neutrinos nobel prize

Neutrinos and the Nobel Prize

Neutrino experiments are difficult and often ground-breaking. In (sometimes long-delayed) recognition of this, a number of pioneers of neutrino physics have been awarded the Nobel Prize for Physics.

1988	Leon Lederman, Melvin Schwartz, Jack Steinberger	for the neutrino beam method and the demonstration of the doublet structure of the leptons through the discovery of the muon neutrino
1995	Frederick Reines	for the detection of the neutrino
2002	Raymond Davis and Masatoshi Koshiba	for pioneering contributions to astrophysics, in particular for the detection of cosmic neutrinos

In addition, Wolfgang Pauli (1945), Enrico Fermi (1938), and Lee and Yang (1957), who made major contributions to neutrino theory, won the Nobel Prize for work not directly connected with neutrinos. Clyde Cowan did not share in the belated prize for the discovery of the neutrino because Nobel prizes are not awarded posthumously.

The Nobel Prize in Physics 2015

The Nobel Prize in Physics 2015

The Nobel Prize in Physics 2015 was awarded jointly to Takaaki Kajita and Arthur B. McDonald "for the discovery of neutrino oscillations, which shows that neutrinos have mass"

Photo © Takaaki Kajita

Takaaki Kajita

Prize share: 1/2

Photo: K. MacFarlane. Queen's University /SNOLAB

Arthur B. McDonald

Prize share: 1/2

Our own genes can block HIV

                              Our own genes can block HIV

       Two groups of researchers at the University of Massachusetts Medical School say a powerful weapon against the AIDS virus may exist in the unlikeliest of places — in our own genes.

The studies, published online yesterday in the journal Nature, found that two genes can block HIV from spreading to other cells, which researchers in the HIV/AIDS field say could open the door to promising new treatments and could even pave the way for a cure.

Two groups of UMass Medical researchers used different methods in each study, but came to the same conclusion: the SERINC5 and SERINC3 genes can shut down the virus, stopping its spread and rendering it inactive.

But a component of the virus — the protein Nef — counteracts the SERINCs inhibiting powers, which is why those genes don’t prevent people from contracting the virus.

The finding, though, could very well lead to treatments that weaken the damaging protein and allow the virus-fighting genes to fend off illness, researchers say.

“Nef is a gene that HIV evolved largely to overcome this anti-viral factor that our cells make,” said Dr. Jeremy Luban, professor of molecular medicine at UMass Medical, an investigator in one of the studies.

“The hope is that there will be 
a way to intervene, perhaps by developing a new drug that 
allows the SERINCs to escape from Nef,” Luban said.

Ideally, the discoveries will lead to the development of treatments in the next five years, though it 
is difficult to estimate, Luban said.

The research, funded primarily by the National Institutes of Health, was done in collaboration with scientists at the Univer-
sity of Trento in Italy and the University of Geneva in Switzerland.

The discovery coincides with new HIV guidelines issued yesterday by the World Health Organization, increasing the number of those infected or at risk who should seek virus-inhibiting therapy by 9 million.

“Advancing science is a critical part of what needs to happen,” said Dr. Carlos Del Rio, chairman-elect of the HIV Medicine Association.

“Gene therapy advances for HIV are very exciting. They could lead to treatments that can cure HIV,” Del Rio said.

Though there are more than 30 of these therapies available, they can cause a range of side effects, from skin rashes and nightmares to weakened bones and cardiovascular disease, according to 
Dr. Daniel Kuritzkes, chief of 
Infectious Diseases at Brigham and Women’s Hospital.

“Not everyone tolerates the currently available regimen equally well,” Kuritzkes said.

“We still need to keep looking for new and improved treatments.”

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Cell Division and Cancer

Cancer cells are cells gone wrong — in other words, they no longer respond to many of the signals that control cellular growth and death. Cancer cells originate within tissues and, as they grow and divide, they diverge ever further from normalcy. Over time, these cells become increasingly resistant to the controls that maintain normal tissue — and as a result, they divide more rapidly than their progenitors and become less dependent on signals from other cells. Cancer cells even evade programmed cell death, despite the fact that their multiple abnormalities would normally make them prime targets for apoptosis. In the late stages of cancer, cells break through normal tissue boundaries and metastasize (spread) to new sites in the body.

How Do Cancer Cells Differ from Normal Cells?

In normal cells, hundreds of genes intricately control the process of cell division. Normal growth requires a balance between the activity of those genes that promote cell proliferation and those that suppress it. It also relies on the activities of genes that signal when damaged cells should undergo apoptosis.

Cells become cancerous after mutations accumulate in the various genes that control cell proliferation. According to research findings from the Cancer Genome Project, most cancer cells possess 60 or more mutations. The challenge for medical researchers is to identify which of these mutations are responsible for particular kinds of cancer. This process is akin to searching for the proverbial needle in a haystack, because many of the mutations present in these cells have little to nothing to do with cancer growth.

Different kinds of cancers have different mutational signatures. However, scientific comparison of multiple tumor types has revealed that certain genes are mutated in cancer cells more often than others. For instance, growth-promoting genes, such as the gene for the signaling protein Ras, are among those most commonly mutated in cancer cells, becoming super-active and producing cells that are too strongly stimulated by growth receptors. Some chemotherapy drugs work to counteract these mutations by blocking the action of growth-signaling proteins. The breast cancer drug Herceptin, for example, blocks overactive receptor tyrosine kinases (RTKs), and the drug Gleevec blocks a mutant signaling kinase associated with chronic myelogenous leukemia.

Other cancer-related mutations inactivate the genes that suppress cell proliferation or those that signal the need for apoptosis. These genes, known as tumor suppressor genes, normally function like brakes on proliferation, and both copies within a cell must be mutated in order for uncontrolled division to occur. For example, many cancer cells carry two mutant copies of the gene that codes for p53, a multifunctional protein that normally senses DNA damage and acts as a transcription factor for checkpoint control genes.