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Even after surgery and chemotherapy, I make sure to shine through cancer and any fear that stares at me.

Shining Through Cancer and Fear

There are differences in prostate cancer treatment intensification adoption between academic and nonacademic physicians.

Treatment Intensification Adoption Differences Across Prostate Cancer

Findings from the IMPLEMENT sub-analysis investigating patients with metastatic castration-sensitive prostate cancer show differences in treatment intensification adoption between academic and nonacademic physicians, according to Dr. Neeraj Agarwal.

2025 ASCO Genitourinary Cancers Symposium

, Agarwal sat down for an interview with CURE® to discuss the trial. In the two-phase study, investigators revealed that, of the identified barriers and facilitators to treatment intensification, nonacademic physicians and low-intensity prescribers more frequently reported obstacles such as knowledge gaps and concerns about side effects, while academic physicians and high-intensity prescribers cited clinical support and survival benefits as key motivators.

Agarwal is a medical oncologist, a professor of medicine and the Presidential Endowed Chair of Cancer Research at the Huntsman Cancer Institute, University of Utah, as well as director of the Genitourinary Oncology Program and the Center of Investigational Therapeutics at the Huntsman Cancer Institute in Salt Lake City.

There is a clear difference between the barriers faced by high intensifiers versus low intensifiers. An approach to solve this problem is going to be physician-specific or practice-specific. From a patient’s perspective, I would urge our patients to talk to their physicians about the different treatment options which are available for them. Unless they ask, they were not going to make them think so.

If, say, there is a low intensifier physician who is not using this therapy, and they're still using, for example, ADT plus bicolutomide, which is a first-generation anti-androgen, and they are happy using that drug instead of a second generation ARPI with or without chemotherapy, if patients ask this question to their doctors, ‘What are the treatment options available for me?’ and ‘What has been developed in the last five or six years?’ that may make those busy physicians and clinicians think about those options and go back and read about them, or at least get to know about those options.

When the patient comes back for the second visit, then they are more ready to discuss those questions with them, with the most recent data, if you will. That's how I think it will impact the patients.

Transcript has been edited for clarity and conciseness.

For more news on cancer updates, research and education, don’t forget to 

subscribe to CURE®’s newsletters here.

Tumor

Dr. Barry W. Goy explains how to interpret PSA levels after prostate cancer treatment and how to manage recurrence based on disease progression.

Understanding How One Must Interpret PSA Levels in Prostate Cancer

Among patients with intermediate-risk prostate cancer, treatment with external-beam radiation therapy (EBRT) with or without six months of neoadjuvant-deprivation-therapy (NADT) showed a high prostate-cancer-specific-survival of 91%, according to research shares in a poster at the 

2025 ASCO Genitourinary Cancers Symposium.

In a comparison of NADT plus EBRT versus EBRT alone, 15-year freedom-from-biochemical-failure; metastases-free survival; prostate-cancer-specific survival; and overall survival were 52% versus 49%; 85% versus 83%; 91% versus 91%; and 53% versus 51%, respectively.

CURE spoke with lead study author and presenter Dr. Barry W. Goy to discuss how to interpret rising prostate-specific antigen (PSA) levels after treatment, and what steps patients can take to manage their disease effectively.

Goy is a physician of Radiation Oncology at Kaiser Permanente, Los Angeles Medical Center, in California.

Most patients will rely on their physicians, and of course, it varies in terms of how PSA failures are approached from one physician to another. At our institution, our initial approach is to find out where the cancer is. We have a PSA-PET scan, which is more accurate these days, but still in the context, the death rate of prostate cancer in this group of patients is still quite low. One has to be able to assess how long these patients are going to live.

If you look at our experience and many others, most patients tend not to die of prostate cancer. Whenever we recommend something, we have to look at what side effects are we causing for them. We usually try to work up where the cancer is. Sometimes, if it's not metastatic by imaging, we'll do a prostate biopsy, and we'll consider salvaged local therapy like cryotherapy or HIFU if the patient has enough longevity. Certainly, if the patient's not going to be around that long, it may be just wise to watch it if the recurrence is indolent. If there are patients where the cancer recurs more quicker or the PSA doubling time is more rapid, like less than a year, and you see visible evidence of metastasis, then it may be worthwhile to put patients on salvage ADT. For many patients that can last them for the rest of their lives.

There was no evidence that CAR T directly caused secondary malignancies, despite FDA warnings, citing prior treatments as the cause, according to research.

A Study Investigates If CAR T Therapy Directly Causes Secondary Malignancies

Despite the Food and Drug Administration (FDA) requesting that approved BCMA- or CD-19-targeted CAR T-cell therapies come with a warning following reports of T-cell malignancies, including CAR-positive lymphoma, among patients who received the treatment, researchers have announced that they have found no evidence that the therapy caused secondary cancer in modified T cells.

That’s according to research published in 

 from the Perelman School of Medicine at the University of Pennsylvania and Penn Medicine’s Abramson Cancer Center.

CAR T-cell therapy, as defined by the National Cancer Institute, utilizes a patient’s T cells, part of the immune system, which are extracted, changed in a laboratory to attack cancer cells, grown in the laboratory and infused back into the patient. The treatment, according to a news release from Penn Medicine, involves the use of engineered viruses to deliver genetic instructions that enable a patient’s T cells to target and eliminate cancer cells. There is, according to the release, a risk of a cancer-associated gene mistakenly being turned on and causing unregulated growth, which is known as insertional mutagenesis.

Researchers drew on data from 783 adult and pediatric patients who received treatment with CAR T-cell therapy at Penn Medicine and Children’s Hospital of Philadelphia in clinical trials, and found 18 cases of secondary cancers, noting that there was no evidence that these cancers were caused by intentional mutagenesis. Instead, researchers cited suppression of the immune system from prior cancer treatments as the cause of the secondary cancers.

 associated with CAR T-cell therapy in Nov. 2023, and 

 to pharmaceutical companies behind CAR T-cell therapies asking that their labeling contain a warning of secondary malignancies and that patient counseling information and medication guide also mention the risk for cancers.

 study’s co-senior author, Dr. Joseph Fraietta, about the findings and what they mean for patients. Fraietta is an assistant professor of microbiology at the Perelman School of Medicine at the University of Pennsylvania.

After looking at over 38 clinical trials of cell therapies and engineered T cell therapies — not only CAR T-cell therapies — with over 2,200 years of total patient follow-up, the frequency of secondary malignancies is very low, actually. Across our trials, none of them were directly attributed to the engineered cell product. In other words, the cell product really didn't grow out and cause any issues.

I hope [the study] puts CAR T-cell therapies more into context in terms of the relative risk with other sorts of therapies as well. And notably, this is our experience at the University of Pennsylvania, although similar studies by other groups, these large safety data sets, they're coming out. But with that, there are also isolated instances of some of these products causing secondary malignancies, but they're very few and far between. I'm not sure how the FDA will look at it, because there's still a risk. However, these secondary malignancies that are directly attributed to the CAR T-cell products are infrequent.

blood cancer

Side Effect Management

Dr. Frederick L. Locke sat down with CURE® to discuss treatment with cema-cel in the ALPHA/ALPHA2 study for relapsed/refractory large B-cell lymphoma.

Breaking Down The Results of The ALPHA/ALPHA2 Study in Large B-Cell Lymphoma

Cemacabtagene ansegedleucel (cema-cel; formerly ALLO-501/A) is an off-the-shelf allogeneic CAR-T cell therapy, Dr. Frederick L. Locke described in an interview with CURE®, saying that treatment with the CAR-T product demonstrated responses in patients with relapsed/refractory large B-cell lymphoma.

These responses were recorded in findings from the phase 1 ALPHA/ALPHA2 study, which were shared in a press release from Allogene Therapeutics, Inc. Among heavily pretreated patients, the selected phase 2 regimen achieved an overall response rate of 67% and a complete response rate of 58%, with a median duration of response of 23.1 months, Locke explained. Moreover, the safety profile was manageable, with no severe cytokine release syndrome (CRS) or neurotoxicity observed.

Locke serves as an investigator of cema-cel, as well as the chair of the Department of Blood and Marrow Transplant and Cellular Immunotherapy at Moffitt Cancer Center and Research Institute, in Tampa, Florida. In the interview with CURE, he expanded on the key takeaways derived from the trial. 

Read more from Locke and learn more about cema-cel here.

The ALPHA/ALPHA2 trial is a phase one, single-arm clinical trial that which tests the safety and efficacy of cema-cel in large B-cell and relapsed/refractory non-Hodgkin lymphoma. The results in patients with large B-cell lymphoma [show] that it can be safely administered and [oncologists are] able to manage side effects. It certainly can cause cytokine release syndrome [CRS] — which is fevers — which are common with autologous CAR-T cell therapy, the FDA-approved CAR-T cell therapies. With cema-cel we only saw CRS in about a quarter of patients, and no severe CRS [was reported]. We didn't see any neurologic toxicity that we commonly see with autologous CAR-T.

We tested [cema-cel] out in patients who had already [been treated with] several lines of treatment and the efficacy results were very intriguing and exciting. We saw that 58% of patients had a response, and 42% of patients had a complete response, or complete disappearance of their lymphoma on the ALPHA/ALPHA2 studies. This this is comparable with autologous CAR-T cell [therapy], but because it's allogeneic, we can give the cells almost immediately to our patients. We don't have to wait a month for the CAR-T cells to be made. [Therefore], it has some advantages over autologous CAR-T.

Transcript was edited for clarity and conciseness.

For more news on cancer updates, research and education,

don’t forget to subscribe to CURE®’s newsletters here.

Cemacabtagene ansegedleucel (cema-cel) is an allogeneic CAR-T cell therapy showing promise in treating relapsed/refractory large B-cell lymphoma. In the phase 1 ALPHA/ALPHA2 study, cema-cel achieved a 67% overall response rate and a 58% complete response rate among heavily pretreated patients, with a median response duration of 23.1 months. The safety profile was favorable, with no severe cytokine release syndrome or neurotoxicity observed. Cema-cel offers advantages over autologous CAR-T therapies, including immediate availability for patients without the need for cell manufacturing delays.

Dr. Frederick L. Locke sat down with CURE® to discuss treatment with cema-cel in the ALPHA/ALPHA2 studies for relapsed/refractory large B-cell lymphoma.

By Brian Koffman, MDCM (retired), DCFP, FCFP, DABFP, MSEd and Dany Habr, M.D.

When Nathan was diagnosed with chronic lymphocytic leukemia (CLL) at just 45 years old, his world turned upside down overnight. As a military veteran and ER nurse, he was no stranger to facing challenges, but this was different. His local oncologist initially recommended chemotherapy without ordering biomarker testing—a decision that could have had devastating consequences for his prognosis.

Unsatisfied with the initial treatment plan, Nathan dove into research, sought new opinions and discovered the importance of understanding his unique biomarker status. This led him to a CLL specialist who ordered the necessary tests, uncovering critical information about his genetic profile and recommending a non-chemotherapy treatment that offered a potentially better outcome. Today, he is in remission and credits biomarker testing with not only transforming his treatment plan but also giving him hope for a healthier future.

 is a powerful example of the life-changing potential of biomarker testing. Yet, for many patients with CLL, his experience remains the exception rather than the rule. Bold scientific advances in cancer treatment have paved the way for more personalized approaches, allowing therapies to align with a patient’s unique biology. But many patients continue to face outdated treatments that fail to address the specific needs of their disease. This gap is especially significant in CLL / small lymphocytic lymphoma (SLL), the most common type of adult leukemia.

CLL / SLL, a slow-growing but life-threatening blood cancer, accounts for one-third of all new leukemia cases diagnosed in adults each year.

 Despite significant progress in treatment options, many patients are still treated with chemotherapy—an approach that often comes with harsh side effects and limited effectiveness, especially for patients with a high-risk genetic profile.

 This reality persists even as biomarker testing, a powerful diagnostic tool, has evolved and provided the potential to guide patients and their doctors toward safer and more effective targeted therapies.

 Unfortunately, biomarker testing in CLL remains underutilized in community clinics.

Why Biomarker Testing is a Game-Changer in CLL

Biomarker testing, conducted through a blood test, provides critical insights into a patient’s genetic profile, identifying molecular features that influence how well a treatment might work, and also helps predict how the disease may progress.

 For example, approximately 50% of CLL / SLL patients have high-risk molecular features that may limit the effectiveness of some treatments like chemotherapy and increase the likelihood of disease progression if not treated correctly.

In fact, of those patients, about 10% of CLL / SLL patients have the high-risk del(17p) and/or TP53 mutation before starting treatment, and about 40% of patients will develop del(17p) and/or TP53 mutations after relapsing or not responding to treatment.

 Biomarker testing before starting treatment can help identify these features, enabling healthcare providers to guide patients toward more targeted therapies tailored to their needs, ultimately improving outcomes.

What’s more, genetic profiles evolve over time, meaning a treatment that worked during an earlier stage of the disease may no longer be effective after progression.

This reinforces the critical need for retesting at each stage to ensure that patients receive therapies aligned with their current disease biology.

Moving Beyond Chemotherapy to Targeted Therapies

For decades, chemotherapy was a go-to treatment for cancer, widely applied in a one-size-fits-all approach. While it has saved lives, it comes at a cost: significant toxicity, immunosuppression, and, for many CLL / SLL patients, limited effectiveness and poorer outcomes.

 High-risk patients with unmutated IGHV, del(17p) and/or TP53 are particularly vulnerable to poor outcomes with chemotherapy.

Thankfully, the rapid pace of innovation in cancer research has paved the way for more precise treatments in CLL / SLL, including a shift toward more targeted therapies. National guidelines, such as those from the National Comprehensive Cancer Network®, now recommend the newer covalent Bruton’s tyrosine kinase (BTK) inhibitors or a B-cell lymphoma 2 (Bcl-2) inhibitor plus a monoclonal antibody over chemotherapy as preferred treatment for nearly all people with CLL / SLL.

 BTK inhibitors block a protein in cancerous B cells called Bruton’s tyrosine kinase, stopping signals that cause CLL / SLL growth.

 Bcl-2 inhibitors push CLL /SLL cells towards cell death or apoptosis. Monoclonal antibodies target cancer cells for destruction by the immune system. These targeted therapies, guided by biomarker testing, can align with the unique biology of each patient, offering potentially improved outcomes and fewer side effects.

Biomarker testing also informs which targeted therapies are best suited for individual patients. For example, it can guide whether to use continuous treatment with a BTK inhibitor versus a fixed-duration regimen.

 In fact, patients with high-risk features like unmutated IGHV, TP53 and del(17p) may have better outcomes with a continuous treatment approach.

A Call to Action in CLL / SLL Care: Test Before Treat

The benefits of biomarker testing should be a universal standard. To achieve this, testing and retesting before all treatments must become the norm—for all CLL / SLL patients, regardless of where they receive care.

For patients and caregivers, the message is clear: advocate for yourself. Ask your doctor about biomarker testing before starting each and every line of therapy or after disease progression. By understanding your unique genetic profile, you can ensure your treatment plan is tailored to your specific needs, just as Nathan did.

Biomarker testing is more than a diagnostic tool—it’s a gateway to more personalized care, a chemo-free future for many, and the key to unlocking potentially better outcomes and improved quality of life for countless CLL / SLL patients. The future of CLL / SLL treatment is here, and it begins when we Test Before Treat. Because as we say at CLL Society, “Smart Patients Get Smart Care.”

Brian Koffman, MDCM (retired), DCFP, FCFP, DABFP, MSEd, is Co-Founder, EVP, Chief Medical Officer at 

, the world’s leading authority for CLL / SLL cancer patients. Dany Habr, M.D., is Head of Medical Affairs, North America & International Markets at 

, a global oncology company developing targeted therapies for CLL / SLL.

Together, BeiGene and CLL Society are advancing Before Treat™, an awareness campaign to promoting biomarker testing to improve patient outcomes in CLL. Learn more at 

NCCN. (2024). NCCN Guidelines for Patients: Chronic Lymphocytic Leukemia. National Comprehensive Cancer Network. 

https://www.nccn.org/patients/guidelines/content/PDF/cll-patient.pdf

Nguyen, T. T., Nhu, N. T., Tran, V. K., et al. (2023). Efficacy and Safety of Bruton Tyrosine Kinase Inhibitor Monotherapy Compared with Combination Therapy for Chronic Lymphocytic Leukemia and Small Lymphocytic Lymphoma: A Systematic Review and Meta-Analysis. Cancers, 15(7), 1996. 

American Cancer Society. What is Chronic Lymphocytic Leukemia? Updated May 10, 2018. Accessed November 2024. 

https://www.cancer.org/cancer/types/chronic-lymphocytic-leukemia/about/what-is-cll.html

American Cancer Society. Key Statistics for Chronic Lymphocytic Leukemia. Updated July 1, 2024. Accessed November 2024. 

Prostate cancer, particularly metastatic castration-resistant prostate cancer (mCRPC), poses significant challenges, especially for older men. Pluvicto® (lutetium Lu 177 vipivotide tetraxetan) offers a novel radioligand therapy for PSMA+ mCRPC, showing improved survival and tumor response rates compared to standard therapies. Patients are encouraged to discuss this option with their doctors, considering its potential side effects and radiation exposure. Support from care partners is crucial in navigating treatment decisions. Pluvicto is not chemotherapy and targets PSMA+ cells, providing a different approach to cancer care.

Barbara Scott

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