Photo by mohamad azaam on Unsplash

Biologic drugs play an important role in treating cancers such as breast cancer and lymphoma, but their high costs can add to the financial burden of cancer care. Now, lower-cost versions known as biosimilars are gaining ground, and a new study led by researchers at the UCLA Health Jonsson Comprehensive Cancer Center suggests their growing use is associated with lower costs for both insurers and patients.

The findings, published in JAMA Oncology, show that patients with cancer who exclusively used biosimilars had average monthly costs that were $3820 (R61 502) lower for insurers and $39.50 (R636) lower out of pocket compared with patients who exclusively used the original branded biologic drugs. The results provide evidence that market competition enabled by entry of biosimilars may help reduce the cost of cancer biologic drugs.

Why it matters

Cancer treatment can place a significant financial burden on patients, with financial hardship associated with medication nonadherence and poorer health outcomes. The high and rising cost of anticancer medications, particularly biologic drugs, which are complex medicines made using living cells, is one contributor to this burden. Previous research has estimated that financial toxicity may affect as many as half of patients with cancer in the United States.

Biosimilars were introduced as one potential way to address the high cost of biologic medicines. Unlike generic versions of conventional drugs, biosimilars are highly similar to, but not identical to, their originator products and have no clinically meaningful differences from them. A federal policy enacted in 2009 was designed to establish an abbreviated regulatory pathway for biosimilars in the US market to increase competition, lower prices and improve access to biologic treatments. By the end of 2024, 13 biosimilars were available for three major cancer biologics: bevacizumab, rituximab and trastuzumab. These drugs are used to treat cancers including breast cancer, lymphoma, colorectal cancer, lung cancer and ovarian cancer.

Previous studies have found that biosimilar competition in other therapeutic areas can lower prices and increase use of these lower-cost alternatives. However, less was known about how biosimilar entry across these three major cancer drugs affected the prices and market share of the original branded biologics and, importantly, whether those changes translated into lower costs for insurers and patients. The new study sought to address this gap by examining the economic impact of biosimilar use in real-world cancer care.

What the study did

Researchers conducted a retrospective cohort study using health insurance claims data to examine the use and costs of three cancer biologics after biosimilars became available for each. They analysed data from 14,655 patient-drug pairs involving people with cancer who initiated bevacizumab, rituximab or trastuzumab between 2020 and 2023. The study included patients with commercial insurance and Medicare-related coverage and tracked their treatment and costs for 12 months after they began treatment with a biologic.

The researchers grouped patients based on whether they exclusively used a biosimilar, exclusively used the originator, switched from the originator to a biosimilar, or switched from a biosimilar to the originator. They compared monthly costs paid by insurers and patients’ out-of-pocket payment, calculated as the sum of deductibles, copayments and coinsurance. They also examined changes in the average sales price and market share of the originators and their biosimilars from before biosimilar entry through 2024 to assess how the introduction of biosimilars affected the market dynamics.

What they found

Among the patient-drug pairs, 59.4% of patients exclusively used a biosimilar during the first 12 months of treatment, while 32.5% exclusively used the originator. About 6.9% of patients switched from the originator to a biosimilar, and 1.2% switched from a biosimilar to the originator. This suggests that biosimilars were adopted primarily by patients starting treatment rather than through switching patients who were already receiving the originator.

Patients who exclusively used biosimilars were associated with substantially lower monthly costs for insurers. After adjusting for differences among patients and treatment patterns, average monthly payer costs were $8,959 (R144 230) for patients who exclusively used biosimilars, compared with $12 779 (R205 751) for those who exclusively used the originator, a difference of $3820 (R61 502) per month. Patients who exclusively used biosimilars also had lower average monthly out-of-pocket costs, $118.90 (R1950) compared with $158.40 (R2550) for those who exclusively used the originator, a savings of $39.50 (R636) per month.

The researchers also found that biosimilar entry was associated with lower prices and declining market share for the originators. The average sales price of the three originators declined by 3.8% per year after biosimilars entered the market, while their market share decreased by about 30% annually among patients with commercial insurance and 31.5% in Medicare Part B. The average sales price of the 12 biosimilars included in the study declined by 12.4% per year.

What this means for patients

The findings suggest that biosimilars could help reduce some of the financial burden associated with cancer treatment for patients while creating savings for the healthcare system.

“Although the savings were substantially greater for insurers than for patients, even modest reductions in out-of-pocket costs may be meaningful for people facing the financial challenges of cancer care – savings that can be used toward other treatment-related expenses or cover living expenses,” said Tina Shih, PhD, director of the Cancer Health Economics Research Program at the UCLA Health Jonsson Comprehensive Cancer Center, professor of Health Economics in the Department of Radiation Oncology, and senior author of the study. 

The study also points to treatment initiation as an important opportunity to expand biosimilar use. Because most patients in the study who received biosimilars started treatment with them, rather than switching from an original biologic, decisions about which drug to use when treatment begins may play an important role in increasing access to lower-cost and equally efficacious alternatives. 

“The FDA has continued to take regulatory actions aimed at further unlocking biosimilar competition recently,” said Xiaoyu Liu, PhD, first author of this study. Our study findings offered further evidence to support patients, providers and insurers in their consideration of biosimilars.”

Source: UCLA Health

Categories : Cancer Obstetrics & GynaecologyTags :

How Can We Cut Gynaecologic Cancer–related Deaths in Low- and Middle-income Countries?

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Female reproductive system. Credit: Scientific Animations CC4.0 BY-SA

Review offers insights on evidence-based strategies.

Low- and middle-income countries (LMICs) bear a disproportionate burden of gynaecologic malignancies – cancers of the cervix, endometrium, ovary, vagina, and vulva. A review published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society, reveals that survival disparities for these cancers are driven by late-stage diagnosis, limited screening coverage, inadequate radiotherapy infrastructure, workforce shortages, and restricted access to essential and novel therapies.

By analysing studies published between 2015 and 2024, investigators observed that LMICs account for approximately 94% of global cervical cancer deaths, with the highest mortality observed in East Africa. Despite persistent survival disparities in LMICs, research has generated evidence that cost-effective and scalable interventions – including single-dose HPV vaccination, screen-and-treat strategies, HPV self-sampling, radiotherapy expansion, and workforce development with international training partnerships – can substantially improve outcomes when embedded within national cancer control policies and supported by sustainable financing mechanisms.

The authors stressed that policy-driven, system-level reforms should prioritise prevention, strengthen service delivery, and expand equitable access to care.

“The survival gap in gynaecologic cancers between low- and middle-income countries and wealthier nations is not inevitable – it is largely the result of delayed diagnosis and under-resourced health systems,” said corresponding author Dr Alfi Sophian, SSi, MSi, of the Indonesian Food and Drug Authority. “Our review shows that proven, cost-effective interventions already exist. What is needed now is stronger political commitment and sustainable financing to embed them into national cancer control policies.”

CANCER’s Editor-in-Chief, Suresh S. Ramalingam, MD, FASCO, who is the Executive Director of the Winship Cancer Institute of Emory University and the Roberto C. Goizueta Chair in Cancer Research at the Emory University School of Medicine, agreed that the review highlights key opportunities to reduce the burden of gynaecological malignancies in low- and middle-income countries. “Gynaecological malignancies claim the lives of far too many women globally; implementation of evidence-based tools consistently and uniformly across the world will save numerous lives,” he said.

Source: Wiley

Categories : CancerTags :

Electric Fields Offer New Hope Against Aggressive Brain Cancer

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Technique developed for treating Parkinson’s disease also disrupts growth of glioblastoma

Postdoctoral researcher Erin Iredale, who has worked on intratumoral modulation therapy since her undergraduate degree, hopes the proposed electric fields treatment will one day be used for patients with brain cancer. (Christopher Kindratsky/Western Communications)

More than a decade ago, Dr Matthew Hebb was treating patients with Parkinson’s disease using deep brain stimulation by implanting tiny electrodes into the brain and delivering electrical signals to control tremors. He wondered if the same basic technology could be used against brain cancer.

Hebb, neurosurgery professor at Western University’s Schulich School of Medicine & Dentistry, took tumour samples removed during surgery back to his laboratory, implanted electrodes and stimulated the cancer cells. The tumours responded.

That unexpected observation set in motion years of research into what is now called Intratumoral Modulation Therapy, or IMT – an original approach that uses low-amplitude electric fields to disrupt the growth of glioblastoma, one of the most aggressive and difficult-to-treat brain cancers.

Now, a Western-led research team has taken another step toward potentially bringing the technology from the laboratory to patients.

The latest study, published in Neuro-Oncology Advances, shows that IMT can safely deliver stronger, dynamic electric fields directly to a glioblastoma tumour while significantly slowing brain tumour growth, in an animal model.

The research team, which included Hebb, physics and astronomy professor Eugene Wong, medical biophysics professor Terry Peters, anatomy and cell biology professor Susanne Schmid and postdoctoral researcher Erin Iredale, observed an eight-fold reduction in tumour growth measured through bioluminescence and a five-fold reduction in tumour volume measured by magnetic resonance imaging (MRI) after seven days of treatment.

For Iredale, the first author on the study and has worked on the IMT project since her undergraduate degree, the results represent another important step toward a treatment she hopes could one day help patients.

“It’s so interdisciplinary,” said Iredale. “We need everyone from different fields, with their own expertise, to come together to solve this huge problem in health care.”

Different kind of electrical treatment

Glioblastoma is a devastating cancer that begins in the cells or tissues of the brain. Even with current treatments, including surgery, radiation and chemotherapy, patients diagnosed with the disease have a median survival of just more than a year. One of the challenges is that glioblastoma cells divide rapidly despite aggressive conventional treatments, leading to recurrence mainly near the site of the surgery. IMT takes direct aim at that process.

Rather than using electricity to acutely burn or destroy the tumour, the treatment delivers chronic low-amplitude electric fields that interfere with the way cancer cells divide.

“When we put this electric field on those cells, it prevents them from dividing properly,” said Iredale. “So, they’re kind of stalled in their cell division process.”

The exact biological mechanisms are still being investigated, but the team has repeatedly observed reduced tumour growth when the electric fields are applied.

The idea grew from Hebb’s early experiments and then expanded as physicists and biomedical researchers joined the project. Deep brain stimulation normally operates at frequencies designed to produce a neurological response. For cancer treatment, however, the goal is different.

The researchers increased the frequency so the stimulation could target the tumour without producing unwanted effects in normal brain tissue. The result is a treatment designed to destroy the cancer while leaving the surrounding brain largely undisturbed.

Finding the sweet spot

Iredale joined the IMT project in 2016 as an undergraduate student when she was studying medical physics and applied mathematics. She was drawn to the possibility of combining physics and mathematics with the practical goal of helping patients – an interest that eventually led to a PhD in medical biophysics, where her research focused on developing a treatment-planning system for IMT.

Iredale’s work in the Hebb lab has helped address one of the central challenges of treating a tumour inside the brain: precisely controlling where the electric field goes and how strong it is.

The latest study, done in rats, marks the first time the team used multiple electrodes in a living brain to create a dynamic electric field. Three electrodes were implanted around the tumour. By shifting the phase of the electrical signals delivered by each electrode, the researchers created an electric field that rotates over time.

The approach helps cover the tumour more completely, reducing the possibility of ‘cold spots’ where cancer cells might escape treatment.

“We’re basically triangulating the tumour,” said Iredale.

“We’re using the electrodes to target very specific areas, making sure the electrical stimulation reaches the tumour while delivering the right amount of energy to each spot.”

– Western postdoctoral researcher Erin Iredale

The researchers used computational modelling to determine how the fields would be distributed through the brain and then confirmed those predictions with direct electrical measurements. Importantly, the treatment produced no neurological adverse effects or imaging evidence of brain injury.

From computer models to the clinic

The new treatment-planning system, devised by Iredale, is designed to eventually help physicians personalise IMT for individual patients. A physician could provide a patient’s MRI, and the system would calculate where electrodes should be implanted and what stimulation parameters should be used to provide the necessary tumour coverage.

The system currently relies on traditional computational methods, including an optimisation algorithm developed by Iredale. Artificial intelligence and machine learning could potentially be incorporated in the future.

The research has progressed from studies in cancer cells to animal models, and while further work will be required before the treatment can be tested in people, the team is already developing a prototype with the goal of moving toward a first-in-human clinical trial.

“In five to 10 years, I would hope to see IMT go through an initial clinical trial to test its efficacy against glioblastoma,” said Iredale. “From there, we could start to see it become part of the treatment options available to patients with brain cancer.”

Source: Western University