“A research team at MedUni Vienna has now discovered specific changes in a protein that drive the growth and spread of prostate cancer. The study was recently published in the journal Molecular Cancer.
In the study, the researchers broke new ground and investigated the role of the protein KMT2C in prostate cancer. KMT2C is a genetic component that essentially functions as a regulator of central cellular processes. If KMT2C loses this regulatory ability due to typical cancer-related mutations, this encourages the proliferation of the cancer gene MYC. This in turn causes cells to divide at an increased rate, driving both growth and spread of the cancer.
…
MYC inhibitors are essentially new cancer treatment drugs that have already been tested in clinical trials and -- if further studies confirm this -- could also be used in metastatic prostate cancer in the next few years.”
Your thoughts? Sounds like we might soon have a way to stop metastasis, even if it’s already gotten a foothold. Am I misreading?
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I'm surprised with MYC being present in a high % of PCa patients, that it is not a path more studied! Form what I've read in the past, and if I recall correctly, don't quote me, lol... It's because the MYC is so intertwined and has such a large footprint, that studying it's effect is then problematic.
Awesome! Metastisis is what kills us-not cancer in prostate. NOTE: previous discussions on “Fruit Pectin” which breaks down the gel like substance that allows cancer cells to cluster.
Also Dr Thomas Seyfried of Boston College has proven in lab that he can stop Metastisis by lowering Glucose and Glycogen levels (see his videos on YouTube ). Trying to raise funds for Human Trial.
I have not yet closely compared the two studies, but here is a similar study published in Nature Cancer with this excerpt from the Princeton Alumni Weekly.paw.princeton.edu/article/p...
When Yibin Kang was a postdoctoral researcher at Memorial Sloan Kettering Cancer Center in the early 2000s, he thought of metastasis as “the elephant in the room.”
“Nobody knows how cancer cells become metastatic,” he says. Now, after more than 15 years of research on a gene known as metadherin, or MTDH, Kang believes he has made a breakthrough.
Kang hopes his findings will lead to new therapeutic interventions for treating common cancers, including breast, lung, colon, liver, and prostate.
In November 2021, Kang, who is the Warner-Lambert/Parke-Davis Professor of Molecular Biology, and his co-authors published two papers in Nature Cancer demonstrating that in mice, blocking the interaction between MTDH and another protein disables its function and prevents metastasis. Kang hopes his findings will lead to new therapeutic interventions for treating common cancers, including breast, lung, colon, liver, and prostate.
During his time as a postdoctoral researcher, Kang, who arrived at Princeton in 2004, became intrigued by breast cancer, which kills more than 40,000 women annually in the United States. “You could have two breast cancer patients with almost the exact same early-stage cancer and treatment, but they could have very different outcomes,” he recalls. “One would be cured, but the other would experience recurrent metastasis a few years later, treatment would fail, and the patient would die.” Kang wanted to know if there was a way to predict whether a patient’s cancer would return and spread.
Kang began to research MTDH, which had been identified as a factor in metastatic breast cancer in mice. In 2009, he published a human study showing that patients with metastatic breast cancer frequently had a higher DNA copy number and gene expression level of MTDH in their tumors — in other words, the MTDH gene was amplified in patients whose cancer resisted treatment.
In 2014, Kang published another set of studies demonstrating that MTDH plays an essential role in promoting metastasis for breast and prostate cancers (as well as lung and intestinal cancers, according to a follow-up study published in 2020). These studies included two notable results. First, Kang showed that removing the MTDH gene in healthy mice had no discernible effect on their health. This suggested that MTDH is probably not essential for normal growth and development, and that targeting it won’t create adverse side effects.
Second, Kang analyzed the crystal structure of the MTDH protein and found that it interacted with another protein, SND1. Two projections on the surface of MTDH fit precisely into cavities in SND1 like a key into a lock. Kang hypothesized that disrupting the relationship between the two proteins could be a way to neutralize MTDH’s harmful activities.
In search of a way to block the “handshake” between MTDH and SND1, Kang turned to the Small Molecule Screening Center in Princeton’s chemistry department. His team spent over two years testing thousands of molecules in the center’s library before it found a compound that could fill one cavity in SND1, essentially disabling MTDH.
Kang says MTDH plays two key roles in helping cancer flourish: It helps tumors resist stress as they grow, and suppresses the body’s immune response to cancer — which he compares to having “a house on fire, [but the] fire alarm is disabled.” In his most recent papers, Kang demonstrates why disabling MTDH is effective in treating cancer. The first paper shows how the blocking mechanism works. The second shows its therapeutic benefit by demonstrating that blocking MTDH in mice with breast cancer is highly effective when combined with anti-PD1 immune checkpoint therapy, a relatively new treatment that disrupts interactions between proteins that suppress the immune system. This combination works by reactivating the tumor’s alarm system so that it can call for help, and then maintaining the stamina of the “firefighters” that respond to the alarm so that they have enough energy to attack the tumor.
Kang hopes to begin clinical trials on humans in two to three years. He has licensed the technology from his latest studies to Firebrand Therapeutics, a Princeton-based biotech startup, which is continuing to develop the compounds for clinical trials. An important step in the process will be substantially reducing the concentration of the MTDH-blocking compound to prevent unwanted side effects in humans.
Andres Blanco *11, who completed his Ph.D. under Kang and took part in some of Kang’s earliest research on MTDH, notes that metastasis is particularly tricky because cancer cells tend to change with each new region of the body they spread to, which means that treating metastasis is “almost like treating multiple diseases.” He believes that Kang’s latest findings have “very high potential.” The key, Blanco adds, is “to find something that the cancer cells are very vulnerable to [but that] normal cells are minimally vulnerable to.”
Liling Wan *14, who also completed her Ph.D. with Kang and is a co-author on the new papers, is excited by Kang’s results — not only for their potential therapeutic use, but also because they prove how sheer persistence in the lab can yield major insights over time. “It’s really encouraging to see how basic research [might] translate to something that is meaningful in patients,” Wan said.
As Hidden alludes, it will be nice when a given experimental moves from mouse studies to people. Or, if I understand the canine connection, we take advantage of the better genetic matchup b/w dogs and humans…assuming we are gentle and kind with the dogs, of course.
I’m not sure if the Science Daily study was with mice or people. I noticed a couple of things from my admittedly quick read — the study leader is affiliated with several organizations, one of which deals with Animal Pathology; however, the article stated clinical trials are already underway. Not sure exactly what that means, but when I searched clinicaltrials.gov for “MYC Inhibitor”, I found a handful of trials — though I’ve not taken much time to drill down for details. Here’s one I found that is interesting (out of a total of six):
… status: recruiting, for mCRPC; one of the interventions is ZEN-369, a BET Bromodomain inhibitor. Here’s a piece of the description:
“ZEN-3694 blocks the expression of the MYC gene to prevent cellular growth in certain types of tumors, including castrate resistant prostate cancer. ”
Frankly I’m trying to not get too excited … typically I assume that if a new therapy or drug has legs, that we’ll hear more about it over months and years. I recall being over-the-top excited when I first read about Lu177 some years ago, but my MO helped slow my roll: if it has legs, we’ll “soon enough” hear a whole bunch more about it. In the Lu177 case, I joke with her that “See? Told ya!”.
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