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Study reveals how mutant p53 protein converts other proteins into cancer drivers (Heparin helps)
Medical Xpress / Instituto Nacional de Ciência e Tecnologia / Communications Chemistry ^ | Sept. 16, 2024 | Elaine C. Petronilho et al

Posted on 09/20/2024 4:56:11 PM PDT by ConservativeMind

Research from has uncovered a critical mechanism by which mutations in the p53 protein—a key tumor suppressor known as the "guardian of the genome"—turn other proteins into cancer-promoting agents.

The study, led by Dr. Jerson Lima Silva, offers fresh insights into a process that plays a pivotal role in the development and progression of many cancers.

p53 is central to the body's defense against cancer, tasked with regulating the cell cycle and triggering the death of damaged cells before they can become malignant. However, in more than 50% of all tumors, mutations in p53 undermine its protective role, converting it into a driver of cancer. In this study, the research team demonstrated that mutant p53 not only loses its tumor-suppressing abilities but also gains the capacity to corrupt other anti-tumor proteins, including p63 and p73.

Through a mechanism known as aberrant phase transition, mutant p53 induces amyloid aggregation in p63 and p73, forming harmful protein clumps known as amyloid structures. These aggregates drive the oncogenic transformation of these proteins, leading to uncontrolled tumor growth.

These findings provide critical new insights into why some tumors, such as glioblastoma, are so aggressive.

"This discovery could be key to designing therapies for aggressive cancers, including glioblastoma, where mutant p53 plays a dominant role," said Dr. Silva.

Using advanced biophysical techniques and fluorescence microscopy, the team investigated three specific p53 mutations: glioblastoma; liver cancer; and breast cancer. They found that each of these mutants not only altered the behavior of p53 but also triggered p63 and p73 to form amyloid-like structures, further driving cancer progression.

Excitingly, the research also revealed that heparin, a widely used anticoagulant, can inhibit the formation of these harmful aggregates. This suggests a potential therapeutic approach to either prevent or reverse the malignancy-enhancing effects of mutant p53.

(Excerpt) Read more at medicalxpress.com ...


TOPICS: Health/Medicine
KEYWORDS: amyloid; cancer; cancerprotein; glioblastoma; medicalxpress; p53; protein; tumor
Heparin appears to inhibit the creation of these amyloid issues from defective p53, p63, and p73 proteins.

Heparin is a common anticoagulant.

1 posted on 09/20/2024 4:56:11 PM PDT by ConservativeMind
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To: Mazey; ckilmer; goodnesswins; Jane Long; BusterDog; jy8z; ProtectOurFreedom; matthew fuller; ...

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2 posted on 09/20/2024 4:57:01 PM PDT by ConservativeMind (Trump: Befuddling Democrats, Republicans, and the Media for the benefit of the US and all mankind.)
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To: ConservativeMind

Had hep injections when I was so sick in hospital. Into the tummy. Slight sting but totally bearable.


3 posted on 09/20/2024 5:02:33 PM PDT by RushIsMyTeddyBear (Nessun Dorma.)
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To: ConservativeMind

p53 is critical. It’s the tumor suppressor. If p53 is screwed up then the outlook is very grim.


4 posted on 09/20/2024 5:04:02 PM PDT by libh8er
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To: ConservativeMind

Heparin doesn’t go in to cells, generally.

This is in vitro.

They expressed the various p53 isoforms with his tags in bacteria and used the enriched fractions for their in vitro studies.


5 posted on 09/20/2024 5:31:37 PM PDT by ifinnegan (Democrats kill babies and harvest their organs to sell)
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