A fast-growing form of breast cancer that is often harder to spot on mammograms now accounts for more than one in ten breast cancer cases in the United States, according to a recent American Cancer Society (ACS) report. Invasive lobular carcinoma, the second most common type of breast cancer, is rising at a rate of about 3% annually, more than triple the growth rate of other breast cancer types, the study published Tuesday morning revealed. With these cases increasing across the U.S., it is worth examining what this cancer is and why its prevalence is climbing.

Rare, Dangerous Type Of Breast Cancer On The Rise In The U.S.

Rates of lobular breast cancer are climbing three times faster than other breast cancers, at 2.8% per year compared with 0.8% per year, according to researchers in the October 7 report published in Cancer.

“Although lobular breast cancer represents just over 10% of all breast cancer cases, the number of new diagnoses each year makes it essential to understand,” said Angela Giaquinto, lead researcher and associate scientist for cancer surveillance research at the American Cancer Society (ACS).

“Furthermore, survival rates beyond seven years are notably lower for lobular breast cancer than the most common type, which emphasizes the urgent need for prevention measures and early detection strategies specifically targeting this subtype,” Giaquinto added in a press release.

What Is Invasive Lobular Carcinoma?

Invasive lobular carcinoma (ILC) is the second most prevalent type of invasive breast cancer. It develops in the milk-producing lobes of the breast and represents roughly 5–15% of all invasive breast cancers. Unlike other breast cancers, ILC grows in single-file lines of cells rather than forming a distinct lump, making it more difficult to detect on mammograms. Symptoms can include thickening or swelling in the breast, changes in breast shape or the nipple, and pain. Surgery is typically part of treatment, while hormone therapy is often central, as ILC is frequently ER-positive.

Invasive Lobular Carcinoma Symptoms

At its early stages, invasive lobular carcinoma may not produce any noticeable symptoms. As it grows, possible signs include:

• Changes in the skin texture or appearance over the breast, such as dimpling or thickening.
• New areas of fullness or swelling in the breast.
• Newly inverted nipples.
• Localized thickening in part of the breast.
• ILC is less likely than other types of breast cancer to form a firm or clearly defined lump.

How Can You Get Invasive Lobular Carcinoma?

The risk factors for invasive lobular carcinoma are similar to those for breast cancer in general. Factors that may increase the risk include:

• Family history of breast cancer: If a parent, sibling, or child had breast cancer, your risk is higher. The risk is particularly elevated if multiple family members were affected or if cancer appeared at a young age. Most people diagnosed with breast cancer, however, do not have a family history.
• Personal history of breast cancer: Having had cancer in one breast increases the risk of developing it in the other breast.
• Personal history of certain breast conditions: Conditions like lobular carcinoma in situ (LCIS) and atypical hyperplasia indicate a higher risk. A biopsy revealing these conditions also raises your risk.
• Early menstruation: Starting your period before age 12 increases the likelihood of developing breast cancer.
• Late menopause: Beginning menopause after 55 increases risk.
• Dense breast tissue: Breasts composed of more dense tissue than fatty tissue increase both risk and difficulty in detection on mammograms. Discuss additional imaging tests with your doctor if you have dense breasts.
• Alcohol consumption: Drinking alcohol elevates the risk.
• Late first pregnancy: Having your first child after age 30 may increase risk.
• Never having been pregnant: Pregnancy lowers the risk; not being pregnant raises it.
• Inherited DNA changes: Certain inherited gene changes, such as BRCA2 and CDH1, raise the likelihood of ILC. BRCA2 also increases ovarian cancer risk; CDH1 is linked to hereditary diffuse gastric cancer syndrome.
• Menopausal hormone therapy: Some hormone therapies combining estrogen and progesterone can increase risk. Stopping these therapies reduces it.
• Obesity: Being overweight raises the risk of breast cancer.
• Older age: ILC is more likely to occur at older ages compared with other breast cancers.
• Radiation exposure: Receiving radiation to the chest in childhood or young adulthood increases risk.

Consult a healthcare professional if you notice any changes in your breasts, including lumps, unusual skin texture, thickened areas, or nipple discharge. Discuss when to begin routine breast cancer screening and how frequently it should be done. Most doctors suggest starting regular screening in your 40s.

For years, people living with chronic fatigue syndrome (ME/CFS), also known as myalgic encephalomyelitis, have struggled to confirm whether they actually have the condition or to recognise its full range of symptoms. Diagnosis has largely depended on ruling out other illnesses such as thyroid problems, anaemia, or depression. As a result, patients have often faced years of uncertainty or received incorrect diagnoses. Now, in a promising scientific development, researchers have identified a blood test that may detect chronic fatigue syndrome with an accuracy rate of 96%.

What Is Chronic Fatigue Syndrome?

Chronic Fatigue Syndrome (CFS), also referred to as Myalgic Encephalomyelitis (ME/CFS), is a long-term, multifaceted illness that leaves sufferers drained of energy in ways that ordinary rest cannot fix. According to the National Institutes of Health, this fatigue deepens after even light physical or mental effort—a hallmark called post-exertional malaise. Many cases worsen because the illness remains unrecognised for years. Gaps in medical training, limited awareness, and confusion about how to identify and manage the disease have all contributed to poor outcomes for patients.

Chronic Fatigue Syndrome Symptoms

The U.S. Centers for Disease Control and Prevention (CDC) lists several key symptoms of ME/CFS. These include severe tiredness that does not ease with rest, exhaustion after any activity (post-exertional malaise), unrefreshing sleep, pain in muscles or joints, headaches, and problems with memory or concentration. Other frequently reported signs are a persistent sore throat, tender lymph nodes, and feeling faint or dizzy when standing.

Additional symptoms that can appear include:

• Flu-like sensations, fever, or chills
• Mood changes such as anxiety, irritability, or depression
• Digestive problems
• Sensitivity to food, smells, or chemicals
• Rapid or irregular heartbeat

Breakthrough Blood Test Can Now Detect Chronic Fatigue Syndrome

A group of researchers from the University of East Anglia (UEA) working with Oxford BioDynamics believe they have overcome one of the biggest hurdles in diagnosing ME/CFS. Their goal was to create a dependable blood-based test capable of identifying consistent biological differences between people with ME/CFS and those without it. To do this, they turned to EpiSwitch 3D Genomics, a technology that studies how DNA folds inside cells. The way DNA loops or folds affects which genes are active, even when the genetic sequence itself remains unchanged.

The study examined blood samples from 47 people with severe ME/CFS and 61 healthy participants. Researchers looked for distinct DNA “folding signatures” that appeared consistently in patients but not in healthy controls. Their findings showed that the test could identify ME/CFS with about 96% accuracy, though individual reports of this figure vary slightly.

If future research confirms these results, this could represent a turning point in how the illness is recognised and treated. A reliable biomarker could help patients receive earlier diagnoses and enable scientists to design better therapies. However, experts urge caution. Independent testing across larger and more diverse groups is crucial before it becomes part of clinical practice.

The discovery is an encouraging advance, but it is still early. For now, the EpiSwitch blood test stands as a hopeful sign, one that brings ME/CFS research closer to validation, but not yet to medical routine.

Nobel Peace Prize 2025: It was 1am at night, when Mary Brunkow's phone began to ring, assuming it to be a spam call, she put it on "do not disturb" and went back to sleep. Her husband too ignored the rings, only to be woken up along with their dog a few minutes later, when the Associated Press photographer showed up at their door. This is when Brunkow realized that she had won a Nobel Prize.

Brunkow along with two other scientists Fred Ramsdell and Shimon Sakaguchi had won the Nobel Prize "for their discoveries concerning peripheral immune tolerance".

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What Is " peripheral immune tolerance"?

It refers to the mechanisms by which the immune system prevents self-reactive immune cells, especially the T-cells from attacking healthy tissues once they are already in the body's circulation.

The three are award for their work that revealed the existence and function of these special class of T-cell, called the regulatory T-cells, which act as brakes on immune responses, preventing autoreactivity. They also discovered the gene FOXP3, whose proper function is essential to the development and operation of regulatory T-cells. Their discovery revealed that mutation in FOXP3 genes is what leads to serious autoimmune disorders.

How Did The Discovery Happen?

Long before FOXP3, Sakaguchi, who is a professor at Osaka University in Japan, resurrected and rigorously defined the concept of regulatory T cells, also called Tregs. In 1995, he published work that showed that a subset of T-cells marked by CD25 along with CD4 could suppress autoimmune responses in mice. Those cells would be later called as the regulatory T-cell. It was his discovery which became the "brake" the immune system needed.

Also Read: Why More U.S. Women Are Being Denied Breast Cancer Therapy

Why Does This Discovery Matter?

Before Sakaguchi's work, the existence of regulatory T-cells was speculative, even controversial. The idea was dismissed because the evidence was murky. His work also opened the possibility that one day we may enhance regulatory T-cell functions in autoimmune diseases or inhibit it in cancer settings.

What Did Brunkow and Ramsdell Do?

While Sakaguchi defined the Treg population, Brunkow and Ramsdell filled the gap by discovering FOXP3, the gene whose expression is necessary for Treg development.

They studied that in mice, a peculiar strain known as "scurfy" mice, spontaneously developed lethal autoimmunity, which was manifested by scaly, flaky skin, enlarged lymph nodes and spleens, and early death. They showed that the scurfy phenotype is caused by a mutation on the X chromosome in a previously unknown gene which they named FOXP3.

Their discovery also showed that in humans, a rare autoimmune syndrome called IPEX, which is characterized by immune dysregulation, polyedendocrinopathy, entropathy, X-linked inheritance is caused by mutations in the human equivalent, FOXP3. They thus, directly connected the mouse mutation and human disease that proved that FOXP3 is central to immune self-tolerance.

Without functional FOXP3, regulatory T-cells fail to form or function, and immune system launches damaging attacks on normal tissues.

What Comes Next?

Their discovery is important as it can be used to treat autoimmune diseases like Type 1 diabetes, systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, and many more.

The scope for cancer immunotherapy and tolerance during organ transplantation also broadens with the discovery. As with the FOXP3, it becomes possible to design therapies that block Treg suppression locally, enabling the immune system to better recognize and attack tumors. In terms of organ transplantation, with Tregs, it may become feasible to engineer Tregs that home to transplanted organs and locally suppress rejection.

The Nobel press release and news sources note that more than 200 clinical trials are already underway based on regulatory T cell / peripheral tolerance ideas.

A recent report from Santé publique France highlights a significant rise in suspected COVID-related visits to emergency departments across the country during the week of September 15–21, 2025 (week 37). Compared with the previous week (September 8–14, week 36), hospital visits linked to COVID increased by 43% among children under 15, with 156 additional visits, and by 29% among adults, with 224 more visits.

Cases among adults had already started climbing the week before. This surge comes as a new SARS-CoV-2 variant, nicknamed “Frankenstein,” becomes increasingly common in France. Here is everything you need to know about this variant, its symptoms, and how to protect yourself.

What Is the Frankenstein Variant?

According to the World Health Organization (WHO), this rise is associated with the emergence of a new variant called XFG. It is nicknamed “Frankenstein” because it is a recombinant, meaning it contains genetic material from two different COVID-19 subtypes, LF.7 and LP.8.1.2. The WHO has classified XFG as a variant under monitoring since June 25, 2025, and it is spreading in several countries worldwide. Current evidence suggests that the public health risk remains low, and approved COVID vaccines are expected to continue preventing severe disease and symptomatic infection. Countries in Southeast Asia have also reported increases in both new cases and hospitalisations in areas where XFG has been widely detected.

Although XFG appears to spread more easily than other variants, experts say it does not seem to cause more severe illness. “The vast majority of infections are mild and resolve within a few days with rest,” said Dr. Gérald Kierzek. Infectious disease specialist Anne-Claude Crémieux added that, so far, there are no signs the variant is more dangerous than previous strains.

Symptoms of the Frankenstein Variant

The symptoms of XFG are similar to those seen with previous COVID-19 variants and are generally mild, resembling a common cold. These may include:

• Sore throat
• Runny or congested nose
• Dry cough
• Fatigue and muscle aches
• Mild fever
• Loss of appetite

Why Is The Variant Called Frankenstein?

The nickname “Frankenstein” reflects the variant’s hybrid nature, as it combines genetic material from multiple COVID-19 subtypes.

Frankenstein Covid Variant: Preventing Infection and Managing Symptoms

There is no treatment specific to XFG, so care follows the same principles used for other COVID variants.

• Vaccination: Current COVID vaccines remain highly effective at preventing severe illness and hospitalisation, even if protection against infection may be slightly reduced.
• Symptom relief: Rest, hydration, fever reducers, and cough medicines can help manage mild symptoms.
• Protective measures: Wearing masks, maintaining hand hygiene, social distancing, and avoiding crowded places remain important.

Research on the Frankenstein variant is ongoing. Since the disease can affect individuals differently, taking personal precautions and consulting a doctor when symptoms appear remain essential.