Tag: breast cancer

Categories : CancerTags :

Ischaemia Speeds Tumour Growth by Aging the Immune System

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Immune cells (red) accumulating within a tumour (blue) and multiplying (green). When blood flow is blocked either in the heart or legs, these immune cells change in a way that enables tumour growth. Credit: NYU Langone

Cutting off blood flow can prematurely age the bone marrow, weakening the immune system’s ability to fight cancer, according to a new study from NYU Langone Health.

Published online August 19 in JACC: CardioOncology, the study showed that peripheral ischaemia, restricted blood flow in the arteries in the legs, caused breast tumours in mice to grow at double the rate seen in mice without restricted flow. These findings build on a 2020 study from the same team that found ischemia during a heart attack to have the same effect.

Ischaemia occurs when fatty deposits, such as cholesterol, accumulate in artery walls, leading to inflammation and clotting that restrict the flow of oxygen-rich blood. When this happens in the legs, it causes peripheral artery disease, which can increase the risk of heart attack or stroke.

“Our study shows that impaired blood flow drives cancer growth regardless of where it happens in the body,” says corresponding author Kathryn J. Moore, PhD, tProfessor of Cardiology at NYU Grossman School of Medicine. “This link between peripheral artery disease and breast cancer growth underscores the critical importance of addressing metabolic and vascular risk factors as part of a comprehensive cancer treatment strategy.”

Importantly, the research team found that restricted blood flow triggers a shift toward immune cell populations that cannot efficiently fight infections and cancer, mirroring changes seen with aging.

Systemic Skewing

To examine the mechanisms behind the link between cardiovascular disease and cancer growth, the study authors developed a mouse model with breast tumours and induced temporary ischaemia in one hind limb. The team then compared cancer growth in mice with and without impaired blood flow.

Their findings build on the nature of the immune system, which evolved to attack invading bacteria and viruses, and under normal conditions detects and eliminates cancer cells. These protective functions rely on stem cell reserves in the bone marrow, which can be activated as needed to produce key white blood cell populations throughout life.

Normally, the immune system responds to injury or infection by ramping up inflammation to eliminate threats, then scaling back to avoid harm to healthy tissue. This balance is maintained by a mix of immune cells that either activate or suppress inflammation. The researchers found that reduced blood flow disrupts this equilibrium. It reprograms stem cells in the bone marrow to favour the production of “myeloid” immune cells (monocytes, macrophages, neutrophils) that dampen immune responses, while reducing output of lymphocytes like T cells that help to mount strong antitumour responses.

The local environment within tumours showed a similar shift, accumulating more immune-suppressive cells, including Ly6Chi monocytes, M2-like F4/80+ MHCIIlo macrophages, and regulatory T cells, that shield cancer from immune attack.

Further experiments showed that these immune changes were long-lasting. Ischaemia not only altered the expression of hundreds of genes, shifting immune cells into a more cancer-tolerant state, but also reorganised the structure of chromatin, the protein scaffolding that controls access to DNA. This made it harder for immune cells to activate genes involved in fighting cancer.

“Our results reveal a direct mechanism by which ischemia drives cancer growth, reprogramming stem cells in ways that resemble aging and promote immune tolerance,” says first author Alexandra Newman, PhD, a postdoctoral scholar in Dr Moore’s lab. “These findings open the door to new strategies in cancer prevention and treatment, like earlier cancer screening for patients with peripheral artery disease and using inflammation-modulating therapies, to counter these effects.”

Moving forward, the research team hopes to help design clinical studies that evaluate whether existing inflammation-targeted therapies can counter post-ischaemic changes driving tumour growth.

Source:

Categories : Cancer ExerciseTags :

Bouts of Exercise Could Help in the Fight Against Cancer

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Photo by John Arano on Unsplash

A single bout of either resistance or high intensity interval training could help in the cancer battle, new research from Edith Cowan University (ECU) has found.

ECU PhD student Mr Francesco Bettariga found that a single bout of exercise increased the levels of myokines, a protein produced by muscles which has anti-cancer effects, and which could reduce the proliferation of cancer growth by 20 to 30 per cent.

“Exercise has emerged as a therapeutic intervention in the management of cancer, and a large body of evidence exists that shows the safety and effectiveness of exercise as medicine, either during or post cancer treatment,” Mr Bettariga said, first author of the study which appears in Breast Cancer Research and Treatment.

His research with survivors of breast cancer measured myokine levels before, immediately after and 30 minutes post a single bout of either resistance of high intensity interval training and found that both sets of exercise had a resultant increase in myokine levels.

While higher levels of myokines were expected in a healthy population, post a vigorous workout, Mr Bettariga investigated whether breast cancer survivors would see the same results, given the impact that cancer treatments and cancer itself often has on the body.

“The results from the study show that both types of exercise really work to produce these anti-cancer myokines in breast cancer survivors. The results from this study are excellent motivators to add exercise as standard care in the treatment of cancer,” Mr Bettariga said.

He added that the long-term implications of elevated myokine levels should be further investigated, particularly in relation to cancer recurrence.

Further research by Mr Bettariga investigated how changes in body composition, following consistent exercise, could impact inflammation, which plays a key role in breast cancer recurrence and mortality by promoting tumour progression.

Persistent inflammation not only promotes tumour progression by influencing cell proliferation, survival, invasiveness, and metastasis, but also inhibits immune function. Given that the cancer itself and the side-effects of treatments can elevate levels of inflammatory biomarkers, survivors of breast cancer are at increased risk of cancer progression, recurrence and mortality.

“Strategies are needed to reduce inflammation which may provide a less supportive environment for cancer progression, leading to a lower risk of recurrence and mortality in survivors of breast cancer,” Mr Bettariga said.

The new research found that by reducing fat mass and increasing lean mass, through consistent and persistent exercise, cancer survivors had a better chance at reducing inflammation.

“If we are able to improve body composition, we have a better chance of decreasing inflammation because we are improving lean mass and reducing fat mass, which is responsible for releasing anti and pro-inflammatory markers,” Mr Bettariga said.

Unfortunately, quick fixes to reduce fat mass would not have the same beneficial effects, Mt Bettariga stressed.

“You never want to reduce your weight without exercising, because you need to build or preserve muscle mass and produce these chemicals that you can’t do through just diet alone.”

Source: Edith Cowan University

Categories : CancerTags :

When Should Preventive Mastectomy be Offered in High Breast Cancer Risk?

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Photo by National Cancer Institute on Unsplash

More women at higher risk of breast cancer should be offered a mastectomy, according to researchers at Queen Mary and London School of Hygiene and Tropical Medicine.

A new analysis, published in JAMA Oncology, has found that the surgical technique was a cost-effective way of reducing the likelihood of developing breast cancer compared to breast screening and medication. Current guidelines on who is offered mastectomy may need to be revised to reflect these new findings. 

Clinicians currently use personalised risk prediction models which combine genetic and other data to identify those women who are at a higher risk of developing breast cancer (BC). Subsequent treatment options – including mammograms, MRI screening, surgery, and medication – are then offered dependent on each woman’s level of risk. 

Risk reducing mastectomy (RRM) is recommended for women at high risk, but in practice this surgery is only clinically offered to those carrying faults (called pathogenic variants) in genes that are known to increase the likelihood they will develop the disease (BRCA1/ BRCA2/ PALB2 PV). 

Professor Ranjit Manchanda from Queen Mary University of London, Dr Rosa Legood from London School of Hygiene and Tropical Medicine, along with colleagues from Manchester University and Peking University created a new economic evaluation model to accurately predict the level of risk that would make RRM a more cost-effective treatment. 

For their model, researchers used guidelines from the National Institute for Health and Care Excellence (NICE) to determine whether a treatment is considered cost-effective. Their model showed that mastectomy was a cost-effective treatment for women aged 30 or above who have a lifetime breast cancer risk greater than or equal to 35%. Offering RRM to women in this cohort could potentially prevent 6,500 of the 58,500 cases of breast cancer that are diagnosed every year in the UK. 

Professor Manchanda, Professor of Gynaecological Oncology at Queen Mary and  Consultant Gynaecological Oncologist, said: “We for the first time define the risk at which we should offer RRM. Our results could have significant clinical implications to expand access to mastectomy beyond those patients with known genetic susceptibility in high penetrance genes- BRCA1/ BRCA2/ PALB2 – who are traditionally offered this. This could potentially prevent can potentially prevent ~6500 breast cancer cases annually in UK women. We recommend that more research is carried out to evaluate the acceptability, uptake, and long-term outcomes of RRM among this group”.. 

Dr Legood, Associate Professor in health economics at the London School of Hygiene & Tropical Medicine, said: “Undergoing RRM is cost-effective for women 30-55 years with a lifetime breast cancer risk of 35% or more. These results can support additional management options for personalized breast cancer risk prediction enabling more women at increased risk to access prevention.”  

Dr Vineeth Rajkumar, Head of Research at Rosetrees, said: “Rosetrees is delighted to fund this truly groundbreaking research that could have a positive impact on women worldwide.” 

The researchers used data from women aged between 30 and 60 with varying lifetime breast cancer risks between 17% and 50%, and who were either undergoing RRM or receiving screening with medical prevention according to currently used predictive models. 

NICE deems a treatment cost-effective if it typically brings one additional year of health for no more than £20 000–£30 000 per patient (known as the ‘willingness to pay’ threshold, or WTP). The researchers’ model used a threshold of £30 000/Quality Adjusted Life Year. 

Source: Queen Mary University London

Categories : CancerTags :

Less Is More: Low-Dose Olanzapine Curbs Chemo-Induced Nausea Without the Sedation

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A recent clinical trial demonstrates 5mg olanzapine’s safety and efficacy for chemotherapy-induced nausea and vomiting

Researchers from Japan found that a 5mg dose of olanzapine, taken after chemotherapy, significantly reduces nausea and vomiting in breast cancer patients, while minimising sedation and cutting costs. This patient-centred approach could reshape global standards for antiemetic care. Credit: Prof Mitsue Saito from Juntendo University, Japan

Chemotherapy-induced nausea and vomiting can severely impact patients’ quality of life and treatment adherence. In a major clinical trial, researchers from Japan tested whether a low, 5mg dose of olanzapine taken at home after chemotherapy could reduce these side effects without causing heavy sedation. The study found that this approach significantly improved outcomes compared to placebo, offering a safer, more affordable strategy that could reshape supportive cancer care, especially in outpatient and resource-limited settings.

Chemotherapy-induced nausea and vomiting are among the most distressing side effects of anti-cancer treatment, particularly for those receiving highly emetogenic regimens such as anthracycline plus cyclophosphamide combinations. This major side effect compromises a patient’s quality of life and willingness to continue therapy. Therefore, there is a crucial need to devise an effective antiemetic management approach for optimizing cancer care and patient well-being.

Against this backdrop, a new study, led by Professor Mitsue Saito and Dr. Hirotoshi Iihara from Japan, was made available online on June 17, 2025, and published in Volume 26, Issue 7 of the journal The Lancet Oncology on July 1, 2025, examined whether a 5mg dose of olanzapine taken at home after chemotherapy could reduce nausea and vomiting in patients with breast cancer while minimising the sedative effects associated with the standard 10mg dose.

“While multiple studies have examined 10mg of olanzapine and confirmed its effectiveness for nausea control, at this dose it often causes sedation, raising safety concerns,” explains lead author Prof Saito. “Beyond the commonly observed sedation, olanzapine at the 10 mg dose can cause serious adverse effects, including sedative effects such as daytime sleepiness and loss of consciousness.”

“The study was inspired in part by three patients with breast cancer who attended an antiemetic guideline meeting at MASCC 2015 in Copenhagen. They spoke about the burdensome sedative side effects of olanzapine, a concern that helped shape the trial’s patient-centred design,” says Prof Saito.

This phase 3, double-blind, placebo-controlled trial enrolled 500 female patients with breast cancer in Japan receiving outpatient anthracycline plus cyclophosphamide-based chemotherapy. Participants were randomly assigned to receive either olanzapine 5mg or placebo in combination with standard triplet antiemetic therapy (palonosetron, dexamethasone, and an NK-1 receptor antagonist). The olanzapine 5mg was taken at home after chemotherapy to help avoid sedation during hospital travel or treatment.

“This study uniquely investigates the timing of olanzapine 5mg administration, given within 5 hours post-chemotherapy administration and before the evening meal, to reduce sedation during hospital visits and transportation. This approach takes into account the onset of nausea and vomiting reported in previous studies. Among highly emetogenic chemotherapies, there is a significant difference between cisplatin, which usually requires hospitalisation for treatment, and other chemotherapies such as anthracycline-based regimens that are typically administered on an outpatient basis,” says Dr Iihara. The primary endpoint of the study was to investigate the proportion of patients achieving complete response, defined as no vomiting and no rescue medication use during the overall phase (0–120 hours post-anthracycline plus cyclophosphamide initiation).

The results demonstrated significant improvement, with 58.1% of patients in the olanzapine 5mg group achieving a complete response during the first 5 days after chemotherapy, compared to only 35.5% in the placebo group. Benefits also extended to delayed nausea and vomiting across a 7-day observation period.

While some patients reported drowsiness, the incidence of severe or very severe concentration impairment was low, occurring in 10% of patients in the olanzapine 5mg group vs 14% in the placebo group. Additionally, no major adverse events were observed in either group, indicating that there were no treatment-related deaths in either group.

The olanzapine 5mg dose offers an important financial and clinical advantage over the commonly used 10mg. By reducing side effects and cost, this strategy may make antiemetic treatment more accessible, particularly in lower-resource settings.

These new findings suggest that an olanzapine 5mg regimen, especially when administered after chemotherapy, can be just as effective, with fewer side effects. Although the study focused on Japanese women with breast cancer, the results are expected to influence international practices and future guideline updates.

In addressing both physical and financial toxicity and putting patients’ voices at the centre of the research, this trial represents more than a treatment tweak. It’s a step toward more humane, equitable cancer care.

Source: Juntendo University

Categories : Cancer GeneticsTags :

Women of African Ancestry May Be Biologically Predisposed to Early-onset or Aggressive Breast Cancers

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Photo by National Cancer Institute

While the incidence of breast cancer is highest for white women, Black women are more likely to have early-onset or more aggressive subtypes of breast cancer, such as triple-negative breast cancer. Among women under 50, the disparity is even greater: young Black women have double the mortality rate of young white women.

Now, research from the University of Notre Dame is shedding light on biological factors that may play a role in this disparity. The study published in iScience found that a population of cells in breast tissues, dubbed PZP cells, send cues that prompt behavioural changes that could promote breast cancer growth.

Funded by the National Cancer Institute at the National Institutes of Health, the study set out to explore what biological differences in breast tissue could be related to early onset or aggressive breast cancers. Most breast cancers are carcinomas, or a type of cancer that develops from epithelial cells. In healthy tissue, epithelial cells form linings in the body and typically have strong adhesive properties and do not move.

The researchers focused on PZP cells as previous studies had shown that these cells are naturally and significantly higher in healthy breast tissues of women of African ancestry than in healthy breast tissues of women of European ancestry. While PZP cell levels are known to be elevated in breast cancer patients in general, their higher numbers in healthy, African ancestry tissues could hold clues to why early-onset or aggressive breast cancers are more likely to occur in Black women.

“The disparity in breast cancer mortality rates, particularly among women of African descent, is multifaceted. While socioeconomic factors and delayed diagnosis may be contributing factors, substantial emerging evidence suggests that biological and genetic differences between racial groups can also play a role,” said Crislyn D’Souza-Schorey, the Morris Pollard Professor of Biological Sciences at Notre Dame and corresponding author of the study.

The study showed how PZP cells produce factors that activate epithelial cells to become invasive, where they detach from their primary site and invade the surrounding tissue.

For example, a particular biological signaling protein known as AKT is often overactive in breast cancers. This study showed that PZP cells can activate the AKT protein in breast epithelial cells, which in part allows them to invade the surrounding environment. PZP cells also secrete and deposit certain proteins outside the cell that guide the movement of breast epithelial cells as they invade.

Overall, the results of the study emphasize multiple mechanisms by which PZP cells may influence the early stages of breast cancer progression and their potential contribution to disease burden.

The researchers also looked at how a targeted breast cancer drug, capivasertib, which inhibits the AKT protein, impacted PZP cells and found it markedly reduced the effects of the PZP cells on breast epithelial cells.

“It’s important to understand the biological and genetic differences within normal tissue as well as tumours among racial groups, as these variations could potentially influence treatment options and survival rates. And consequently, in planning biomarker studies, cancer screenings or clinical trials, inclusivity is important,” said D’Souza-Schorey, also an affiliate of Notre Dame’s Berthiaume Institute for Precision Health and Harper Cancer Research Institute.

Source: University of Notre Dame

Categories : Cancer Obstetrics & GynaecologyTags :

Breastfeeding’s Protective Effect Against Breast Cancer Explained by Metabolism

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Study shows a mother’s mitochondria determine if lactation is protective or not against breast cancer—and points to a possible intervention to increase the benefit to more women

Photo by Wendy Wei

Breastfeeding is often linked with better health for both mothers and babies, but it does not protect all women against breast cancer. The reason remains unknown. Since breast cancer in young women is on the rise, understanding why breastfeeding is protective in some women but not others is critical. 

A new study, led by a team of researchers from The Tisch Cancer Institute at the Icahn School of Medicine at Mount Sinai and published in the journal Nature Communications, addressed this question. 

The study was performed in mice, which exhibit a similar phenomenon: lactation strongly protects some mice against breast cancer, but others are more susceptible. The researchers studied female mice that had the same basic DNA but different types of mitochondria. The team found that the way the body responds to breastfeeding could change depending on the mother’s mitochondria.  

In mice with specific types of mitochondria, the researchers found, lactation allowed a certain group of cells similar to those found in postpartum breast cancer in humans to expand and grow, explains Edmund Jenkins, PhD, Assistant Professor of Medicine (Hematology and Medical Oncology) at the Icahn School of Medicine at Mount Sinai. Dr Jenkins served as the bioinformatics expert on the study. 

“We’ve always thought that breastfeeding is good for all women when it comes to lowering breast cancer risk,” said senior author Doris Germain, PhD, Professor of Medicine (Hematology and Medical Oncology) at the Icahn School of Medicine at Mount Sinai. “But our study shows that it really depends on a woman’s metabolism and how her body responds to lactation at the cellular level.” 

The researchers also discovered that they could change the way the body reacts during breastfeeding by using a natural dietary supplement. In the mice that were at higher risk of developing postpartum breast cancer, this treatment switched their response from harmful to protective. This finding opens the door to a possible way to help more women benefit from breastfeeding by supporting their bodies in the right way.  

“Our research raises the possibility that one day, doctors might be able to identify women whose breastfeeding response puts them at risk and then offer them a simple, natural dietary intervention to change that,” said first author Mrittika Chattopadhyay, PhD, Assistant Professor of Medicine (Hematology and Medical Oncology) at the Icahn School of Medicine at Mount Sinai. 

The team is now studying human breast milk with the goal of identifying milk metabolites that can show whether a woman’s body is reacting to breastfeeding in a way that is helpful or harmful. They also plan to develop a study in humans. One question then will be whether, because this dietary supplement may impact the development of the child, it should be tested only in mothers after they have stopped giving milk to their newborns.  

Source: Mount Sinai

Categories : CancerTags :

FDA-Approved Drug Halts EBV-Driven Lymphoma by Disrupting a Key Cancer Pathway

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Swollen lymph nodes. Credit: Scientific Animations CC0

Scientists at The Wistar Institute have discovered that a class of FDA-approved cancer drugs known as PARP1 inhibitors can effectively combat Epstein-Barr virus (EBV)-driven lymphomas. The findings, published in the Journal of Medical Virology, demonstrate that these drugs, which work by blocking the activity of the PARP1 enzyme, can halt tumour growth by interfering with the EBV’s ability to activate key cancer-promoting genes.

“We’ve uncovered a completely different mechanism for how PARP inhibitors work in EBV-positive cancers,” said Italo Tempera, PhD, associate professor at Wistar’s Ellen and Ronald Caplan Cancer Center and senior author of the study. “Instead of preventing DNA damage from repairing itself in the tumours, like these drugs do in other cancers, they essentially cut off the virus’s ability to hijack cellular machinery to drive cancer growth. This opens up exciting possibilities for repurposing existing FDA-approved drugs to treat EBV-associated cancers.”

EBV infects over 90% of the global population. While most people with the virus remain symptom-free, immunocompromised individuals such as people with HIV and transplant recipients have an increased risk of EBV causing several types of cancer, including various lymphomas and carcinomas. Despite the virus’s clear role in driving these malignancies, no specific therapies currently target EBV-driven cancer.

In search of such a therapy, Tempera and his research team focused on PARP1, a cellular protein that is known primarily for its role in DNA repair. In cancer treatment, PARP inhibitors typically work by preventing cancer cells from repairing their DNA, causing them to die. However, Tempera’s team had previously discovered that PARP1 plays a very different role in EBV infection: It helps control which genes are accessible and active, essentially acting as a master regulator of gene expression.

“Think of PARP1 as a key that opens up DNA to make certain genes readable,” explained Tempera. “EBV uses this key to unlock cancer-promoting genes. When we block PARP1, we’re essentially taking away the key so the virus can’t get in and use our DNA for its own purposes.”

Using a mouse model of EBV-driven lymphoma, the researchers treated the animals with BMN 673 (talazoparib/talzenna), a PARP inhibitor that has already been approved for breast cancer treatment. Compared to controls, the treated mice showed an 80% reduction in tumour growth, and the cancer’s ability to spread to other organs was significantly reduced. Further, when the team analysed the tumours, they found no increase in DNA damage in the treated animals – the hallmark of how PARP inhibitors typically work. Instead, they discovered that PARP1 inhibition disrupted a critical partnership between the viral protein EBNA2 and the cellular oncogene MYC.

“EBNA2 is like the conductor of an orchestra, directing cellular genes to play a cancer symphony,” said Tempera. “It specifically turns on MYC, which is one of the most important cancer-promoting genes. When we inhibit PARP1, EBNA2 can’t effectively activate MYC anymore, and the whole cancer program falls apart.”

The findings have significant therapeutic implications. Because PARP inhibitors are already FDA-approved and their safety profiles are well established, the path to clinical application could be accelerated compared to developing entirely new drugs.

The research also suggests this approach might work beyond EBV-associated lymphomas. The team is now investigating whether PARP inhibitors could be effective against other EBV-driven cancers, including nasopharyngeal and gastric carcinomas. Additionally, given EBV’s suspected role in autoimmune diseases, the researchers are exploring whether PARP1’s regulation of viral gene expression might contribute to these conditions.

“This work really showcases the power of understanding fundamental viral biology,” said Tempera. “We’re taking insights from basic virology research and translating them into potential therapies. With further development, this approach could provide new hope for patients with EBV-associated cancers who currently have limited treatment options.”

Source: Wistar Institute

Categories : CancerTags :

Celebrate Christmas in July with PinkDrive

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Cold Nights, Warm Hearts, Festive Vibes – and Support for Early Detection

Think log fires, festive cheer, a three-course dinner and dancing to a live band – all wrapped up in the joy of giving. On Saturday, 5th July 2025, PinkDrive will host a Christmas in July dinner at the Indaba Hotel in Johannesburg, a night of holiday cheer and hope in action: raising funds for a life-changing cause. And you’re invited.

PinkDrive is a non-profit (NPC) committed to prolonging lives through the early detection of gender-related cancers. It delivers essential health services to thousands of South Africans every year by bringing mobile mammography units directly to communities that need them most, from rural villages to peri-urban areas across the nine provinces. These trucks provide clinical breast exams, mammograms, pap smears, and PSA testing, helping to detect cancer early in areas where healthcare access is often limited or unavailable.

Like many non-profits, PinkDrive depends on the support of corporate partners, sponsors, government, and the public to sustain its vital work, among them, Lee-Chem Laboratories. “This is a cause that is close to our hearts,” says Bhavna Sanker, Marketing Manager at Lee-Chem Laboratories. “Each year, we proudly support PinkDrive through our Mandy’s brand sponsorship, focusing on spreading awareness, sharing survivor stories, and making sure people understand their healthcare options.”

As part of their continued support, every guest at the Christmas in July function will receive a goodie bag from Lee-Chem, filled with products from their Mandy’s brand. “We are truly honoured to have Lee-Chem and the Mandy’s brand as valued sponsors of our Christmas in July Dinner fundraiser,” comments Nelius du Preez, Operations Manager at PinkDrive NPC. “Their continued support, alongside our other generous sponsors, makes events like this possible and helps us not only raise vital funds but also amplify the message of early detection and health education across South Africa.”

The fundraiser will spotlight the resilience of breast cancer survivors, with Deputy Minister of Electricity and Energy, Samantha Graham-Maré, sharing her personal journey with cancer. PinkDrive CEO and Founder, Noelene Kotschan, a passionate advocate for early detection prolonging  lives, will also address guests, and your charming host for the evening? A dashing Mister Global SA finalist will take the mic as MC, steering the evening from heartfelt reflections to lively fundraising with raffles and auctions featuring holiday packages, original artworks, and other exclusive prizes.

“We call the event ‘a night of giving back’ because it is occasions like these that allow us to keep our mobile health units on the road, reaching men and women who might otherwise not have access to screening services,” says du Preez. “Together with compassionate partners like Lee-Chem, we are driving change and prolonging lives, one screening at a time. And we are grateful to every corporate and individual who supports the event by purchasing tickets,” he adds.

All proceeds from the evening will be ringfenced to build and operate a new mobile mammography unit, expanding PinkDrive’s reach to screen more South Africans and detect cancer early, when treatment is most effective. “We encourage the public to join us in this mission by purchasing tickets and supporting the evening’s fundraising efforts,” concludes Sanker.

Tickets for the Christmas in July dinner are R600 per person and available now at pinkdrive.org. Don’t miss this chance to dress up, give back, and help bring hope where it’s needed most.

Categories : Cancer Neurodegenerative DiseasesTags :

Breast Cancer Treatment Linked to a Reduction in Alzheimer’s Disease Risk

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Photo by National Cancer Institute on Unsplash

A Korean population-based cohort study investigated the risk of Alzheimer’s disease (AD) among breast cancer survivors compared to age-matched controls without cancer. The study, published in JAMA Network Open, found that breast cancer survivors had an 8% lower risk of AD than controls, with a significant association in survivors over 65 years old – though the effect did not persist past five years. Radiotherapy was associated with a lower risk of AD among breast cancer survivors – but not other treatments.

Breast cancer survivors may experience long-term health consequences, including cognitive function and risk of dementia. The risk of AD among breast cancer survivors is still unclear and may vary depending on age at diagnosis, treatment received, and time since treatment.

Previous studies reported mixed results on the risk of AD among breast cancer survivors, with some finding no increase in risk and others finding a 35% increased risk for those diagnosed at age 65 or older. These studies have been hampered by a number of methodological issues, including not accounting for risk factors.

Cytotoxic chemotherapy can cause cognitive decline termed ‘chemobrain’. Other chemotherapy drugs such as anthracycline may reduced AD risk by reducing the formation of amyloid deposits. Endocrine therapy may increase the risk of dementia by lowering oestrogen, but studies suggest that the use of tamoxifen and aromatase inhibitors is associated with a lower risk of AD. An increase in dementia is seen in radiotherapy for head and neck cancers.

To investigate the risk of AD among breast cancer survivors, researchers used the Korean National Health Insurance Service (K-NHIS) database, exploring whether there is an association with cancer treatment and various confounding factors.

Among 70 701 breast cancer survivors (mean age, 53.1 years), 1229 cases of AD were detected, with an incidence rate of 2.45 per 1000 person-years. Survivors exhibited a slightly lower risk of AD compared with cancer-free controls, especially among individuals 65 years or older (SHR, 0.92; 95% CI, 0.85-0.99). But landmark analyses found that this lower risk did not persist beyond five years of survival. Radiotherapy was associated with reduced risk of AD among survivors, while chemotherapy and endocrine therapy had no significant impact. Anthracycline use, however, did show a non-significant decrease in risk.

Differences in doses and timing of radiotherapy may influence the effects. The incident exposure to the brain is estimated to be 0.2Gy from a breast cancer radiotherapy dose of 50Gy. A pilot study found that patients with AD who received low-dose whole-brain radiotherapy at 3Gy showed a temporary improvement in cognitive function. This improvement is believed to be due to a neuroprotective effect on microglia. Other studies have noted a transient risk reduction for AD in breast cancer radiotherapy; however, patients receiving radiotherapy usually do so in conjunction with breast-conserving surgery – those opting for this procedure are younger, with fewer comorbidities and smaller tumours.

The study suggests that cancer treatment may have benefits against AD development, but the risk of AD may differ depending on the duration of survival.

The findings indicate that breast cancer treatment may not directly lead to AD, and that managing modifiable risk factors for AD, such as smoking and diabetes, is a feasible option to lower AD risk among breast cancer survivors.

Categories : CancerTags :

South African Study Identifies Two New Breast Cancer Genes in Black Women

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Genetic factors contribute to some 30% of breast cancer cases in SA, necessitating investment in genomic research in African contexts.

Photo by National Cancer Institute

A seminal genetic study published in Nature Communications has discovered two genetic variants linked to breast cancer in black South African women, deepening knowledge about the genetic basis for this disease in African populations.

The genome-wide association study (GWAS) of breast cancer is the first to have been done in African women living on the continent.

A GWAS is a powerful research method that scans the entire DNA of many people to find genetic differences associated with a specific disease or trait.

In this case, the scientists at the Sydney Brenner Institute for Molecular Bioscience (SBIMB) scanned for breast cancer and found consistent genetic patterns in black South African women.

The SBIMB researchers discovered genetic signals around the gene RAB27A, a member of the RAS oncogene family, and USP22, a gene which is highly active in breast cancer cells and associated with a poor health prognosis.

“These genes have not been associated with the disease before, which is an important advance in understanding breast cancer risk and biology in women of African ancestry,” says Dr Mahtaab Hayat, the lead author of the study.

The two new genetic variants were identified in black South African women with breast cancer enrolled in the Johannesburg Cancer Study, compared to women without cancer in the Africa Wits-INDEPTH Partnership for Genomic Research (AWI-Gen) study.

Until now, most breast cancer genetics research has focused on European and Asian populations, with studies of African ancestry limited primarily to African- American women, who largely descend from West African populations.

A tool that estimates lifetime cancer risk based on DNA, the polygenic risk score (PRS), performed poorly in distinguishing South African women with breast cancer from those without.

“This is because most PRSs were developed in European populations, and their inaccuracy in African populations highlights the urgent need for ancestry-specific tools in cancer risk prediction,” says Dr Jean-Tristan Brandenburg, also in the SBIMB and a lead author.

Breast cancer is the second most common cancer in South Africa and the most common cancer in women globally, with genetic factors contributing to about 30% of cases. “Our study makes a compelling case for investing in genomic research rooted in African contexts,” notes Hayat.

The potential for precision medicine

If further studies confirm these findings, the USP22 and RAB27A genes could be specific targets for new drugs. “We could potentially target harmful cancer cells while sparing healthy tissue, which is ideally what we want when administering cancer treatment,” says Distinguished Professor at the SBIMB, Chris Mathew, and a lead project investigator.

Furthermore, if a specific gene is associated with poorer survival, it can be used as a biomarker to identify more aggressive cancers and help predict which patients may need more intensive treatment and monitoring.

Understanding the genetic architecture of complex diseases helps scientists figure out the biological processes leading to these conditions and find drug targets and treatments for groups of individuals with similar disease risk profiles.

Genomic diversity in Africa is unparalleled

African populations have more genetic variation than any other population in the world, but they have been significantly underrepresented in genomic research. This means that the global understanding of disease risk, and the tools and treatment developed from it, is limited.

“The study reveals that more people can benefit from genetic discoveries. It proves that new risk factors are still out there, waiting to be found,” says Hayat.

Source: University of the Witwatersrand