"A revolution in cancer treatment?"

[billfenley2]

I don't see a specific reference to prostate cancer in this article in today's NYTimes. But it's about multiple cancers, and the idea, spoken of here before, is that patients with cancers formerly called terminal are living longer and longer as multiple drug treatments may come close to turning these into "chronic" conditions. nytimes.com/2023/06/16/opin...

[HikerWife]

This was excellent, thanks for posting! Shared it with Eric.

[Spyder54]

locked behind a NY Times paywall

[billfenley2 in reply to Spyder54]

Thanks Spyder. I copied/pasted, below, as much as I could.

[Seasid in reply to Spyder54]

Put the title of the article into a Google search and click then from the result there. It works for me and it always works that way.

[Don_1213]

Good article - outlines treatments used to keeping metastatic patients alive - sequential treatment using multiple treatment regimes: They describe it as crossing a brook on stepping stones - you go from one treatment that might stop working to the next treatment and stay on it until it stops working, then onto the next.. etc. and they talked a bit about what new treatments are working and under development (immunotherapy, and new less damaging forms of chemotherapy.)

Good article.

[anony2020 in reply to Don_1213]

The possible problem with sequential is that the human body weakens while the disease gets stronger.

Dont mind me. I am just a layman.😊

[Seasid in reply to anony2020]

I am only on ADT Degarelix injection alone for 5 years and I still feel OK. I understand it require luck to make proper treatment decisions. Good luck.

[billfenley2 in reply to Seasid]

Keep up the good work, Sid!

[Seasid in reply to billfenley2]

OK, I had early chemotherapy and although I am polimetastatic I irradiated my prostate on the ground that my prostate was the only visible cancerous site in my body on the psma pet scan.

The cancer in the prostate at some point stops responding to global treatments. Therefore I wanted to remove that only visible CRPC in my body and to continue with firmagon injections alone extending its use further instead of jumping to the next possible option like Abiraterone. I still believe I am a gambler. I really wonder when the rest of the cancer will follow the cancer in my prostate and become CRPC?

My biggest nightmare is the spread of the cancer to my brain as I have Mets in my neck and spine. My last PSA was 0.23 a drop from 1.4 before the SBRT of my prostate six months ago.

I was thinking about starting enzalutamide or abiraterone, but I feel treasonably OK now.

I had a vertigo recently and I should do the MRI of my brain and c spine. The waiting list is 2 months long in my hospital. I could speed this up but I don't want to overreact. Maybe if my PSA stops dropping. I really hope that it will go down for one more year. This is an uncharted territory. We will see.

[billfenley2]

By Kate Pickert

Carol MacKenzie had just finished playing a round of golf when she noticed some swelling and pain in her neck. It was 2014, and 18 years had passed since Ms. MacKenzie finished treatment for breast cancer. But it had returned. This time the cancer was growing inside several lymph nodes around her neck, plunging her back into treatment long after she thought that was all behind her.

Doctors do not know exactly why or how breast cancer can go dormant in a patient’s body for so long, not advancing for years, until it suddenly begins to grow. But that’s what had happened. Without treatment, Ms. MacKenzie’s cancer would most likely have made its way to her vital organs and killed her.

But in the nine years since Ms. MacKenzie’s cancer reappeared, her physician, Dr. Nancy Lin, a medical oncologist at Dana-Farber Cancer Institute in Boston who specializes in treating and studying advanced breast cancer, has prescribed a series of eight drug regimens for her, including three as part of clinical trials. Ms. MacKenzie, 71, of Massachusetts, switches from one medication to another when it becomes clear that a treatment doesn’t work or has stopped working because her cancer has figured out how to resist its effects. Some of these regimens have lasted only a few months, while others have kept Ms. MacKenzie’s cancer under control for longer. Of an oral type of chemotherapy she tried as her fifth line of treatment, she said: “I was excited. I got 12 months out of that one.”

Like a hiker who comes upon a wide creek and gingerly steps from one partially submerged stone to the next, Ms. MacKenzie has moved from one regimen to another, each drug or drug combination keeping her cancer in check long enough to get to the next one — until finally, in 2020, she started taking a medicine that for more than two glorious years has stopped her cancer from growing and given her a quality of life that’s very close to normal.

“Of all the things I’ve been on, it’s the easiest,” Ms. MacKenzie said. These days, she is more focused on her grandchildren’s hockey and football games than the fact that she has a supposedly fatal disease. In January, she and her husband celebrated their 50th wedding anniversary.

If you know someone with late-stage cancer, this kind of treatment regimen might be familiar to you. The approach is increasingly becoming a standard of care for patients facing diagnoses that were once death sentences.

Thanks to a combination of forces, cancer drug development is now happening fast enough that for patients like Ms. MacKenzie, it is outpacing the growth of cancer cells inside their bodies. For these patients, cancer is more like a chronic disease than a one-time catastrophic event.

Every time a new cancer treatment approach emerges, oncologists and overexcited journalists have a habit of declaring that a cure for cancer is imminent. What’s happening now is different. Rather than a single breakthrough therapy or discovery, a variety of scientific advances are exerting downward pressure on cancer mortality in new ways and at the same time. As a result, the landscape for many cancer patients has changed tremendously in just the past five years. The Cancer Moonshot, a multibillion-dollar initiative championed by President Biden, aims to cut the cancer death rate by 50 percent in the next quarter century. The goal is lofty, but recent progress against cancer means it’s now less far-fetched than it might have once seemed.

“The pace of progress is most certainly accelerating,” said Dr. Jedd Wolchok, an oncologist and director of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine. “There are so many things converging.”

In some cases, patients like Ms. MacKenzie with cancer that has spread inside their bodies — called metastatic disease — are able to stay alive much longer than previously predicted. Some are cured altogether by new drugs, a reversal of fortune that patients and doctors dared not contemplate just a few years ago. In a growing number of cases, patients with metastatic cancer are not cured but have access to so many treatment options that they are able to leap from one to the next, changing course whenever their cancer becomes resistant to a drug, always staying ahead of their disease.

This is a new paradigm. Until recently, the prevailing wisdom in oncology was that many early-stage cancer patients could be cured, but metastatic disease was almost always incurable. This thinking drove cancer research, treatment and care for decades. Oncologists often threw the kitchen sink at early-stage cancer patients, performing invasive surgeries and administering heavy doses of chemotherapy — which can make patients sick to their stomachs, prone to infection and bald, but can also have long-term side effects including infertility, heart damage, numbness in hands and feet, brain fog and fatigue. The belief was that the only chance to save the lives of such patients was to eliminate the possibility of their cancer’s spreading. Since metastatic disease was usually considered incurable, research focused on early-stage disease. For unfortunate patients who developed advanced cancer, care typically consisted of additional rounds of chemotherapy and palliative approaches. Now there is new hope for many of these patients.

[Jeremiad53]

Click bait, I won't pay they won't allow me to read. The media is often the handmaiden of pharma.

[billfenley2 in reply to Jeremiad53]

I've copied most of the article in the post above yours.

[Seasid in reply to Jeremiad53]

You could read it if you put a title of this article into a Google search and kick on the result there. It works for me and always works that way.

[garyjp9]

Here is another article from the immunotherapy field that I found interesting. We can hope.

Regulatory T cells lacking SRC-3 gene mediate long-lasting tumor eradication

Reviewed by Megan Craig, M.Sc.May 29 2023

Researchers at Baylor College of Medicine have discovered a crucial regulator of the anti-cancer immune response that could change the game in the fight against cancer. Published in the Proceedings of the National Academy of Sciences, the study shows that in animal models of breast and prostate cancer, eliminating the gene SRC-3, specifically in a type of immune cell called regulatory T cells (Tregs), triggered a lifelong anti-cancer response that eradicated the tumor without the typical side effects observed with other therapies.

Furthermore, transferring Tregs without SRC-3 to animals carrying breast cancer tumors also resulted in long-term elimination of the tumor without negative side effects. The findings encourage pursuing further investigations to determine the value of this approach to treat the human disease.

More than 30 years ago, my lab discovered a protein we called steroid receptor coactivator (SRC) that is required for the effective regulation of gene activity. Since then, we have discovered that a family of SRCs (SRC-1, SRC-2 and SR-3), regulates the activity of a variety of cellular functions."

Dr. Bert W. O'Malley, corresponding author, chancellor and professor of molecular and cellular biology at Baylor

Over the years, the O'Malley lab and colleagues have been particularly interested in SRC-3 and its role in cancer. SRC-3 is not only highly expressed in all human cancers and plays a role in cancer growth, but it is also strongly expressed in Tregs that regulate the immune response to cancer. Intrigued by the abundance of SRC-3 in Tregs and suspecting that it might play a role in controlling cancer progression, O'Malley and his colleagues investigated the effect of eliminating the gene SRC-3 in Tregs on breast cancer growth.

The team generated mice lacking the SRC-3 gene only in Tregs (SRC-3 knock-out) and then compared breast cancer progression in these mice with the progression in mice that had the SRC-3 gene.

"We were surprised by the results," O'Malley said. "Breast tumors were eradicated in the SRC-3 knock-outs. A subsequent injection of additional cancer cells in these mice did not give rise to new tumors, showing that there was no need to generate additional SRC-3 knock-outs to sustain tumor resistance. Importantly, transferring these cells to animals carrying pre-established breast tumors also resulted in cancer eradication. We obtained similar results with prostate cancer."

The team also discovered that Tregs lacking SRC-3 mediated long-lasting tumor eradication by effectively modifying the environment surrounding the tumor into one that favored its elimination.

Using a variety of laboratory techniques, O'Malley and his colleagues discovered that the modified Tregs proliferated extensively and preferentially infiltrated breast tumors where they released compounds that generated an anti-tumor immune response. On one side, the compounds facilitated the entrance of immune cells – T cells and natural killer cells – that directly attacked the tumor and, on the other side, modified Tregs blocked other immune cells that attempted to stop the anti-tumor response.

"Other published treatments seem to reduce tumor burden or eliminate the cancer for some time, but in most cases it returns. Our findings in animal models are the first to show that Tregs lacking SRC-3 eradicate established cancer tumors and appear to confer long-lasting protection against recurrence," said first author Dr. Sang Jun Han, associate professor of molecular and cellular biology and in the Center for Reproductive Medicine at Baylor. He also is a member of Baylor's Dan L Duncan Comprehensive Cancer Center. "We are very excited about the results; altogether they warrant continuing our investigations to translate the findings into a novel, more effective and longer-lasting cancer therapy."

Other contributors to this work include senior scientists David M. Lonard and Cliff C. Dacso and lab members Prashi Jain, Yosef Gilad, Yan Xia, Nuri Sung, Mi Jin Park, Adam M. Dean, Rainer B. Lanz, Jianming Xu, all at Baylor.

This work is partly supported by funding from the National Institutes of Health grants R01HD07857, R01HD08188 and R01HD098059 and CoRegen, Inc.

Baylor has partnered with CoRegen, Inc. to commercialize these groundbreaking discoveries. All the patents and intellectual property underlying these discoveries have been licensed to CoRegen, Inc. (coregeninc.com)

Source:

Baylor College of Medicine

[billfenley2 in reply to garyjp9]

Good one Gary, Thanks. A side note -- look at the names of those Baylor contributors -- thank God for the melting pot that is America, may it ever last!

[Spyder54 in reply to garyjp9]

Man,, it seems they are really on to something !

“On one side, the compounds facilitated the entrance of immune cells – T cells and natural killer cells – that directly attacked the tumor and, on the other side, modified Tregs blocked other immune cells that attempted to stop the anti-tumor response.”

As TA has said before, not all mouse studies transfer well to humans. Hopefully this is one that does. T-regs lacking SRC-3 seems promising.

Mike

[garyjp9 in reply to Spyder54]

Thanks, Mike. Agree.

[garyjp9]

True enough, thanks Bill