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The September issue of ONCOLOGY features a rare case study on glioblastoma, discussions on end-of-life care, and insights into the field of pediatric oncology. 

September ONCOLOGY Publication

Dealing with Insurance Companies as an Oncologist: How Has the Process Changed?

As cancer care becomes more expensive, many patients rely on their health insurance to afford the already-high, and still rising, costs of treatment. CancerNetwork® spoke with Loretta Nastoupil, MD, about how the physician-insurance company interaction has shifted over the years that she has been an oncologist.

Initially, she noted that there are more barriers to pursuing an approval. Oncologists and their staff, particularly at community cancer centers, are forced to remain determined in getting approval from these companies. While most providers stick to the NCCN guidelines that enforce standards of care across various disease types, Nastoupil noted that even considering those standards, it may be more difficult to get the insurers to agree. Specifically, more modern therapies, like Bruton’s tyrosine kinase (BTK) inhibitors, can require more work to get the insurance companies to improve.

Nastoupil, a practicing oncologist at Southwest Oncology in Durango, Colorado, iterated that it’s crucial to remain patient and endure the wait times necessary to get proper approval for the treatments that can provide patients the best experience possible. These insurance companies and payers, as she said, are aware that they have the luxury of time, whereas oncologists and patients do not.

Have you noticed any differences when dealing with insurance companies over the years you’ve been practicing?

There appear to be more barriers instituted to see if you have the staff or the determination to stick with it, or if you’ll potentially quickly move on to something that’s potentially more financially feasible. Most oncologists will rely on NCCN guidelines to know what is essentially a standard-of-care option. Payers and insurers will also look at that as the standard of care. Most of your practicing oncologists in the community are going to fall within those guidelines, and they’re generally not asking for things that are not FDA-approved or outside the window of being a standard-of-care option.

Even with those guardrails, we see that with some of our more modern therapy, particularly in the form of oral targeted agents—BTK inhibitors, for instance—you’ll see that it often takes longer for insurers to even agree to it. That’s even before we learn what the patient’s copayment is or what their responsibility might be. If you don’t have the patience or the luxury of time with the patient in front of you, it’s sometimes easier to move on to that standard chemotherapy option that’s been around for many years because you know you’ll potentially get it approved faster. That’s where the practice of oncology has probably changed the most over the last 10 years.

You have to understand that we need to have patience on our side and we need to have patience with our staff who are negotiating on these payment plans, but you also need to manage the patient and their family’s expectations. That’s where people start to cave under the pressure in most situations, because it’s so much communication and a lot of managing what a realistic wait time is vs what’s unacceptable. But you’re also doing that when you’re busy seeing patients in front of you. That’s where payers and insurers know that they probably have an upper hand because they have the luxury of more time, they’re not patient-facing, and they don’t have to deal with the questions every day of why this is taking so long.

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Over the past 10 years, more barriers have become apparent in the process of getting insurance companies to approve cancer treatments, according to Loretta Nastoupil, MD.

“By examining patterns across countries and population groups, we can provide governments and individuals with more specific information to help prevent many cancer cases before they start,” according to study author André Ilbawi, MD.

Approximately 4 of 10 cancer cases in 2022 may have been averted by avoiding exposure to key preventable risk factors, according to findings from a global analysis study published in 

Of 18.7 million cancer cases recorded in 2022, approximately 7.1 million (37.8%) were linked to modifiable risk factors. Cancer cases due to modifiable risk factors were reported in 29.7% of women with cancer compared with 45.4% of men. The highest cancer burden for female populations was observed in sub-Saharan Africa, where 38.2% of cases were linked to modifiable risk factors; male populations experienced the highest burden in East Asia, where 57.2% of cases were associated with such risk factors.

Across the world, new cancer cases in women were typically linked to infections (11.5%), smoking (6.3%), and high body mass index (BMI; 3.4%). Among men, the most common risk factors associated with cancer cases included smoking (23.1%), infections (9.1%), and alcohol consumption (4.6%).

Data showed that 477,869 new lung cancer cases among women were preventable, as these diagnoses were related to smoking (60.5%), air pollution (27.5%), and occupational exposures (12.0%). Among men with lung cancer, 1,326,453 cases were preventable; these diagnoses were linked to smoking (69.4%), air pollution (15.8%), and occupational exposure (14.7%). In female populations, other cancer diagnoses that were attributable to preventable risk factors included breast cancer (n = 453,515), cervical cancer (n = 662,004), and stomach cancer (n = 272,763); for male populations, preventable cancer diagnoses included stomach cancer (n = 511,309), liver cancer (n = 461,985), and colorectal cancer (n = 371,331).

“This is the first global analysis to show how much cancer risk comes from causes we can prevent. By examining patterns across countries and population groups, we can provide governments and individuals with more specific information to help prevent many cancer cases before they start,” study author André Ilbawi, MD, who is from the Department of Communicable and Noncommunicable Diseases at the World Health Organization (WHO) and serves as WHO team lead for cancer control, stated in a press release regarding these findings.

Study authors sought to provide estimated incidences for cancer types that are associated with a wide range of modifiable risk factors. Risk factors of interest included tobacco smoking, consumption of alcohol, high BMI, insufficient physical activity, suboptimal breastfeeding, air pollution, ultraviolet radiation, infections, and occupational exposures. Investigators collected data on cancer incidences from 185 countries in 2022.

Regarding potential policy implications stemming from these findings, study authors noted that reducing exposure to modifiable risk factors may be an effective, sustainable strategy for preventing new cancer cases. New policies focusing on tobacco control measures and strengthened vaccination or screening programs, for example, may help address local disease patterns and prevalent risk factors. The authors also noted a need for gender-sensitive approaches, which may include increased human papillomavirus vaccination access.

“This landmark study is a comprehensive assessment of preventable cancer worldwide, incorporating, for the first time, infectious causes of cancer alongside behavioral, environmental, and occupational risks,” senior study author Isabelle Soerjomataram, MD, PhD, deputy head of the Cancer Surveillance Unit at the International Agency for Research on Cancer, said in the press release.

 “Addressing these preventable causes represents one of the most powerful opportunities to reduce the global cancer burden.”

According to the study authors, variable data quality across countries represented a key limitation to their investigation. The available data also facilitated assumptions of consistent relative risks and simplified modeling that treated exposures independently despite known clustering and interactions. The authors noted that these limitations may have introduced uncertainty and yielded underestimations of true preventable cancer burdens, especially in areas with limited surveillance.

Fink H, Langselius O, Vignat J, et al. Global and regional cancer burden attributable to modifiable risk factors to inform prevention. 

Published online February 3, 2026. doi:10.1038/s41591-026-04219-7

Four in ten cancer cases could be prevented globally. News release. World Health Organization. February 3, 2026. Accessed February 4, 2026. https://tinyurl.com/3cz7f8an

Articles

Global analysis data reveal that lung, stomach, and cervical cancers represent approximately half of preventable cancers.

Modifiable Risk Factors Suggest Potential for Improving Cancer Prevention

The developers noted that no serious adverse effects were likely attributable to study agents or devices.

Treatment with light-activated TLD-1433 (Ruvidar) displayed early efficacy among patients who have disease progression following standard-of-care therapy for BCG-unresponsive non–muscle-invasive bladder cancer (NMIBC) carcinoma in situ (CIS) and who are not candidates for radical cystectomy in a single-arm phase 2 trial (NCT03945162), according to a news release from the developer, Theralase.

Specifically, among 87 patients treated with TLD-1433 who were evaluable for efficacy, the complete response (CR) rate was 64.4% (n = 56; 95% CI, 48.6%-80.2%), with a total response rate of 73.6% (n = 64; 95% CI, 56.7%-90.5%). The total response rate includes those who experienced an indeterminate response (IR), defined as having negative cystoscopy results and positive or suspicious urine cytology results.

Moreover, among 47 evaluable responders, 40.4% (n = 19; 95% CI, 23.8%-57.1%) experienced a sustained CR at 450 days and 42.6% (n = 20; 95% CI, 26.6%-58.5%) experienced a sustained total response. Additional interim data revealed that the 2- and 3-year CR rates were both 21.3% and that 2.1% of patients sustained a CR after 7 years.

“Enrolling and treating 90 patients in our phase 2 registration clinical study represents a significant milestone for the company. With the targeted enrollment now completed, we can focus on compilation of the clinical data for Health Canada and FDA regulatory approval,” Roger DuMoulin-White, BSc, PEng, ProDir, president and CEO of Theralase, said in a separate news release on the trial.

 “2026 will be a pivotal year for the company as we complete our bladder cancer study, embark on a combinational clinical study for bladder cancer, and launch numerous phase 1/2 adaptive clinical studies for brain, lung, muscle-invasive bladder, pancreatic, and colorectal cancers.”

Patients enrolled in the trial received a single intravesical instillation of TLD-1433 at 0.70 mg/cm

 via bladder instillation and photodynamic therapy.

 After TLD-1433 was rinsed from the bladder, patients received subsequent photodynamic therapy with a separate TLC-3200 system.

The primary end point of the trial was CR rate. Secondary end points included 3-year CR and IR rates as well as duration of response. An exploratory end point was safety.

Regarding safety, the developers noted that no serious adverse effects were likely attributable to study agents or devices. Moreover, they noted that the results of the trial exceed the International Bladder Cancer Group’s recommended guidelines for CR rates of 50% and 30% at 6 and 12 months, respectively, among CIS populations.

The trial completed enrollment and successfully treated 90 patients with TLD-1433 on February 2, 2026. Moreover, the developers plan to compile clinical data for a 2026 presentation to the FDA and Health Canada for an expected regulatory approval decision in 2027.

Those eligible for enrollment in the phase 2 trial were 18 years or older with histologically confirmed NMIBC CIS with or without resected Ta/T1 papillary disease who were not candidates for or refused radical cystectomy. Additionally, patients must have had an ECOG performance status of 0 to 2 and the ability to retain study drugs for a minimum of 60 minutes to be enrolled in the trial.

Exclusion criteria included those who experienced past or current muscle invasion, had concurrent extravesical non–muscle-invasive transitional cell carcinoma of the urothelium, or had active gross hematuria. Additionally, those receiving treatment with a prohibited concomitant therapy, those with an additional malignancy requiring treatment for progression, or those who had contraindications to general or spinal anesthesia were ineligible to enroll in the study.

Theralase(R) provides update on bladder cancer clinical study. News release. Theralase. February 4, 2026. Accessed February 4, 2026. https://tinyurl.com/4dz8ca3m

Theralase(R) completes enrollment in bladder cancer clinical study. News release. Theralase. February 2, 2026. Accessed February 4, 2026. https://tinyurl.com/mr2ut6em

Intravesical photodynamic therapy ("PDT") in BCG-unresponsive/​intolerant non-muscle invasive bladder cancer ("NMIBC") patients. ClinicalTrials.gov. Updated November 24, 2025. Accessed February 4, 2026. https://tinyurl.com/4skudub6

Of 78 patients with NMIBC in the phase 2 clinical trial, 64.4% experienced a complete response with TLD-1433.

TLD-1433 Exhibits Early Efficacy in BCG-Unresponsive NMIBC CIS

The immune system is a “critical player” in the emergence, therapeutic responses, and outcomes associated with newly diagnosed multiple myeloma (NDMM), according to Manoj Bhasin, PhD, MS.

 about research that he and colleagues published in 

 describing a single-cell atlas that may effectively characterize the bone marrow immune microenvironment among patients with NDMM. By generating profiles of 1,397,272 single cells from the bone marrow of 337 patients with NDMM, investigators determined specific attributes that may correlate with tumor growth and factors that can help improve stratification for the prediction of survival.

In a breakdown of his team’s research, Bhasin highlighted different cytogenetic risk-based evaluations, signaling analyses, and other processes as part of a comprehensive investigation into the bone marrow immune microenvironment. Additionally, he outlined potential future initiatives aiming to translate these data into more comprehensive risk-stratification models and novel antimyeloma therapies.

Bhasin is a professor in the Department of Pediatrics and in the Department of Biomedical Informatics at Emory University School of Medicine. He is also director of genomics, proteomics, bioinformatics, and systems biology and director of the Single Cell Biology Program at Aflac Cancer and Blood Disorders Center, both at Children’s Healthcare of Atlanta.

CancerNetwork: What was the rationale for generating the bone marrow microenvironment Immune Atlas associated with NDMM?

If you look at the landscape of multiple myeloma, all the risk staging and stratification are mainly tumor genetic [centered]. We are mainly focused on the tumor part and some clinical features, whereas the extrinsic factors like the immune system are not taken into consideration when we are stratifying the patient into high risk or standard risk. The basis for this study was to figure out [whether] the immune system is playing a role in the emergence of multiple myeloma, the therapeutic response, as well as the outcome. This was one of the first comprehensive studies where we profiled more than 1.4 million cells from newly diagnosed [patients with] myeloma before they were given any therapy. This was a study to answer some of the important questions because it was built up on the Multiple Myeloma Research Foundation CoMMpass registry study [NCT01454297]. That is a study with 8 to 10 years of follow-up on the patients with very comprehensive tumor genetics along with the clinical information to understand if the immune system plays a role in multiple myeloma. This is the study we planned 5 years back.

What did findings show regarding the utility of this single-cell atlas? What did the cytogenetic risk-based analysis demonstrate?

What we learned from this study is that [the atlas] generated a comprehensive profile of the immune landscape of the bone marrow microenvironment in multiple myeloma. We profiled 106 different major cell types, subtypes, or states of immune cells and then correlated them with the outcomes of multiple myeloma at [a] broader level. What we learned is that the patients who have an accumulation of these dysfunctional effector T cells at baseline usually have poor outcomes. This is true for whether they have a standard risk or high risk based on tumor genetics. The immune system is a key player in driving the outcomes.

Broadly speaking, patients with multiple myeloma are put into 2 bins. One is high risk, and [another] is standard risk, based on the cytogenetics of their lesions. What we learned is that cytogenetics affects the immune system, but [not] all high-risk cytogenetic lesions have the same effect. Most of the high-risk cytogenetic lesions have depletion of interferon type I response. But what we observed is that one of the high-risk lesions, which carries deletion of 17p13, these specific lesions have enrichment of interferon type I response. That looks counterintuitive, but what we learned is that T cells, myeloid cells, and the tumor cells themselves produce humongous amounts of this interferon I, specifically in the lesions with 17p13 deletion. Then, if you look at the second major cytogenetic alteration-carrying myeloma lesions...these lesions have accumulation of these dysfunctional T cells, along with senescent and exhausted T cells, which are associated with the poor outcomes in these lesions. The cytogenetics of lesions seem to be [quite] different from each other. Not all the high-risk lesions have the same immune imprint.

What were the key findings from the signaling analyses? Are there any particular factors associated with potential tumor growth and survival?

The proinflammatory signaling and immune-expressive signaling in the bone marrow microenvironment, which are driven by interferon I or interferon gamma, activate T and NK [natural killer] cells. They also activate macrophages and monocytes. On one side, it is like putting an escalator on T and NK cells to make them antitumor. They also activate the macrophages to create an immunosuppressive environment. It’s like you’re putting a foot on both escalators as well as on the brake of a car. It is making the cells get exhausted, and that is associated with the poor outcomes.

There is a great thing going on where a proliferation-inducing ligand [APRIL] binds with a TACI receptor on the plasma cells. The monocytes and macrophages, which are enriched in high-risk patients and patients who show very rapid progression, produce more amounts of this APRIL receptor that binds with the TACI on the surface of plasma cells to make them survive and cause the therapeutic resistance. In the patients who have nonprogressive disease, they produce B-cell activating factor [BAFF] instead of APRIL. When they produce BAFF, they bind with the B cells and make them differentiate. It can also bind with TACI on plasma cells, but with very low affinity. It looked like the balance of this signaling of APRIL, TACI, and BAFF is shifted in the patients of high risk and the patients who are showing a rapid progression. That provides us [with] a therapeutic opportunity; we can try to intervene in this interaction and try to design new therapies for multiple myeloma that fix the immune microenvironment.

How might integrating immune cell signatures with known tumor cytogenetics help with the prediction of survival in NDMM?

The current prognostic system or staging system is clinical feature driven and tumor genetic centric. What we learned from this study is that tumor-extrinsic factors like the immune system, the accumulation of these dysfunctional late effector T cells, are associated with poor outcomes. Adding those components into the staging system will improve the stratification of the patients. Right now, based on the current staging system, we observe that some of the high-risk patients don’t have progression of their disease whereas some of the standard-risk patients show a rapid progression of the disease because the immune component is missing. Maybe adding that immune component will bring accuracy into our prognostication system.

In addition to looking at all the clinical parameters and all the tumor genetics parameters, maybe [we can] look into the immune compartment of bone marrow by doing some flow- or CyTOF [cytometry by time of flight]-based immune profiling so that we can know if the patients have this dysfunctional T cell at baseline, they have a chance of rapid progression of disease. Taking the next step, how can we have a simple assay that can capture the immune microenvironment of bone marrow? Then, based on how the immune system is looking for a patient, a clinician can decide what the optimal therapy is. It is like we are trying to bring a personalized tumor genetics–, clinical-, and immune system–driven model for improving the progression-free survival as well as overall survival in multiple myeloma.

What are the next steps for further researching the immune microenvironment and potential factors correlating with survival in NDMM?

This study, Immune Atlas, is mainly focused on gene expression profiling, where we looked at the profile of each of the cells from the bone marrow. From genes, we need to move on to the protein. As a next step in this direction, we are focusing on profiling the proteome profile of each of these cells in the bone marrow microenvironment. We figured out from this study that these dysfunctional late effector T cells are the key drivers of outcomes of multiple myeloma. We need to further characterize them by doing functional assays, by doing some T-cell receptor sequencing or repertoire profiling, so that we can figure out what the clonality of these dysfunctional T cells looks like.

Then we are looking at the immune components of the bone marrow microenvironment. We also need to look into the stromal compartment that has these fibroblasts, hematopoietic stem cells, and the osteoblast. We need to start looking at endothelial cells. We should start looking into those cells because they might also be playing a key role, in addition to the immune system plus tumor genetics, on the outcomes. Then [we are] converting this research-grade assay into a clinical assay by using flow cytometry or by using another approach that can be quickly done with very high sensitivity in the clinical setting.

What do you hope your colleagues take away from this research?

Maybe the biggest thing we want to say from this study is that the immune system is a critical player in the outcome of multiple myeloma, its emergence, and its therapeutic response. It is not a byproduct; it is a major driver of the outcomes. We need to start working toward more comprehensive risk-stratification models that have tumor-intrinsic factors. We already have them, like genetics and clinical parameters, but then we need to add the immune component into it to further improve the stratification strategy. [Additionally], all high-risk multiple myeloma lesions are not the same. They have very different immune imprints. We should look at the immune imprints of them, further comprehensively study them, and then help in designing immune therapies that fix the immune dysregulation that is associated with each cytogenetic alteration [instead of] thinking that all high-risk cytogenetic lesions of myeloma are all [the] same.

Pilcher WC, Yao L, Gonzalez-Kozlova E, et al. A single-cell atlas characterizes dysregulation of the bone marrow immune microenvironment associated with outcomes in multiple myeloma. 

 2026;7(1):224-246. doi:10.1038/s43018-025-01072-4

Research may support the development of more comprehensive risk-stratification models accounting for different tumor-intrinsic factors.

How Is the Immune System a “Critical Player” in NDMM Outcomes?

Findings from a phase 2 study demonstrate the feasibility of conducting genomically driven trials among patients with meningiomas.

Abemaciclib (Verzenio) demonstrated clinical activity in patients with recurrent or progressive meningiomas harboring somatic 

 or CDK pathway alterations, according to data from the phase 2 Alliance A071401 trial (NCT02523014) published in 

. The study represents a milestone as the first national investigation of precision medicine in genetically defined subclasses of meningioma, a disease with historically limited systemic treatment options once surgery and radiation have failed.

The trial met its primary end point of progression-free survival (PFS) at 6 months. Among the first 24 evaluable patients, the observed PFS rate at 6 months was 58.3% (95% CI, 36.6%-77.9%), which significantly exceeded the prespecified success threshold of 8 patients. No complete or partial responses were observed; however, the best response was stable disease in 16 of 24 patients (67%; 95% CI, 44.7%-84.4%).

The median overall survival (OS) reached 29.1 months (95% CI, 26.3-not evaluable) in the primary evaluation cohort. Among the first 24 evaluable patients, the median PFS was 10.1 months (95% CI, 3.6-20.2). Exploratory analyses revealed that patients with 

 alterations alone experienced a significantly longer median PFS of 12.1 months (95% CI, 7.6-20.6) compared with 2.4 months (95% CI, 1.6-not evaluable) in those with CDK pathway alterations alone and 2.0 months (95% CI, 1.5-not evaluable) in those with both alterations (

 = .0094). Additionally, higher levels of p16 expression by immunohistochemistry were associated with clinical benefit with abemaciclib.

“In conclusion, we demonstrate that genomically driven trials for patients with meningiomas are feasible,” wrote lead study author Priscilla K. Brastianos, MD, of Massachusetts General Hospital Cancer Center, and coauthors in the paper. “Abemaciclib was well tolerated and showed encouraging activity in patients with recurrent or progressive high-grade meningioma with CDK pathway or 

The Alliance A071401 trial was a genomically driven umbrella study evaluating targeted therapies in patients with recurrent or progressive meningiomas. The abemaciclib arm specifically enrolled patients with World Health Organization (WHO) grade 2 or 3 tumors. The treatment regimen consisted of abemaciclib administered as an oral continuous dose at 200 mg twice daily. Patients received a mean of 9 treatment cycles, with 33% requiring a treatment delay in at least 1 cycle.

Eligibility criteria required patients to have intracranial grade 2 or 3 meningioma, measurable disease, and documented somatic 

 mutations or alterations in the CDK pathway. Patients must have had progressive or residual disease, defined as residual measurable disease immediately following surgery for grade 2 or 3 tumors, or an increase in lesion size by 25% or more over 25 months. Most enrolled patients had an ECOG performance status of 0 or 1 (88%) and had previously undergone at least 2 prior treatment modalities (96%), including surgery and radiation.

The safety analysis included 36 patients who received at least 1 dose of abemaciclib. Overall, the toxicity profile was consistent with the known safety patterns of CDK4/6 inhibitors. Treatment-related adverse events (TRAEs) of grade 3 occurred in 9 patients, while grade 4 TRAEs were reported in 2 patients. The specific grade 4 toxicities included aspartate aminotransferase elevation/alanine aminotransferase elevation and vomiting. Additionally, seven patients discontinued treatment due to AEs or complications. Other notable grade 3 TRAEs included anemia, decreased neutrophil count, and diarrhea. A treatment delay in at least 1 cycle was noted in 12 patients (33%).

Brastianos PK, Dooley K, Geyer S, et al. Abemaciclib in meningiomas with somatic NF2 or CDK pathway alterations: the phase 2 Alliance A071401 trial. 

Published online January 16, 2026. doi:10.1038/s41591-025-04141-4

Abemaciclib Shows Encouraging Activity in Recurrent/Progressive Meningioma

Targeting Metabolic Vulnerability: Fasting Mimicking Diets and TNBC Sensitization

Triple-negative breast cancer (TNBC) is a challenging subtype to treat due to its aggressive nature and lack of targeted hormonal receptors. However, emerging research suggests that the metabolic landscape of TNBC may be its "Achilles’ heel."

In this interview, Ifeoma Dikeocha, PhD candidate, spoke with CancerNetwork

 and discussed the synergistic potential of fasting mimicking diets (FMDs) when paired with standard-of-care chemotherapy. Dikeocha explored the mechanistic rationale behind why metabolic restriction—specifically the reduction of circulating glucose, insulin, and insulin growth factor 1—sensitizes TNBC cells to cytotoxic agents such as doxorubicin and cyclophosphamide. By exploiting the inherent metabolic vulnerabilities of this subtype, FMD represents a promising adjunctive strategy to enhance therapeutic index and improve survival outcomes.

Dikeocha is a PhD candidate from the University of Adelaide.

Basically, triple-negative breast cancer repeatedly shows strong sensitization signals on the metabolic restriction, and this is very well seen when this metabolic procedure is combined with chemotherapy. In our study and in the preclinical studies, fasting mimicking diet, when combined with an agent like doxorubicin [or] cyclophosphamide, would reduce tumor growth and it improves survival. From the literature, we saw those triple-negative models.

When we think about it mechanistically, the rationale was [that] while triple-negative breast cancer may be more responsive, it also aligns with the other vulnerabilities that dietary interventions, like fasting mimicking diets, are designed to exploit, essentially reducing circulating glucose, also reducing insulin and IGF-1—that’s insulin-like growth factor 1—which basically reduces apoptosis and slows down inflammation in the system as well. In summary, we can say that triple-negative breast cancer appears to be a metabolically vulnerable subtype and diets like fasting mimicking diets or calorie restriction can exploit this vulnerability, especially when chemotherapy is introduced. This would then enhance the treatment responses.

Dikeocha IJ, Wardill HR, Coller JK, Bowen JM. Dietary interventions and tumor response to chemotherapy in breast cancer: a comprehensive review of preclinical and clinical data. 

. 2024;63:462-475. doi:10.1016/j.clnesp.2024.06.048

Ifeoma Dikeocha, PhD candidate, explains why triple-negative breast cancer is uniquely sensitive to fasting mimicking diets. 