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Breast Cancer Growth: Study Reveals Surgery Delays Have Minimal Impact

New analysis indicates inaccuracies in initial scans are more often to blame for staging changes than tumor progression.

Fears that breast cancer may significantly advance while patients await surgery are largely unfounded, according to groundbreaking research. A novel analytical method developed at Fox Chase Cancer Center provides the most detailed look yet at how tumors grow and how pre-operative delays affect cancer staging.

Understanding Tumor Progression

The study, led by **Dr. Richard Bleicher**, Chief of Breast Surgery at Fox Chase Cancer Center, utilized pathologic tumor sizes—the actual dimensions after surgical removal—to understand growth rates. This method offers a more precise view than clinical assessments made via imaging before surgery.

“It is the first study ever to use pathologic tumor sizes to determine how fast tumors of different sizes and traits grow in the patient while they’re waiting for treatment.”

Dr. Richard Bleicher, MD, FACS, Study Lead Author and Chief, Division of Breast Surgery, Fox Chase Cancer Center

“Patients who are diagnosed with breast cancer are always worried about how fast breast cancer grows while they wait for their surgery and the likelihood that it will spread from that growth,” **Dr. Bleicher** explained. “This study finally gives patients and their physicians that information for tumors of different sizes and types to make the best decisions they can.”

Upstaging Linked to Scan Accuracy

The research found that the rates of upstaging—when cancer is found to be more advanced than initially diagnosed—are relatively small and consistent with previous findings. Even prolonged delays between diagnosis and surgery have been linked to only minor increases in mortality risk.

“Many patients fear that delays in care will allow their cancer to grow and spread beyond the point of cure,” **Dr. Bleicher** stated. “This study provides the most comprehensive evaluation of how treatment delays may affect the likelihood that a tumor will be upstaged or be at a more advanced stage at the time of surgery than initially estimated at diagnosis.”

The team’s innovative approach compared initial clinical tumor sizes with post-operative pathologic sizes to calculate growth and upstaging risks. This technique more accurately reflects associated risks by accounting for limitations in clinical staging.

Data from Over One Million Patients

Analyzing data from the National Cancer Database for over one million patients treated between 2010 and 2020, the study focused on individuals with non-metastatic, non-inflammatory breast cancer receiving surgery as their initial treatment.

“Interestingly, a significant proportion of the observed upstaging is not from tumor progression, but from the inaccuracy of clinical staging,” **Dr. Bleicher** noted. “In other words, when breast cancers are upstaged at surgery, it’s more likely because we didn’t appreciate the initial extent of disease than because the tumor had time to spread.”

The findings offer crucial data to help guide conversations with newly diagnosed patients, improving the understanding of treatment timelines. As diagnostic tools advance, the risk of upstaging is expected to decrease further.

A recent report from the American Cancer Society indicates that an estimated 287,590 new cases of invasive breast cancer will be diagnosed in women in the U.S. in 2024 (American Cancer Society, 2024). This study aims to alleviate patient anxiety by providing a clearer picture of the actual impact of waiting periods.

“We may not be able to stop time, but armed with this new knowledge, we can use it more wisely, empowering patients to ensure that they feel urgency and not fear,” **Dr. Bleicher** concluded.

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Here’s a rewritten version of the article, focusing on clarity and conciseness while retaining the key details:

New Gene Signature Could Predict aggressive Pancreatic Cancer

San Diego, CA – Researchers at the University of California San Diego School of Medicine have identified a crucial link between cellular stress, inflammation, and the progression of pancreatic ductal adenocarcinoma (PDAC), one of the deadliest forms of cancer. This revelation could lead to an early warning system for the disease, potentially allowing for detection before it becomes life-threatening.

Previous research indicated that inflammation and cellular stress activate a protein called STAT3 in pancreatic cells, contributing to tumor growth and treatment resistance. The new study sheds light on how STAT3 achieves this.

The UC San Diego team found that in the face of inflammatory signals and low oxygen levels (a common stressor), STAT3 activates specific genes essential for cell adaptation. Notably, they discovered that STAT3 turns on the gene integrin β3 (ITGB3) in both mouse and human pancreatic cells.

Key findings from the study include:

ITGB3’s Role: Increased expression of ITGB3 was found to promote the initial advancement and accelerate the progression of PDAC tumors.
Chemotherapy’s Impact: Inflammation and stress caused by chemotherapy also activated STAT3, leading to higher ITGB3 levels in PDAC cells.
Blocking the Pathway: Inhibiting the STAT3 pathway that controls ITGB3 expression slowed down tumor initiation.
The “STRESS” Signature: STAT3 activates a group of 10 genes, including ITGB3, which the researchers have named the “STRESS” gene signature. This signature proved to be a more accurate predictor of pancreatic cancer development and tumor aggressiveness compared to existing gene signatures.

These findings hold significant promise for precision medicine. The “STRESS” signature could be used to develop early screening tools for precancerous cells. Furthermore,it may help clinicians identify patients at higher risk of aggressive disease and predict their response to traditional treatments as the cancer progresses.

The researchers are now investigating molecules that can block the inflammation-driven activation of ITGB3. This approach could potentially be applied to other cancers that affect tissue surfaces,such as lung,breast,and skin cancers,to prevent tumor progression,spread,and drug resistance.

Source: University of California – San Diego
Journal Reference: Campos,A. D., et al. (2025). A STAT3/integrin axis accelerates pancreatic cancer initiation and progression. Cell Reports. doi.org/10.1016/j.celrep.2025.116010

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Air Pollution Linked to Brain Tumor Risk

Study of 4 Million Danes Reveals Association with Meningioma

Long-term exposure to common air pollutants may increase the likelihood of developing meningioma, a tumor originating from the membranes surrounding the brain and spinal cord. This finding emerges from a large-scale Danish study, adding to evidence of air pollution’s detrimental effects beyond cardiovascular and respiratory systems.

Pollutants and Tumor Development

The comprehensive cohort study, which tracked nearly 4 million adults since 1991, identified a consistent link between increased meningioma risk and exposure to ultrafine particles (UFPs), fine particulate matter, nitrogen dioxide, and elemental carbon. These associations were observed even after accounting for various individual and area-level factors.

Study Methodology

Researchers utilized nationwide Danish registries to gather data on participants’ addresses and relevant covariates. Air pollution levels at residential locations were assessed using a validated model, with contributions from local traffic and other sources quantified through a national emission inventory. The study’s primary focus was the incidence of primary central nervous system (CNS) tumors, including meningiomas, gliomas, cranial nerve tumors, and other CNS tumors, as reported in the Danish Cancer Registry.

Key Findings on Tumor Types

Over 16,000 CNS tumors were identified in the study group. Meningiomas constituted 28% of these cases. For meningioma, a 10-year mean exposure to UFPs, fine particulate matter, nitrogen dioxide, and elemental carbon each showed an associated increased risk. Sensitivity analyses indicated that traffic-related UFPs had a stronger association compared to non-traffic UFPs, while both traffic and non-traffic fine particulate matter demonstrated similar risk increases. Notably, no clear links were found between air pollutants and glioma risk, although nitrogen dioxide showed a negative association with cranial nerve tumors.

Expert Commentary

“Our study suggests that long-term exposure to air pollution from traffic and other sources may play a role in the development of meningioma and adds to the growing body of evidence that air pollution can affect the brain — not just the heart and lungs.”

Ulla A. Hvidtfeldt, PhD, Danish Cancer Institute

The findings highlight a significant public health concern, particularly given that ambient particulate matter pollution levels in many urban areas globally exceed World Health Organization guidelines. For instance, the average annual PM2.5 concentration in London was 10.3 µg/m³ in 2022, exceeding the WHO guideline of 5 µg/m³ (IQAir 2022).

Limitations and Future Research

The researchers acknowledged certain limitations, including a strong intercorrelation among pollutants and uncertainty in pollution estimates, which could affect the precise attribution of effects and personal exposure classification. Factors such as genetic predisposition, radiation exposure, and lifestyle variables were not fully accounted for, potentially leading to residual confounding. The study also noted potential biases from differential tumor detection and reliance on emission inventories of varying accuracy for distinguishing traffic from non-traffic pollution sources.

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