Angel, who is the leader of the GoodNews Church (Spirit Embassy), reportedly accuses Java of extortion and blackmail.

Java was married to late opposition MP and former prime minister Morgan Tsvangirai’s daughter Vimbai, who died following a car accident in 2019.

Batsirai Java is a brother to another Mnangagwa and ZANU PF apologist and self-proclaimed prophet Panganai “Passion” Java.

Last month, Java’s security aide Nigel Dutiro approached the police about the alleged South African assassins.

Dutiro confirmed to The Standard that he made the report under RRB number 141472. He said:

It’s true. I made a police report because there was a threat to life.

Dutiro, however, said he could not reveal more details about the report because the matter was now being handled by the police.

The alleged murder plot was exposed by a woman identified as Sharon Munro, who is said to be based in South Africa.

Munro was allegedly in Zimbabwe on March 31 where she was overhead by patrons at an upmarket bar in Borrowdale, Harare, talking about the alleged plot against Java.

She left the country on April 3 via the Robert Mugabe International Airport.

The Standard reported sources as saying the alleged murder plot was supposed to involve two South Africans only identified as Mkhwananzi and Ndimande.

The alleged hitman entered Zimbabwe through Beitbridge and were later transported as far as Harare.

The South Africans returned home without accomplishing the task after the woman allegedly linked to Angel leaked the details of the plot.

Java was last Sunday summoned by the police as part of the investigations. He said:

l am aware that someone from my church has made a report to the police, and we are waiting for investigations.

Zimbabwe Republic Police (ZRP) spokesperson Assistant Commissioner Paul Nyathi said he was yet to get a briefing from Harare police where the matter was reported.

The person who picked up Munro’s phone reportedly said she had no idea what the publication was enquiring about when asked for a comment. She later posted the same questions on her WhatsApp status.

Angel did not respond to questions sent to him by The Standard two weeks ago.

Early last year, Angel was at the centre of a documentary by Al Jazeera’s Investigative Unit called “Gold Mafia” that exposed illicit gold trade and money laundering by powerful figures in Zimbabwe and the southern African region.

Angel was secretly recorded telling undercover journalists that he could facilitate the smuggling of gold and launder millions of cash by abusing his diplomatic privileges.

More: Pindula News

Working with human breast and lung cells, Johns Hopkins Medicine scientists say they have charted a molecular pathway that can lure cells down a hazardous path of duplicating their genome too many times, a hallmark of cancer cells.

The findings, published May 3 in Science, reveal what goes wrong when a group of molecules and enzymes trigger and regulate what’s known as the “cell cycle,” the repetitive process of making new cells out of the cells’ genetic material.

The findings could be used to develop therapies that interrupt snags in the cell cycle, and have the potential to stop the growth of cancers, the researchers suggest.

To replicate, cells follow an orderly routine that begins with making a copy of their entire genome, followed by separating the genome copies, and finally, dividing the replicated DNA evenly into two “daughter” cells.

Human cells have 23 pairs of each chromosome — half from the mother and half from the father, including the sex chromosomes X and Y — or 46 total, but cancer cells are known to go through an intermediate state that has double that number – 92 chromosomes. How this happens was a mystery.

“An enduring question among scientists in the cancer field is: How do cancer cell genomes get so bad?” says Sergi Regot, Ph.D., associate professor of molecular biology and genetics at the Johns Hopkins University School of Medicine. “Our study challenges the fundamental knowledge of the cell cycle and makes us reevaluate our ideas about how the cycle is regulated.”

Regot says cells that are stressed after copying the genome can enter a dormant, or senescent stage, and mistakenly run the risk of copying their genome again.

Generally and eventually, these dormant cells are swept away by the immune system after they are “recognized” as faulty. However, there are times, especially as humans age, when the immune system can’t clear the cells. Left alone to meander in the body, the abnormal cells can replicate their genome again, shuffle the chromosomes at the next division, and a growing cancer begins.

In an effort to pin down details of the molecular pathway that goes awry in the cell cycle, Regot and graduate research assistant Connor McKenney, who led the Johns Hopkins team, focused on human cells that line breast ducts and lung tissue. The reason: These cells generally divide at a more rapid pace than other cells in the body, increasing the opportunities to visualize the cell cycle.

Regot’s lab specializes in imaging individual cells, making it especially suited to spot the very small percentage of cells that don’t enter the dormant stage and continue replicating their genome.

For this new study, the team scrutinized thousands of images of single cells as they went through cell division. The researchers developed glowing biosensors to tag cellular enzymes called cyclin dependent kinases (CDKs), known for their role in regulating the cell cycle.

They saw that a variety of CDKs activated at different times during the cell cycle. After the cells were exposed to an environmental stressor, such as a drug that disrupts protein production, UV radiation or so-called osmotic stress (a sudden change in water pressure around cells), the researchers saw that CDK 4 and CDK 6 activity decreased.

Then, five to six hours later, when the cells started preparations to divide, CDK 2 was also inhibited. At that point, a protein complex called the anaphase promoting complex (APC) was activated during the phase just before the cell pulls apart and divides, a step called mitosis.

“In the stressed environment in the study, APC activation occurred before mitosis, when it’s usually been known to activate only during mitosis,” says Regot.

About 90% of breast and lung cells leave the cell cycle and enter a quiet state when exposed to any environmental stressors.

In their experimental cells, not all of the cells went quiet.

The research team watched as about 5% to 10% of the breast and lung cells returned to the cell cycle, dividing their chromosomes again.

Through another series of experiments, the team linked an increase in activity of so-called stress activated protein kinases to the small percentage of cells that skirt the quiet stage and continue to double their genome.

Regot says there are ongoing clinical trials testing DNA-damaging agents with drugs that block CDK. “It’s possible that the combination of drugs may spur some cancer cells to duplicate their genome twice and generate the heterogeneity that ultimately confers drug resistance,” says Regot.

“There may be drugs that can block APC from activating before mitosis to prevent cancer cells from replicating their genome twice and prevent tumor stage progression,” says Regot.

Reference: McKenney C, Lendner Y, Guerrero Zuniga A, et al. CDK4/6 activity is required during G2 arrest to prevent stress-induced endoreplication. Science. 2024;384(6695):eadi2421. doi: 10.1126/science.adi2421

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