Contagious Blood Cancer Spreads Among Clam Species
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A contagious blood cancer jumped from one species of clam to another and spread among clams living in the Atlantic Ocean and Mediterranean Sea, shows a study published today in eLife.
The findings add to evidence that cancers may spread among different species of bivalve shellfish and suggest that human activities may be inadvertently contributing to the spread of these cancers to new locations and species.
Contagious cancers have been identified in dogs, Tasmanian devils, and bivalves such as clams and mussels. These diseases usually spread among individuals of the same species. But previous studies have documented at least two cases of contagious cancers spreading among bivalve species.
“We set out to confirm whether a leukemia-like blood cancer found in some bivalves also infects Venus verrucosa, otherwise known as warty venus clams that are found in the seas of southern Europe,” says Daniel García-Souto, a postdoctoral researcher in genetics at the University of Santiago de Compostela - USC, Galicia, Spain, and a co-first author of the study alongside Alicia Bruzos and Seila Diaz at USC.
The researchers collected 345 warty venus clams from the coastal areas of Spain, Portugal, France, Ireland and Croatia. They found a type of blood cancer called hemic neoplasia in warty venus clams collected from two different coastal regions of Spain. One group of infected clams was found along the country’s Atlantic coast, while the other group was found more than 1,000 nautical miles away in the Mediterranean Sea.
The team used a technique called whole-genome sequencing to reveal that the cancer originated in a single clam, later became infectious, and spread among warty venus clams. The cancer contained genetic sequences from both the warty venus clam and another unknown species of clam. By comparing the unknown genetic sequence to a genetic database of bivalve species, the researchers were able to identify the mystery clam as Chamelea gallina, or the striped venus clam.
Further testing of DNA taken from the cell mitochondria and nucleus in both clam species confirmed that the cancer had jumped from the striped venus clam to the warty venus clams.
“The genetic similarity of the cancer cells found in warty venus clams in both the Atlantic Ocean and Mediterranean Sea suggests that human shipping activities may have transported the cancer from one region to another,” says co-first author Alicia Bruzos, who was a Researcher PhD Student at USC at the time the study was carried out, and is now at the Francis Crick Institute in London, UK. This idea is supported by a previous study in eLife* which showed that mussels carried a contagious cancer across the Atlantic by hitching a ride on ships.
The team now hopes to carry out further studies to determine the age of the tumours in their clam specimens and to explore for how long cancer may have been spreading among these species.
“Our work confirms that contagious cancers can jump between marine clam species,” concludes senior author José Tubío, Researcher in Genomes and Disease at USC. “As this may pose a potential threat to marine ecology, we need to keep studying and monitoring pathogens including cancers to help protect these species.”
Reference: Garcia-Souto D, Bruzos AL, Diaz S, et al. Mitochondrial genome sequencing of marine leukaemias reveals cancer contagion between clam species in the Seas of Southern Europe. eLife. 2022;11:e66946. doi: 10.7554/eLife.66946
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Comedian Louie Anderson Hospitalized for Blood Cancer Treatment: Reports
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The Baskets star was diagnosed with diffuse large B-cell lymphoma, the most common type of non-Hodgkin lymphoma
Comedian Louie Anderson is undergoing treatments for blood cancer, according to multiple reports.
The Baskets star, 68, was diagnosed with diffuse large B-cell lymphoma, the most common type of non-Hodgkin lymphoma, and is currently getting treated at a Las Vegas hospital, his rep confirmed to Rolling Stone.
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“Iconic comedian Louie Anderson is currently in a Las Vegas hospital being treated for diffuse large B cell lymphoma, a form of cancer,” Glenn Schwartz, told the outlet in a statement. “He is resting comfortably.”
PEOPLE has reached out for further comment.
According to the Lymphoma Research Foundation, more than 18,000 people in the U.S. are diagnosed with diffuse large B-cell lymphoma (DLBCL) a year. And “despite being an aggressive lymphoma, DLBCL is considered potentially curable.”
Anderson has previously dealt with heart problems, and in 2003 underwent two procedures to correct an unspecified issue.
Last March, Anderson shared that he’s been working on losing weight, and has lost around 40 lbs. during the COVID-19 pandemic.
“I started the pandemic at about 370 or 380 pounds depending on what I was leaning on,” Anderson joked to host Conan O’Brien during an appearance on Conan on Tuesday. “And now I’m 340. I’m trying to get 275 so I can get into some of my mom’s actual clothes,” he added, referring to his female character on Baskets.
RELATED VIDEO: Louie Anderson ‘Knew It Was Right’ to Play a Woman on ‘Baskets’
Anderson said he’s been doing intermittent fasting, though he also poked fun at the weight loss strategy.
“I’m on the intermittent fast. One minute I’m eating, the next minute I’m not. Then I’m eating again. I figure, that way, I’m only eating for 30 minutes out of 60, which is half. I’m trying to get down to 40/20 so I’m not eating for 40 and eating for 20.”
Anderson first talked about losing weight for his health in 2018, when he opened up about growing up in a housing project as one of 11 children of an alcoholic father, and how he used food for protection.
Therapy offers hope to patients with recurring blood cancers
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Through a partnership with the Moffitt Malignant Hematology and Cell Therapy Clinic, a South Florida resident was qualified as a candidate for a therapy called CAR-T.
PEMBROKE PINES, Fla. – Large B-cell lymphoma is a fast-growing and aggressive form of blood cancer and now a recently approved therapy is offering hope to patients whose cancer returns after standard treatment.
Leticia Lopez was a healthy woman with no medical issues until 2007.
“That’s when it started with this headache, journey whatever you want to call it,” she said.
Lopez was diagnosed with Large-B-Cell Lymphoma, the most common of the Non-Hodgkin’s form of blood cancers, and began standard of care treatment.
“About 60% of patients can be cured with that line of therapy however the problem is when the disease comes back,” said Dr. Jose Sandoval-Sus, a hematologist-oncologist with Memorial Healthcare’s Memorial Hospital West Cancer Center.
When that happened to Lopez, Sandoval-Sus gave her hope.
Through a partnership with the Moffitt Malignant Hematology and Cell Therapy Clinic, Lopez was qualified as a candidate for a therapy called CAR-T.
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Special T-cells are removed, modified in a lab, then implanted back in the patient.
“And as the cells grow, they actually grow very fast inside of the body, and then they kill cancer. We can offer it to a larger group of patients that are actually in dire need sometimes of this treatment,” Sandoval-Sus said.
Lopez underwent the procedure in September 2021.
Follow-up scans have shown no signs of the disease, leaving her feeling almost like nothing ever happened.
“Ta-da! Great!,” she said with a laugh.
CAR-T therapy has also become a breakthrough for patients with relapsed leukemia and multiple myeloma.
New blood cancer gene defect can be treated with existing drugs
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Newswise — A defective gene, normally found in blood cancers, could be treated with drugs already available for cancers with similar gene defects, scientists at Queen’s University Belfast and the University of Birmingham have revealed.
The research team, funded mainly by Cancer Research UK and the Medical Research Council, found that tumours with mutations in the SF3B1 gene respond to PARP inhibitors, a type of drug used to treat cancers which have similar mutations in the BRCA1 and BRCA2 genes.
The researchers believe that PARP inhibitors could be used to treat patients with tumours carrying the defective SF3B1 gene. This mutation is most often found in blood cancers, including chronic lymphocytic leukaemia, as well as some rare cancers like uveal melanoma.
Dr Kienan Savage, lead author and Reader at the Patrick G Johnson Centre for Cancer Research at Queen’s, said: “Our findings have clinical implications for the treatment of many cancers. We specifically focused on this genetic mutation as it is found in several difficult to treat leukaemias and other cancers, and it affects so many cancer patients. By deepening our understanding of this gene mutation, we have identified new ways of treating these cancers that could improve survival rates.”
PARP inhibitors, which include olaparib and rucaparib, are used to treat some patients with ovarian, breast, prostate and pancreatic cancers – usually patients who have inherited a faulty BRCA1 or BRCA2 gene. Around 1 in 400 people have a faulty BRCA1 or BRCA2 gene.
The research, published today in Cancer Research, a journal of the American Association for Cancer Research, found that the SF3B1 mutation produces similar effects to the faulty BRCA1 gene by damaging DNA, preventing it from being repaired properly, and stopping it from making normal copies of itself. PARP inhibitors target the cell’s DNA repair tools by locking them in place on the DNA. This stops DNA repair, causing the cancer cells to die.
The scientists found that cancer cells with the SF3B1 mutation were sensitive to olaparib, the most common PARP inhibitor, some specific chemotherapies and to radiotherapy. The scientists believe that the SF3B1 mutation disrupts the cell’s ability to make DNA repair proteins, leaving it vulnerable to drugs which target these proteins.
The SF3B1 mutation occurs in up to 30% of blood cancers called myelodysplastic syndromes, where blood cells don’t form properly. They are difficult to treat as they occur predominantly in older patients who may not be considered fit for treatment. The mutation is also common among uveal melanoma or cancers of the eye, which currently have limited treatment options.
Dr Katrina Lappin, from Queen’s and first author of the study, added: “Our research shows that cancers with these specific mutations, may be treated effectively with PARP inhibitor therapy drugs, which are less toxic, better at killing cancer cells with these mutations and can be taken at home in tablet form. This could have huge implications for improving outcomes and quality of life of people with these cancers.”
“This work will pave the way for clinical trials using PARP inhibitors for the treatment of patients with this commonly associated cancer mutation, allowing a more personalised approach to the treatment of these cancers.”
The researchers now want to test PARP inhibitors in clinical trials with patients who have the SF3B1 mutation to see if they can stop their cancer from spreading.
Co-author Professor Grant Stewart, of the University of Birmingham, said: “Our work demonstrates that a molecular understanding of how a specific gene mutation affects a cancer cell’s ability to repair damaged DNA can be exploited clinically to specifically tailor the anti-cancer therapy used to treat an individual’s tumour. This will increase the effectiveness of the therapy and hopefully, reduce the chances of re-occurrence.”
Michelle Mitchell, Chief Executive of Cancer Research UK, said: “Our scientists helped to discover the BRCA gene over 25 years ago and since then we’ve led the way in developing PARP inhibitors to treat cancers with BRCA gene faults.
“It’s really exciting to hear about a new mutation, which behaves like the BRCA1 mutation and could in the future be treated in the same way. With PARP inhibitors already widely available, there is huge potential to help people with some of the rarest and most difficult-to-treat cancers known to us.
“Over the past two decades, PARP inhibitors have saved thousands of lives worldwide, and it will be interesting to see if this research in the future could lead to a similar impact for people with rarer cancers.”
The research was funded by the UK Medical Research Council, Cancer Research UK, Blood Cancer UK, Leukaemia and Lymphoma NI and Great Ormond Street Hospital Children’s Charity.
CASI’s partner Juventas’ CNCT19 for blood cancer gets FDA orphan drug status
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