Tag Archives: cancer

Cancer researchers predict 10,000 more deaths in 10 years

There is a new warning Thursday night about the impact of COVID-19 on cancer. Researchers predict there could be at least 10,000 more deaths in the next decade all because of delays in screenings and treatment.Dr. Richard Bold, Physician-in-Charge at UC Davis Comprehensive Cancer Center explained the number could possibly be an underestimate because new data only focuses on two forms of cancer. “It doesn’t include all of the other patients who didn’t seek medical care who are going to see their doctor with advanced staged cancer, which their chance of cure is much less,” he said. Dr. Bold explained that many people haven’t received routine screenings like mammograms, colonoscopies and pap smears. “Particularly at the beginning of last year, we didn’t think we were going to be in COVID for this long or even longer, so a delay of three months might have been reasonable. We’re now a year into it and that’s an unreasonable delay in screening,” he said. Doctors believe there are a number of reasons for the delayed screenings. Stay-at-home orders restricted patients from going to the doctor and many people have fear of contracting COVID-19 at the doctor’s office.“The medical centers are really safe. They’re probably safer than just any other place than your home for the possible contraction of COVID. The health care providers for the most part are vaccinated so COVID is not going to be transferred from a healthcare provider to a patient,” Dr. Bold said. “If you put off your mammogram, go get it. If you put off the colonoscopy, it’s time for that,” he said. UC Davis recently took part in a study that showed patients with cancer have a higher chance of dying from COVID-19. So UC Davis has put cancer patients in the next tier to get the vaccine. They hope to begin vaccinations for cancer patients some time in February.

There is a new warning Thursday night about the impact of COVID-19 on cancer. Researchers predict there could be at least 10,000 more deaths in the next decade all because of delays in screenings and treatment.

Dr. Richard Bold, Physician-in-Charge at UC Davis Comprehensive Cancer Center explained the number could possibly be an underestimate because new data only focuses on two forms of cancer.

“It doesn’t include all of the other patients who didn’t seek medical care who are going to see their doctor with advanced staged cancer, which their chance of cure is much less,” he said.

Dr. Bold explained that many people haven’t received routine screenings like mammograms, colonoscopies and pap smears.

“Particularly at the beginning of last year, we didn’t think we were going to be in COVID for this long or even longer, so a delay of three months might have been reasonable. We’re now a year into it and that’s an unreasonable delay in screening,” he said.

Doctors believe there are a number of reasons for the delayed screenings. Stay-at-home orders restricted patients from going to the doctor and many people have fear of contracting COVID-19 at the doctor’s office.

“The medical centers are really safe. They’re probably safer than just any other place than your home for the possible contraction of COVID. The health care providers for the most part are vaccinated so COVID is not going to be transferred from a healthcare provider to a patient,” Dr. Bold said.

“If you put off your mammogram, go get it. If you put off the colonoscopy, it’s time for that,” he said.

UC Davis recently took part in a study that showed patients with cancer have a higher chance of dying from COVID-19.

So UC Davis has put cancer patients in the next tier to get the vaccine. They hope to begin vaccinations for cancer patients some time in February.

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Dustin Diamond Wonders if He Got Cancer from Cheap Hotels

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New Research Has Solved A 100-Year-Old Mystery About Cancer

It was the great German doctor and Nobel laureate Otto Warburg who, back in 1921, discovered that cancer cells don’t use sugar as fuel the way we thought they would. Rather than “burning” sugar using oxygen like most cells in our body prefer, cancer cells adopt a tactic known to be used by yeast cells: fermentation.

This specialized fermentation process (known as the Warburg effect) is rapid and preferred by cancer cells to produce ATP (used by cells for energy) even in conditions where oxygen is available. However, it is not the most effective way to tap into all of the energy stored within sugar molecules and therefore left scientists intrigued for many years as to why cancer cells do this. 

Many proposed ideas have surfaced over the years since Warburg coined the term. One hypothesis was that cancer cells have faulty mitochondria (the powerhouse of the cell), the organelle within cells where sugar is “burned” and turned into energy very effectively. However, the hypothesis has not stood the test of time, as it was found that the mitochondria within cancer cells work as they should, and hence it could not have been the reason why cancer cells prefer the fermentation route to acquire energy from sugar. 

Now, researchers at the Sloan Kettering Institute led by Dr Ming Li have published a potential explanation in the journal Science. Using biochemical and genetic experiments, the researchers showed that it all comes down to an important growth factor signaling molecule called PI3 kinase, an enzyme involved in a wide range of cellular activities such as cellular division, proliferation, growth, and survival.

“PI3 kinase is a key signaling molecule that functions almost like a commander-in-chief of cell metabolism,” Dr Li said in a statement. “Most of the energy-costly cellular events in cells, including cell division, occur only when PI3 kinase gives the cue.”

PI3 kinase has been extensively studied as part of a key signaling pathway involved in proliferation and cancer metabolism. As cancer cells start to shift and use the Warburg effect, the levels of PI3 kinase increases within the cells. This in turn, via a cascade of downstream events, leads to the cells becoming more committed to dividing. This is of course a hallmark of cancer: rapid division and proliferation. 

“PI3 kinase is a very, very critical kinase in the context of cancer,” Dr Li says. “It’s what sends the growth signal for cancer cells to divide, and is one of the most overly active signaling pathways in cancer.”

To study this, researchers turned to another cell type in our bodies that has the ability to use the “ineffective” Warburg effect to investigate this phenomenon: immune cells. When certain types of T-cells are alerted of a nearby infection and need to rapidly divide to increase in number, they too are capable of turning off the sugar “burning” method of energy production, and turn on the Warburg effect to produce ATP and aid their proliferation. 

As the authors explain in the press release, this “switch” from using oxygen to starting to use the fermentation process is controlled by an enzyme called lactate dehydrogenase A (LDHA). In turn, LDHA is regulated by the amount of PI3 kinase activity within the cell. By using mice that lack the LDHA enzyme, the researchers found that animals could not maintain their normal levels of PI3 kinase within their T-cells, and were unable to fight off infections, because the T-cells didn’t divide properly as the PI3 kinase levels were not what it should be. 

This cemented the idea that the metabolic LDHA enzyme was somehow regulating the cells’ PI3 kinase signaling molecule. 

“The field has worked under the assumption that metabolism is secondary to growth factor signaling,” Dr Li says. “In other words, growth factor signaling drives metabolism, and metabolism supports cell growth and proliferation. So the observation that a metabolic enzyme like LDHA could impact growth factor signaling through PI3 kinase really caught our attention.”

The researchers go on to explain that like most enzymes, PI3 kinase uses ATP as an activating source of energy to perform its functions, like enforcing cellular division. As the Warburg effect ultimately results in ATP production, a positive feedback loop is established between the two molecules where ATP drives the activity of PI3 kinase, and with more PI3 kinase available, it results in rapid cell division and growth.

The findings challenge the accepted textbook view that cell signaling drives metabolism in cancer, as the researchers demonstrate in immune cells that use the Warburg effect, metabolic enzymes could be driving signaling molecules which in turn drives cellular division and growth, explaining a long-standing mystery as to why cancer cells might preferentially use the fermentation process to their advantage.

Although more research needs to be done using cancer cells instead of immune cells to test this, the current findings open up an exciting therapeutic avenue in the future where one might be able to target cancer growth and proliferation by targeting LDHA, instead of the more commonly focused on PI3 kinase signaling enzyme. 



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Dustin Diamond completes first round of chemotherapy for cancer treatment

A representative for the actor said on Thursday that Diamond, known for playing Samuel “Screech” Powers on the hit ’90s teen series, has completed his first round of chemotherapy treatment, with another to follow.

“Dustin is looking forward to spending more time with his girlfriend, playing his bass guitar/video games, as well as making videos for his fans on social media,” a statement from Roger Paul, Diamond’s representative, said.

Diamond, who revealed his diagnosis last week, will begin physical therapy soon, Paul added.

Diamond played Screech for more than a decade, appearing in four different incarnations of the “Saved by the Bell” franchise.

Peacock is home to a reboot of the series, which Diamond has not appeared in.

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Jason Segel stars in a sugarcoated cancer drama

Casey Affleck and Jason Segel in Our Friend
Photo: Gravitas Ventures

The opening scene of Our Friend, a tender indie tearjerker built from the blueprint of a wrenching true story, finds a husband and wife on the precipice of a difficult conversation. It’s time for Nicole (Dakota Johnson) and Matt (Casey Affleck) to talk to their children. Nicole, we’ll soon learn, is sick, and though it’ll be another hour before the film reveals the specific nature of what they’ll disclose, it’s clear that the discussion won’t be an easy one. At least they have one helpful instruction from the doctors: Avoid euphemisms. Give it to them straight. Because there should be no misunderstanding about what’s coming. They have to face reality head on and together.

There’s a certain irony to this in media res prologue—one that will be clear to anyone who’s read the source material, Matthew Teague’s “The Friend: Love Is Not A Big Enough Word.” In his prizewinning essay, published in Esquire in 2015, the journalist recounts the time he spent caring for his wife after she was diagnosed with ovarian cancer, and also how his best friend, Dane Faucheux, moved in to help out during this impossible crucible for the family. It’s an unflinchingly honest memoir, candidly cataloging every ugly detail—medical and psychological—to the point where a truly faithful adaptation would be more upsetting than any horror movie released last year. Our Friend is not that film. It’s sweet and involving and occasionally even moving, but also, in its selective dramatization, a lot easier. Which is to say, it approaches the story itself rather euphemistically, handling the audience with kid gloves by eliding the most unpleasant truths of the family’s experience.

Directed by Gabriela Cowperthwaite, who pulled fewer punches in her documentary Blackfish, Our Friend doesn’t so much deviate from Teague’s account as supply it a new shape and a certain seriocomic Indiewood luster. As the title suggests, the focus is partially on Dane (Jason Segel), a close college friend of the couple who offers to come stay at their Alabama home for a few days after Nicole’s diagnosis—an arrangement that became indefinite, as those days bled into weeks and then months and then more than a year, Dane basically pausing (if not outright abandoning) his life in New Orleans to help look after their two daughters, Molly (Isabella Kai) and Evangeline (Violet McGraw). The script, by Brad Ingelsby, introduces a flashback structure, cutting away from present-day scenes of hospital visits and worsening conditions to fill in the history of a friendship en route to a medical crisis.

In his essay, Teague makes few attempts to crack or explain Dane’s sacrifice: Among other things, it’s an awed, grateful tribute to his friend’s selfless insistence on just being there through the whole gauntlet of heartache and horror. Divorced of a purely first-person perspective, Our Friend strains for understanding it doesn’t always find: One can admire its dramatic theories—the faint suggestion that Dane’s endless supportiveness stemmed partially from a desire to give more meaning to his own life, low on romantic or professional “success”—while still feeling that Segel is playing more saint than man. The flashbacks offer backstory but not a lot of extra dimension.

Our Friend
Photo: Gravitas Ventures

Segel has, of course, spent much of his career exploring the vagaries of male bonding, from the goofy-sweet Apatovian bromance of I Love You, Man to the pricklier quasi-friendship of The End Of The Tour. It’s no surprise, perhaps, that Our Friend hits its stride when centering the relationship between Dane and Matt, finding conflict at its origins (the false alarm of romantic competition) and in its margins. Affleck, too, is in his wheelhouse: Four years after his tremendous, Oscar-winning performance of crystalized guilt and grief in Manchester By The Sea, he’s playing another man numbed by unfathomable hardship. (His voice, which ranges from whisper to mutter, is uniquely suited to characters almost choked silent by their feelings.)

Yet Our Friend keeps us on the outside of that pain, never offering the kind of window into Teague’s heart and mind that his writing intrinsically could. Is this a case of a story perfected in its original format—a personal essay molded imperfectly into cinema? The film fares best when at its most specific, zeroing in on the dismaying inevitability of well-meaning friends disappearing when the going gets tough or moments of casual tragedy, like Matt taking note of what braiding is in anticipation of having to do that for his daughter. Other times, Cowperthwaite’s approach suggests an elegant yada yada: Rather than steep us in the nitty-gritty, the film often flutters through a vaguely Malickian montage of bucket-list excursions and anguished embraces.

One begins to wonder if the achronological structure is just a way to put off everything inconveniently messy in Teague’s essay, like a tough conversation it’s trying to avoid. “We don’t tell each other the truth about dying,” the author writes, early into his article. “It’s grotesque. It’s undignified.” But Our Friend spares us the gory details at almost every turn, cleaning up a story whose power stemmed, heavily, from its willingness to be gruelingly truthful about what cancer can do to the body. Cowperthwaite barely seems willing to even deglamorize Johnson, who never really loses her movie-star glow, even when her character—the most underdeveloped of the film’s trio—becomes unrecognizable to those in her life. At one point, Nicole begins wearing a wig around the house to entertain visitors, doing a performance of good health rather than let anyone see the reality of her condition. It’s as good a metaphor as any for the way Our Friend softens its own blows.

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