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‘Fusion genes’ drive formation and growth of colorectal cancer – Medical Xpress

July 12, 2017 by George Lowery Mouse intestinal organoids that scientists genetically engineered to study colon cancer. Using gene editing technology, the investigators fused together the genes Ptprk and Rspo3 to determine their effect on cancer development. Credit: Cornell University

Genetic mutations caused by rearranged chromosomes drive the development and growth of certain colorectal cancers, according to new research conducted by Weill Cornell Medicine investigators.

Many of the genetic mutations present in colorectal cancer have been known for decades. But their exact role in cancer's development and progression has not been clear. "We knew that these mutations existed, but not whether they contribute to the disease," said Lukas Dow, an assistant professor of biochemistry in medicine and a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine. "So we are interested in whether they are actually driving cancer and whether they can potentially be targets for drugs that treat it."

In a paper published July 11 in Nature Communications, Dow and his colleagues describe how large pieces of chromosomes are deleted or inverted, resulting in new, mutated so-called fusion genes created from parts of two other genes that are responsible for the formation of some colon cancers.

The researchers used the gene editing technology CRISPR, which allows scientists to easily alter any piece of DNA in an organism, to cut the DNA in normal human intestinal cells and create fusion genes. In this way, they engineered the genetic mutations in two genes Rspo2 and Rspo3 known to be associated with colorectal cancer. They then created mice containing these genes to study the genes' effect on colon cancer development.

Though CRISPR has received a lot of attention in the last several years, this is the first time the tool has been used this way. "We created the first CRISPR-based transgenic animal model for inducing large-scale chromosomal rearrangements," Dow said.

These chromosomal rearrangements in the Rspo genes did in fact initiate growth of colon cancer in the mice. The mice containing the engineered genes developed multiple precancerous tumors that are the precursors to colorectal cancer. "This is the first evidence that these specific fusions can drive tumor development," Dow said.

Dow's team went on to treat the mice that developed cancer with an experimental drug, LGK974, which blocks a protein necessary for Rspo fusion genes to cause disease. "The tumors shrank and the mice were fine as long as they continued to take LGK974," Dow said. In addition, the drug only suppressed growth of the cancer cells; it had no obvious negative effect on healthy cells in the mouse intestine.

The study's results hold particular promise for the treatment of colorectal cancer in humans, Dow said. This form of cancer has historically been a difficult disease to treat. Chemotherapy drugs have limited impact against colorectal cancer and developing targeted therapies drugs that target aspects of cancer cells that make them different from healthy cells has proven difficult. "Our results give us confidence that if we can deliver LGK974 effectively to patients with these fusion genes," Dow said, "then we should be able to see some tumor response with these targeted agents."

Explore further: Novel gene editing approach to cancer treatment shows promise in mice

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'Fusion genes' drive formation and growth of colorectal cancer - Medical Xpress

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Gene mutation found to drive prostate cancer subtype – Medical Xpress

March 14, 2017 by Heather Lindsey Prostate organoids from genetically engineered mouse models. Credit: Mirjam Blattner and Dennis Huang

A newly discovered genetic mutation that is found in a subtype of prostate cancer is integral to the disease's development and growth, according to research from Weill Cornell Medicine scientists. Their findings could pave the way for new targeted treatment approaches.

A mutation of the gene Speckle Type BTB/POZ Protein, or SPOP, occurs in about 10 percent of men with prostate cancer. Roughly 20,000 men per year in the United States will be diagnosed with prostate cancers harboring SPOP mutations. But until now, SPOP's role in driving cancer was largely unknown. In a study published March 13 in Cancer Cell, researchers found in mice that the SPOP mutation leads to prostate cancer that grows in a distinctively different way from other common subtypes.

"This is important because now we have to think about SPOP cancers differently," said co-senior author Dr. Mark Rubin, director of the Caryl and Israel Englander Institute for Precision Medicine and the Homer T. Hirst III Professor of Oncology in Pathology at Weill Cornell Medicine. "This may have implications for how people respond to treatment and how amendable they are to certain drugs."

Prostate cancer containing the SPOP mutation was first discovered in 2011 by Weill Cornell Medicine researchers, who found that the malignancy has unique molecular features that characterize it as a distinct subtype.

"The key is we discovered these mutations several years ago, but because there are many mutations in cancer, knowing which ones are causing the disease and changing the biology of cells requires scientists to do some additional experiments," said co-senior author Dr. Christopher Barbieri, an assistant professor of urology at Weill Cornell Medicine.

In the new study, the research team, which included doctoral student and first author Mirjam Blattner, showed that the SPOP mutation drives prostate cancer formation in genetically engineered mice. This is a critical step in understanding the importance of mutations found in human cancers, Barbieri said. Additionally, they demonstrated that the SPOP mutation activates two major pathways in prostate cancer androgen receptor signaling and phosphoinositide 3-kinase (PI3K) signaling which are both important to cell survival and growth, and are processes that contribute to malignancy.

The androgen receptor is one of the main signaling pathways that underlies the growth of the prostate and prostate cancer, said Barbieri, who is a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine and a urologic surgeon at NewYork-Presbyterian/Weill Cornell Medical Center. Consequently, it is a main therapeutic target for men who have the disease. In recent years, researchers have shown that the androgen receptor works with the enzyme PI3K to promote prostate cancer cell survival.

Typically, these two pathways balance each other out, meaning the activation of one keeps the other in check and prevents cells from growing too out of control. "So, the fact that SPOP activates both pathways breaks the normal balance between the two, allowing cells to grow in an uncontrolled fashion," Barbieri said.

Now that scientists have a better understanding of the signaling pathways that are activated in this prostate cancer subtype, "we could potentially design therapies for it or use combinations of therapies that already exist to successfully target the cancer," Barbieri said.

The researchers are evaluating clinical trial data of patients being treated with androgen receptor antagonists and PI3K inhibitors to see whether they have SPOP mutations and how well they are responding to treatment. They're also investigating new agents to directly target SPOP cancers, pursuing a precision medical approach to treatment.

"This is a significant advancement for precision oncology," said Dr. Howard R. Soule, executive vice president and chief science officer of the Prostate Cancer Foundation, which helped fund the study through three research awards to Rubin and Barbieri. "Dr. Barbieri, Dr. Rubin, Blattner and team have identified the molecular mechanisms by which SPOP gene mutations, which define one of the most frequently occurring prostate cancer subtypes, drive prostate cancer. This provides a roadmap for developing precision treatment strategies for patients with this tumor type, which may shift towards improved outcomes."

Explore further: Gene mutation can allow proteins to gather, spark tumor growth

More information: http://www.cell.com/cancer-cell/fulltext/S1535-6108(17)30047-8

Journal reference: Cancer Cell

Provided by: Cornell University

Prostate cancer is generally treated as if it's a single disease. But researchers have discovered a new type of the cancer that appears to affect 15 percent of patients, a finding that paves the way for better diagnosis and ...

Mayo Clinic researchers have shed light on a new mechanism by which prostate cancer develops in men. Central to development of nearly all prostate cancer cases are malfunctions in the androgen receptorthe cellular component ...

Mutations in a protein called SPOP (speckle-type POZ protein) disarm it, allowing another protein called steroid receptor coactivator-3 (SRC-3) to encourage the proliferation and spread of prostate cancer cells, said researchers ...

The gene SPOP is mutated in up to 15 percent of all cases of prostate cancer, making it one of the most mutated genes in the disease. However, when the gene is functioning properly, it acts as a tumor suppressor. Despite ...

A collaborative expedition into the deep genetics of prostate cancer has uncovered a distinct subtype of the disease, one that appears to account for up to 15 percent of all cases, say researchers at Weill Cornell Medical ...

The steroid dexamethasone could potentially deter the growth of a prostate cancer subtype that was previously thought to be difficult to treat with medications, Weill Cornell Medicine researchers report. Their findings were ...

A new study reveals that African-Americans have measurable differences in the number and type of bacteria that live in the colon - and those differences are related to their higher-than-average colon cancer risk.

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The first of a new class of medication that delivers a combination of drugs by nanoparticle may keep melanoma from becoming resistant to treatment, according to Penn State College of Medicine researchers.

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A clinical trial of an antibody-drug conjugate that combines the active portion of a chemotherapy drug with an antibody targeting a molecule expressed on tumor cells appears promising for the treatment of metastatic triple-negative ...

A newly discovered genetic mutation that is found in a subtype of prostate cancer is integral to the disease's development and growth, according to research from Weill Cornell Medicine scientists. Their findings could pave ...

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Breast cancer's many drivers

Public release date: 20-Jun-2012 [ | E-mail | Share ]

Contact: Nicole Davis ndavis@broadinstitute.org 617-714-7152 Broad Institute of MIT and Harvard

Breast cancer is not a single disease, but a collection of diseases with dozens of different mutations that crop up with varying frequency across different breast cancer subtypes. Deeper exploration of the genetic changes that drive breast cancer is revealing new complexity in the leading cause of cancer death in women worldwide.

In one of the largest breast cancer sequencing efforts to date, scientists from the Broad Institute, the National Institute of Genomic Medicine in Mexico City, Beth Israel Deaconess Medical Center, and Dana-Farber Cancer Institute have discovered surprising alterations in genes that were not previously associated with breast cancer. They report their results in the June 21 issue of Nature, which is publishing a series of papers characterizing the genomic landscape of breast cancer.

One of the team's new findings, a recurrent fusion of the genes MAGI3 and AKT3 in what is known as a translocation event, was observed in tumors from a rare but aggressive form of breast cancer known as triple-negative breast cancer. This cancer does not respond to conventional hormone therapy because its tumors lack three receptors that fuel most breast cancers: estrogen receptors, progesterone receptors, and human epidermal growth factor receptor 2 (known as HER2). But the biological pathway that is affected by the MAGI3-AKT3 reshuffling is already the target of experimental drugs.

The other new alteration reported by the team occurred in two transcription factor genes. Recurrent mutations were detected in the gene CBFB and deletions of its partner RUNX1. Cancer-causing rearrangements of these two genes are common in blood cancers, such as acute myeloid leukemia, but their discovery in breast cancer marks the first time they have been seen in a solid cancer.

"These genes wouldn't top the list of genes you think would be mutated in breast cancer," said Alfredo Hidalgo Miranda, co-senior author of the paper and head of the cancer genomics laboratory at the National Institute of Genomic Medicine, known by its Spanish acronym INMEGEN. "That's exactly the point of doing this type of analysis. It gives you the opportunity to find those genes that you never thought would be involved in the breast cancer process."

The scientists studied two kinds of samples. They sequenced the whole exomes - the tiny fraction of the genome that encodes proteins of 103 breast cancer tumors and DNA from normal tissue from patients in Mexico and Vietnam. They also sequenced the entire genomes of 22 breast cancer tumors and matched normal tissue.

Their analysis confirmed the presence of previously known mutations, but it also turned up the unsuspected alterations.

"One of the lessons here is the real diversity of mutations in breast cancer. I think it's clear there are going to be roughly 50 or so different mutated genes in breast cancer," said Matthew Meyerson, co-senior author of the paper, Broad senior associate member, and professor of pathology at Dana-Farber Cancer Institute and Harvard Medical School. "There's a big diversity of driver genes in cancer. We don't understand what all of them are, but larger data sets will enable us to identify them."

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Breast cancer's many drivers

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Black History Month: Remarkable moments at the School of Medicine – Wayne State University

The art mural commemorating African American progress in the medical field in Detroit includes a portrait of Dr. Alexa Canady, far left, who was the first black woman neurosurgeon in the United States..

February is Black History Month in the United States. The Wayne State University School of Medicine has a storied history of African Americans students, faculty and graduates that dates back to a mere year after the medical school was founded.

Joseph Ferguson, M.D., graduated from what was then Detroit Medical College, in 1869. He became the first Black man in Detroit and most likely in Michigan to earn a medical degree.

Fast forward more than 150 years, and the school hit another milestone in 2019 the 50thanniversary of the Post-Baccalaureate Program, founded in 1969. It was the first of its kind in the nation. Initially launched to address the dearth of Black students entering medical schools, the free program immerses students into a year-long education in biochemistry, embryology, gross anatomy, histology and physiology. Many who graduated from the program were accepted into the WSU School of Medicine, but the program also served for several years as a major pipeline for Black students into medical schools across the nation. Today, the program accepts economically or educationally disadvantagedfirst-generation college students.

In between, the school continued to play a major role in addressing the physician workforce in America and bridging the gap in health disparities and health outcomes.

The WSU School of Medicine was founded in 1868 by four Civil War veteran physicians. At the same time, the first medical school in the county that was open to all people, Howard University Medical Department, opened in Washington, D.C., under the direction of Civil War veteran and Commissioner of the Freedmens Bureau, Gen. Oliver Howard. One year later, in 1869, the Detroit College of Medicine and Howard University graduated their first Black physicians.

Albert Henry Johnson, M.D., became the third Black graduate of the Detroit College of Medicine, in 1893. Dr. Johnson was one of the founders of Dunbar Hospital, the first Black non-profit hospital in Detroit.

In 1926, Chester Cole Ames, M.D., graduated from the Detroit College of Medicine and Surgery. He was the first Black physician to obtain an internship in Urology at a white hospital in Detroit, but he was never allowed to join the staff. Dr. Ames was Detroits first Black intern, resident and member of the Wayne University medical faculty. He cofounded three Black hospitals in Detroit, but was never granted privileges to practice his specialty in white hospitals.

Some 17 years later, Marjorie Peebles-Meyers, M.D., graduated from the Wayne University College of Medicine, the schools first Black female graduate. She was also the first Black female resident at Detroit Receiving Hospital, the first Black chief resident at Detroit Receiving Hospital, the first Black female appointed to the WSU medical faculty and the first Black female to join a private white medical practice in Detroit. After retiring, she began a second career as the first Black female medical officer at Ford Motor Co. World Headquarters. Dr. Peebles-Meyers received many awards and honors, including induction into the Michigan Womens Hall of Fame.

The same amount of time elapsed before physicians Thomas Flake Sr., M.D., Class of 1951; Addison Prince, M.D.; William Gibson, M.D.; and James Collins, M.D., were appointed to the staff at Harper Hospital, thereby integrating the Detroit Medical Center hospital staff.

Five years later, Charles Whitten, M.D.,became the first Black physician to head a department in a Detroit hospital when he was named clinical director of Pediatrics at Detroit Receiving Hospital. He was also a co-founder of the aforementioned Post-Baccalaureate Program.

In 1981, Alexa Canady, M.D., became the first Black woman neurosurgeon in the United States. Dr. Canady went on to serve as professor in the WSU Department of Neurosurgery. She was named one of the countrys most outstanding doctors by Child magazine in 2001.

Around 1988, two School of Medicine students Don Tynes, M.D. 95, and Carolyn King, M.D. 93, -- established Reach Out to Youth to introduce children 7 to 11 in underrepresented populations to the possibility of careers in science and medicine. Since then, the hands-on, workshop- and activity-focused program has been presented annually by the School of Medicines Black Medical Association, a chapter of the Student National Medical Association.

In 1995, Professor of Pediatrics and Sickle Cell Detection and Information Center Founder Charles Vincent, M.D., was appointed to the Membership Committee of the American Medical Association, making him the first Black doctor appointed to the committee after the AMAs founding 148 years earlier.

In 2017, Cheryl Gibson Fountain, M.D., FACOG, a 1987 graduate, was named president of the Michigan State Medical Society. The obstetrician/gynecologist served a one-year term as the societys first Black woman president.

In September 2022, members of the community and area churches came together with Wayne State University officials and students at the Wayne State University School of Medicine to celebrate a new outdoor mural commemorating African American progress in the medical field in Detroit. The mural, the product of a public humanities initiative to connect a multidisciplinary team of physicians, artists, students and activists with the broader community to celebrate the history of diversity in medicine and public health at WSU and in the city, was installed that June on the 375-foot-long public-facing concrete wall along the sidewalk north of Scott Hall, on the south side of Canfield Street.

In 2023, the School of Medicines End Race-Based Medicine Taskforce was launched to dispel and extinguish the misguided belief that individual races are biologically distinct groups determined by genes, and terminate medical practices and research that adhere to that concept. Co-created by Ijeoma Nnodim Opara, M.D., assistant professor of Internal Medicine and Pediatrics, and Latonya Riddle-Jones, M.D., M.P.H., assistant professor of Internal Medicine and Pediatrics, the taskforce includes representation from institutional leadership, students, residents, faculty, and community members and leaders, including those from the School of Medicine, Wayne Health, the Detroit Medical Center, the Barbara Ann Karmanos Cancer Institute, the Detroit Health Department and the Michigan State Medical Society.

Today, the push for further diversity, more inclusion and the elimination of health disparities continue to shape the future of the School of Medicine, from student-led efforts to longitudinal research projects dedicated to the health of Black Americans.

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Lessons in Chemistry book and TV show differences – Cosmopolitan UK

As much as bookworms want to hold onto their beloved original stories, bringing books to life visually on-screen is bound to bring about some changes. Bonnie Garmus's debut novel,

Now, the wildly popular New York Times bestseller is also a hit Apple TV+ miniseries starring (and co-produced by) the Brie Larson. And, yes, the show absolutely, 100%, without-a-doubt, does the book justice...and more! Even with all the changes in the storyline, it still exudes the same heart and great storytelling that Garmus was able to pull off with her written words. The TV adaptation also adds even more layers and nuance to the story by tweaking certain details, both big and small.

Warning! Spoilers ahead.

1. In the book: Elizabeth Zott is a chemist at the Hastings Research Institute, with her own lab technicians and a whole team working under her supervision. However, she is underestimated, mocked, and disrespected by her colleagues. This is because they see her as an overly-ambitious scientist, especially since she only has a Master's in Chemistry and not a PhD.

On the show: Though Elizabeth is clearly qualified to be a chemist, she is underemployed as a lab tech. Many of her male colleagues perceived her just as a pretty face and as a glorified secretary.

2. In the book: Calvin and Elizabeth have a fateful encounter, outside of work while outside a theatre. He got food poisoning after a date and accidentally throws up on her, and she winds up taking him home and caring for him.

On the show: This whole scene takes place at a Little Miss Hastings pageant held by their employer. Elizabeth is forced to participate in the pageant, which highlights the sexist demands of her job. But it also allows Calvin to take notice of her as the only unhappy contestant. As Elizabeth grabs her coat to make an early exit, she encounters Calvin, who then vomits on her due to an allergic reaction to Mrs. Donatti's perfume.

3. In the book: Readers meet Harriet Sloane much later in the book, as Elizabeth and Calvin's neighbour. She is an older white woman whose four grown children have already flown the coop, and is left at home with her sexist, abusive, alcoholic husband whom she doesn't love.

On the show: Harriet, played by none other than Aja Naomi King, is introduced early on in the series as a young Black woman whose husband is serving overseas in the Korean War. Aside from being a mother to two young kids, she also works as a legal aide, an environmentalist, and a civil rights activist. Her role in the series is much larger, and an important addition to the plot as it brings more diversity and injects a much-needed social commentary on race during that time.

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4. In the book: In her university days, Elizabeth was sexually assaulted by an old, sleazy professor named Dr. Meyers. He brutally attacks her one night when he finds her still working and running tests for his latest research project. She's able to stop her assailant by stabbing him with a pencil, but this leads to her losing her place in her programme after she refuses to offer a statement of regret.

On the show: Young Elizabeth was able to stop her assailant in the exact same way, with the same consequences. The difference is that in the series, it's someone she considers a friend and mentor who sexually assaults her. Dr. Bates a character invented for the show's purposes pushes himself on her despite her telling him that she doesn't see him that way.

5. In the book: Calvin proposes to Elizabeth at the Hastings cafeteria in front of all their colleagues. He does this, despite the fact that Elizabeth has expressed that she doesn't see herself getting married. She says no, and this leads to a big fight, which they eventually settle when they agree to move in together.

On the show: As their relationship progresses, Elizabeth makes it very clear to Calvin that she has no intention to get married or have kids. She explains that she wants to put her career first, and achieve all her ambitions. He accepts all of this without question.

6. In the book: Though Elizabeth doesn't want to have children, that doesn't mean she doesn't want to be a dog mum! After moving in together, she and Calvin agree that they want a dog in their lives. As it so happens, a dog follows Elizabeth home from a nearby deli. They wind up keeping him, and he gets a funny name after Elizabeth mishears Calvin. When he asks her what the pup's name is, she mishears him and reads the time: Six-Thirty.

On the show: Six-Thirty appears much earlier in the series. In the second episode, Elizabeth finds him sniffing around in her backyard by the trash cans. She takes pity on the poor pup and feeds him. It becomes clear that she's adopted her new furry friend when she brings him to Calvin's house. When he asks her what the dog's name is, she says it's Six-Thirty because of the time he wakes her up in the morning just like clockwork.

7. In the book: Elizabeth blames herself for Calvin's untimely death. She was the one who insisted that he be vigilant about keeping Six-Thirty on a leash whenever they went on runs together. Calvin took this seriously. But one night, during their walk, Six-Thirty gets frightened by a loud noise in front of a parking lot. He tries to run away from Calvin. Calvin then trips and hits his head. He then gets run over by a police car.

On the show: Six-Thirty hates his new leash, and is stubborn about running with it. It's the dog's behaviour that leads Calvin to be run over by a bus.

8. In the book: Another character who is majorly different in the books is Fran Frask, the head of personnel at Hastings. Fran is much more jealous and cruel in the novel, as she seems almost happy because of Elizabeth's misery. She delights in seeing her torn apart by grief. And when Fran finds out that Elizabeth is pregnant (before Elizabeth even realises it herself), she uses this to get her fired from Hastings.

But Fran gets a great character development arc, and eventually works for Calvin's friend, Reverend Wakely, as his secretary.

On the show: After Calvin's death, Fran is shown as someone who is much more sympathetic. From the very beginning, she is portrayed as much more caring than the character in the book. She doesn't get fired because Fran tells on her, but rather once it became apparent to her boss that she was unmarried and pregnant.

9. In the book: Elizabeth names her daughter Mad in a similar way as Six-Thirty. It was an accident! Elizabeth was exhausted, frustrated, and still grieving. With all the emotions running through her, she thought the nurse had asked her how she was feeling after labour. The nurse was actually asking for the baby's name. And, thus, Mad Zott it was.

On the show: After giving birth, the nurse told Elizabeth to name the baby after how she was feeling in the moment.

10. In the book: At a young age, it becomes clear that Mad is a brilliant kid who gets her smarts from her genius parents. But instead of encouraging her, Mad's teacher treats her awfully because of how smart she is.

On the show: Mad's teacher acknowledges that she doesn't belong at the school, and instead recommends her to a private school where she can truly thrive as a student.

11. In the book: Elizabeth takes the job for the cooking show Supper at Six after she felt she had no other great options financially. She had just quit Hastings (after she returned post-firing due to pregnancy) following an incident wherein Donatti stole her research. And she also felt guilty because one of Mad's classmates had told her they were poor.

On the show: Elizabeth needed the Supper at Six gig in order to pay for Mad's private school tuition.

12. In the book: Elizabeth refuses to endorse sponsorin a product she sees as vile and immoral for Supper at Six. She even goes as far as discouraging her audience from buying anything from the brand. Elizabeth's boss Phil intended to punish her for this, and attempts to sexually assault her. But she was prepared, threatening him by pulling out a kitchen knife from her bag. He suffers a heart attack and faints on the spot.

On the show: Elizabeth doesn't react as dramatically to the proposed sponsorship as she did in the book. Her refusal to endorse the product results in a three-day suspension during which Supper at Six plays reruns instead.

13. In the book: Reverend Wakely and Calvin became friends after a lecture Calvin gave at his university. They hit it off and became pen pals, talking about everything from the existence of God to their mundane lives. But their friendship ended abruptly when Calvin wrote that he wished his own father was dead. He was unaware that Reverend Wakely's father was critically ill at the time. But when Wakely learned of Calvin's death, he feels guilty, and decides to preach at his old friend's funeral.

On the show: Wakely and Calvin remained friends, and wrote to each other until the day he died.

14. In the book: Walter is the single father of Amanda, Mad's elementary school friend. His wife had left him, but he finds love once more with Harriet who ends up divorcing her husband.

On the show: The miniseries's version of Harriet is in a loving relationship with her soldier husband. It didn't make sense to give her and Walter, the TV producer who pitched Supper at Six, a love connection. But he does find love with Fran. The two confess their feelings for one another in the show's finale.

15. In the book: Elizabeth's happy ending is that she becomes the Head of Chemistry at Hastings replacing Donatti.

On the show: Elizabeth finds joy in her new role as a chemistry teacher.

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3 things the world’s oldest people regret, according to longevity researchers – IOL

As people journey through life, it is common for them to reflect on past decisions and actions, often leading to feelings of regret.

This phenomenon has intrigued researchers and psychologists for decades, and there is a growing understanding of the science behind why people experience regret as they grow older.

Regret can be defined as a negative emotion associated with a person's belief that they could have achieved a better outcome if they had chosen differently in the past.

It often arises from unmet expectations, perceived mistakes, or the feeling of wasted opportunities.

Anyone may experience regret about various facets of their lives, including relationships, career choices, educational pursuits, and personal achievements.

One of the key components of regret is memory, particularly the phenomenon of selective recall.

This selective recall can magnify the significance of missed opportunities or poor decisions, intensifying the emotional impact of regret.

According to Ben Meyers and Fabrizio Villatoro, researchers at LongeviQuest, an organisation that verifies the ages of supercentenarians (people who live to 110 or older) worldwide, the oldest individuals have shared their most common regrets.

Meyers, CEO of LongeviQuest, and Villatoro, Latin America research president, have had the opportunity to speak with these remarkable individuals, gathering insights on longevity and the things they wish they had done differently.

Meyers noted that many of the centenarians they spoke to had endured incredibly challenging lives, having lived through significant events such as war, the Great Depression, and decolonisation.

Despite this, he pointed out that their regrets were relatable and "pretty human", much like those of the general population.

Working too hard

One common regret expressed by centenarians was not spending enough time with family. Meyers described this as a "typical" regret among the supercentenarians they encountered.

Villatoro added that some regretted life's hardships and world events that disrupted their stability and prevented them from having more children.

Another regret that emerged was working too hard. Villatoro shared the story of Juan Vicente Prez Mora from Venezuela, the oldest validated person ever at the age of 114.

Quality time with loved ones

Mora had wished he had worked less, as he had dedicated his life to hard physical labour on his family's farm.

Villatoro explained that Mora's family had spoken about his regrets of not exploring different career paths, which would have allowed him to spend more time with his loved ones.

This sentiment resonates with findings from previous studies, which indicated that many individuals in hospice and palliative care also regretted prioritising work over family time.

Not travelling more

Not travelling more was another common regret expressed by centenarians. For instance, Evangelista Luisa Lpez, who grew up in Santa Fe province, Argentina, and later moved to Mar del Plata, wished she had travelled more throughout her life.

This sentiment aligns with the findings of Karl Pillemer, a professor of gerontology in medicine at Weill Cornell Medicine.

In his book "30 Lessons for Loving: Advice from the Wisest Americans on Love, Relationships, and Marriage", Pillemer highlighted that older Americans also regretted not having travelled more, particularly during their younger years.

Despite the intrinsic challenges associated with regret, ageing also offers the potential for wisdom and self-reflection.

Coping with regret can be a challenging and emotionally taxing experience. However, there are several effective coping mechanisms that individuals can employ to navigate and manage feelings of regret.

Coping strategies

Understanding and implementing these coping strategies can help individuals cultivate resilience, promote self-growth, and ultimately move forward in a constructive and empowered manner.

Reflecting on experiences

Thinking about past experiences can help you see regret as a way to learn and grow, rather than just something negative.

Being kind to yourself

Treating yourself with kindness and understanding, especially when facing challenges or regret, can help you acknowledge mistakes without being too hard on yourself. This can build resilience and improve how you see yourself.

Embracing mindfulness and acceptance

Practising mindfulness, like meditation and deep breathing, can help you stay present and be aware of your thoughts and emotions without being judgmental.

Set realistic expectations

Recognising and managing your expectations is important when dealing with regret. Having realistic expectations and letting go of perfectionism can ease the weight of regret and strengthen your self-acceptance and emotional strength.

Doing things that matter

Getting involved in activities that bring joy and fulfilment can help manage regret. Hobbies, volunteering, or creative pursuits can boost your self-worth and shift your focus to positive experiences and personal growth.

Get help from a professional

If regret affects your mental well-being, talking to a therapist or counsellor can offer valuable support and guidance. Professional interventions like cognitive-behavioural therapy can provide effective strategies to deal with regret and its emotional impact.

Talking to friends, family, or others in your support network can give you comfort, different perspectives, and valuable insights. Sharing your feelings can offer understanding and help you heal.

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3 things the world's oldest people regret, according to longevity researchers - IOL

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