Author Topic: Lek protiv Raka i...nikom nista?  (Read 7875 times)

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zakk

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Why shouldn't things be largely absurd, futile, and transitory? They are so, and we are so, and they and we go very well together.

scallop

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Re: Lek protiv Raka i...nikom nista?
« Reply #2 on: 17-12-2012, 15:56:07 »
Proveriću još danas sa Jelenom i Caletom, pa javljam.
Never argue with stupid people, they will drag you down to their level and then beat you with experience. - Mark Twain.

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Re: Lek protiv Raka i...nikom nista?
« Reply #3 on: 17-12-2012, 20:43:17 »
Hm, a ko može da potvrdi da ovo nije još jedna patka?


Ghoul

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Re: Lek protiv Raka i...nikom nista?
« Reply #5 on: 17-12-2012, 23:22:24 »
a šta ako su u šumi?!

zakk

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Why shouldn't things be largely absurd, futile, and transitory? They are so, and we are so, and they and we go very well together.

Meho Krljic

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Re: Lek protiv Raka i...nikom nista?
« Reply #7 on: 23-08-2013, 14:36:41 »
Nego, lek za rak nije pronađen, ali za lenjost, izgleda da su na dobrom putu. Dobro, ne lek za lenjost, ali lek koji otklanja posledice lenjosti  :lol:

www.scripps.edu/newsandviews/e_20130729/burris.html

Quote

Drug Candidate Leads to Improved Endurance   By Eric Sauter
 
An international group of scientists has shown that a drug candidate designed by scientists from the Florida campus of The Scripps Research Institute (TSRI) significantly increases exercise endurance in animal models.
These findings could lead to new approaches to helping people with conditions that acutely limit exercise tolerance, such as obesity, chronic obstructive pulmonary disease (COPD) and congestive heart failure, as well as the decline of muscle capacity associated with aging.
The study was published July 14, 2013, by the journal Nature Medicine.
The drug candidate, SR9009, is one of a pair of compounds developed in the laboratory of TSRI Professor Thomas Burris and described in a March 2012 issue of the journal Nature as reducing obesity in animal models. The compounds affect the core biological clock, which synchronizes the rhythm of the body’s activity with the 24-hour cycle of day and night.
The compounds work by binding to one of the body’s natural molecules called Rev-erbα, which influences lipid and glucose metabolism in the liver, the production of fat-storing cells and the response of macrophages (cells that remove dying or dead cells) during inflammation.
In the new study, a team led by scientists at the Institut Pasteur de Lille in France demonstrated that mice lacking Rev-erbα had decreased skeletal muscle metabolic activity and running capacity. Burris’ group showed that activation of Rev-erbα with SR9009 led to increased metabolic activity in skeletal muscle in both culture and in mice. The treated mice had a 50 percent increase in running capacity, measured by both time and distance.“The animals actually get muscles like an athlete who has been training,” said Burris. “The pattern of gene expression after treatment with SR9009 is that of an oxidative-type muscle— again, just like an athlete.”
The authors of the new study suggest that Rev-erbα affects muscle cells by promoting both the creation of new mitochondria (often referred to as the “power plants” of the cell) and the clearance of those mitochondria that are defective.
The study, “Rev-Erbα Modulates Skeletal Muscle Oxidative Capacity by Regulating Mitochondrial Biogenesis and Autophagy” was led by Estelle Woldt and Yasmine Sebti (first authors) and Bart Staels and Hélène Duez (senior authors) of Institut Pasteur de Lille, France. Other contributors include Christian Duhem, Jérôme Eeckhoute, Charlotte Paquet, Stéphane Delhaye and Philippe Lefebvre of Institut Pasteur de Lille, France; Laura Solt, Youseung Shin, Thomas Burris and Theodore M. Kamenecka of TSRI; Steve Lancel and Rémi Nevière of Université Lille Nord de France; and Matthijs K.C. Hesselink, Gert Schaart and Patrick Schrauwen of Maastricht University Medical Center, Maastricht, the Netherlands. For further information, see http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.3213.html

The study was supported by a Marie Curie International Reintegration Grant (FP7), the European Commission (FP7) consortium Eurhythdia, Région Nord Pas-de-Calais/FEDER, a CPER “starting grant,” the European Genomic Institute for Diabetes (ANR-10-LABX-46), an unrestricted ITMO/Astra Zeneca grant, a joint Société Francophone du Diabète MSD research fellowship, Research Grant from the European Foundation for the Study of Diabetes, National Institutes of Health grant (MH093429 and DK080201) and a VICI Research grant for innovative research from the Netherlands Organization for Scientific Research (918.96.618).

FAK JEA!!!! Zgutam pilulu i to je isto ko da sam radio sklekove i trčao čuku vremena!! Pa to čekamo celog života!!!

Meho Krljic

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Re: Lek protiv Raka i...nikom nista?
« Reply #8 on: 03-09-2013, 09:50:00 »
Dakle, naučnici američkog nacionalnog zavoda za srce i pluća su otkrili da ako čačkaju po jednom jedinom genu kod miševa, mogu da im produže životni vek za oko 20 procenata. Ne samo da mišonje duže požive nego su im i pod stare dane pamćenje i ravnoteža bolji. Avaj, kosti su im lošije a i imunosistem je slabiji, pa nisam siguran da je trejdof vredan.

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Meho Krljic

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Re: Lek protiv Raka i...nikom nista?
« Reply #10 on: 11-09-2013, 09:26:38 »
Gore sam pominjao produženje života kod miševa za 20 procenata, ali to nije ništa u odnosu na produženje života kod... er... kvasca za pedeset posto. Tim genetičara sa Novog zelanda i iz Japana je čačkao ribozomalnu DNK i produžio kvascu život za pola. Zvuči suludo ali navodno ljudski i kvaščani geni su u ovom domenu dosta slični i može se špekulisati da bi ovo moglo da dovede do kreacije "leka" za starenje kod ljudi.

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zakk

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Re: Lek protiv Raka i...nikom nista?
« Reply #12 on: 12-09-2013, 13:26:50 »
http://www.sciencedaily.com/releases/2013/09/130911141746.htm



AIDS Vaccine Candidate Appears to Completely Clear Virus from the Body in Monkeys


Sep. 11, 2013 — An HIV/AIDS vaccine candidate developed by researchers at Oregon Health & Science University appears to have the ability to completely clear an AIDS-causing virus from the body. The promising vaccine candidate is being developed at OHSU's Vaccine and Gene Therapy Institute. It is being tested through the use of a non-human primate form of HIV, called simian immunodeficiency virus, or SIV, which causes AIDS in monkeys. Following further development, it is hoped an HIV-form of the vaccine candidate can soon be tested in humans.

These research results were published online today by the journal Nature. The results will also appear in a future print version of the publication.
"To date, HIV infection has only been cured in a very small number of highly-publicized but unusual clinical cases in which HIV-infected individuals were treated with anti-viral medicines very early after the onset of infection or received a stem cell transplant to combat cancer," said Louis Picker, M.D., associate director of the OHSU Vaccine and Gene Therapy Institute. "This latest research suggests that certain immune responses elicited by a new vaccine may also have the ability to completely remove HIV from the body."
The Picker lab's approach involves the use of cytomegalovirus, or CMV, a common virus already carried by a large percentage of the population. In short, the researchers discovered that pairing CMV with SIV had a unique effect. They found that a modified version of CMV engineered to express SIV proteins generates and indefinitely maintains so-called "effector memory" T-cells that are capable of searching out and destroying SIV-infected cells.
T-cells are a key component of the body's immune system, which fights off disease, but T-cells elicited by conventional vaccines of SIV itself are not able to eliminate the virus. The SIV-specific T-cells elicited by the modified CMV were different. About 50 percent of monkeys given highly pathogenic SIV after being vaccinated with this vaccine became infected with SIV but over time eliminated all trace of SIV from the body. In effect, the hunters of the body were provided with a much better targeting system and better weapons to help them find and destroy an elusive enemy.
"Through this method we were able to teach the monkey's body to better 'prepare its defenses' to combat the disease," explained Picker. "Our vaccine mobilized a T-cell response that was able to overtake the SIV invaders in 50 percent of the cases treated. Moreover, in those cases with a positive response, our testing suggests SIV was banished from the host. We are hopeful that pairing our modified CMV vector with HIV will lead to a similar result in humans."
The Picker lab is now investigating the possible reasons why only a subset of the animals treated had a positive response in hopes that the effectiveness of the vaccine candidate can be further boosted.
This research was funded by several grants from the National Institutes of Health, funding from the International AIDS Vaccine Initiative and a CAVD grant from the Bill & Melinda Gates Foundation.


Source: http://www.ohsu.edu/xd/about/news_events/news/2013/09-11-ohsu-vaccine-candidate-a.cfm

Why shouldn't things be largely absurd, futile, and transitory? They are so, and we are so, and they and we go very well together.

Meho Krljic

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Re: Lek protiv Raka i...nikom nista?
« Reply #13 on: 12-09-2013, 13:38:23 »
Lepo. Afrika će ovo pozdraviti aplauzom ako sve bude kako treba. Ja ću da ostanem bez posla, ali ajde, nije mi žao  :lol:

zakk

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Re: Lek protiv Raka i...nikom nista?
« Reply #14 on: 12-09-2013, 13:45:23 »
Uvek možeš da se posvetiš lečenju bele kuge u Srbiji!
Why shouldn't things be largely absurd, futile, and transitory? They are so, and we are so, and they and we go very well together.

Meho Krljic

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Re: Lek protiv Raka i...nikom nista?
« Reply #15 on: 12-09-2013, 13:59:43 »
Naravno, moja firma se i time bavi, ali pošto su međunarodne pare rađe ponuđene da se sprečava širenje jedne relativno teško zarazne i generalno ne preterano oštro razvijajuće bolesti nego da se prave bebe, onda je i balk naših aktivnosti vezan za HIV i AIDS. Jebiga...

Meho Krljic

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Re: Lek protiv Raka i...nikom nista?
« Reply #16 on: 13-01-2014, 10:47:44 »
Nije lek za rak ali je interesantan tretman metastaza:

Nanoparticles catch cancer cells that make it into the blood streamAnd then politely request that they die.



Quote
More than nine in ten cancer-related deaths occur because of metastasis, the spread of cancer cells from a primary tumor to other parts of the body. While primary tumors can often be treated with radiation or surgery, the spread of cancer throughout the body limits treatment options. This situation could change if work done by Michael King and his colleagues at Cornell University delivers on its promises, as he has developed a way of hunting and killing metastatic cancer cells.
When diagnosed with cancer, the best news can be that the tumor is small and restricted to one area. Many treatments, including non-selective ones such as radiation therapy, can be used to get rid of such tumors. But if a tumor remains untreated for too long, it starts to spread. It may do so by invading nearby healthy tissue or by entering the bloodstream. At that point, a doctor’s job becomes much more difficult.
Cancer is the unrestricted growth of normal cells, which occurs because mutations in a normal cell cause it to bypass a key mechanism called apoptosis (or programmed cell death) that the body uses to clear old cells. However, since the 1990s, researchers have been studying a protein called TRAIL, which on binding to the cell can reactivate apoptosis. But so far, using TRAIL as a treatment of metastatic cancer hasn’t worked, because cancer cells suppress TRAIL receptors.
When attempting to develop a treatment for metastases, King faced two problems: targeting moving cancer cells and ensuring cell death could be activated once they were located. To handle both issues, he built fat-based nanoparticles that were one thousand times smaller than a human hair and attached two proteins to them. One is E-selectin, which selectively binds to white blood cells, and the other is TRAIL.
He chose to stick the nanoparticles to white blood cells because it would keep the body from excreting them easily. This means the nanoparticles, made from fat molecules, remain in the blood longer and thus have a greater chance of bumping into freely moving cancer cells.
There is an added advantage. Red blood cells tend to travel in the center of a blood vessel, and white blood cells stick to the edges. This is because red blood cells are lower density and can be easily deformed to slide around obstacles. Cancer cells have a similar density to white blood cells and remain close to the walls, too. As a result, these nanoparticles are more likely to bump into cancer cells and bind their TRAIL receptors.


King, with help from Chris Schaffer, also at Cornell University, tested these nanoparticles in mice. They first injected healthy mice with cancer cells; after a 30-minute delay, they injected the nanoparticles. These treated mice developed far fewer cancers compared to a control group that did not receive the nanoparticles.
“Previous attempts have not succeeded, probably because they couldn’t get the response that was needed to reactivate apoptosis. With multiple TRAIL molecules attached on the nanoparticle, we are able to achieve this,” Schaffer said.
The work has been published in the Proceedings of the National Academy of Sciences. While these are exciting results, the research is at an early stage. Schaffer said that the next step would be to test mice that already have a primary tumor.
“While this is an exciting and novel strategy,” according to Sue Eccles at London’s Institute of Cancer Research, “it would be important to show that cancer cells already resident in distant organs (the usual clinical reality) could be accessed and destroyed by this approach. Preventing cancer cells from getting out of the blood in the first place may only have limited clinical utility.”
But there is hope for cancers that spend a lot of time in blood circulation, such as blood, bone marrow, and lymph node cancers. As Schaffer said, any attempt to control the spreading of cancer is bound to help. It remains one of the most exciting areas of research and future cancer treatment.The Conversation height=1
PNAS, 2014. DOI: 10.1073/pnas.1316312111 (About DOIs).
This article was originally published at The Conversation.


lilit

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Re: Lek protiv Raka i...nikom nista?
« Reply #18 on: 11-06-2016, 08:03:32 »
jes da je časopis sa jadnim impakt faktorom i jes da su mu ga rumena i stojan dali po inspiraciji i krenuli da recikliraju teorije iz sedamdesetih, al nije loše za dolivanje ulja na paranoidnu vatru sagite :lol:

The final checkpoint. Cancer as an adaptive evolutionary mechanism

Rumena Petkovaa & Stoyan Chakarovb*

The mechanisms for identification of DNA damage and repair usually manage DNA damage very efficiently. If damaged cells manage to bypass the checkpoints where the integrity of the genome is assessed and the decisions whether to proceed with the cell cycle are made, they may evade the imperative to stop dividing and to die. As a result, cancer may develop. Warding off the potential sequence-altering effects of DNA damage during the life of the individual or the existence span of the species is controlled by a set of larger checkpoints acting on a progressively increasing scale, from systematic removal of damaged cells from the proliferative pool by means of repair of DNA damage/programmed cell death through ageing to, finally, cancer. They serve different purposes and act at different levels of the life cycle, safeguarding the integrity of the genetic backup of the individual, the genetic diversity of the population, and, finally, the survival of the species and of life on Earth. In the light of the theory that cancer is the final checkpoint or the nature's manner to prevent complex organisms from living forever at the expense of genetic stagnation, the eventual failure of modern anti-cancer treatments is only to be expected. Nevertheless, the medicine of today and the near future has enough potential to slow down the progression to terminal cancer so that the life expectancy and the quality of life of cancer-affected individuals may be comparable to those of healthy aged individuals.

http://www.tandfonline.com/doi/full/10.1080/13102818.2016.1152163
Some things you have to do yourself.

lilit

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Re: Lek protiv Raka i...nikom nista?
« Reply #19 on: 27-07-2016, 18:43:36 »
ovo bi moglo da ide i na topik gojaznost al da ne preplašim debeljuce :lol:

upravo izašla studija koja nam otkriva da ako već treba da dobijemo kancer dobro bi bilo da nismo gojazni.
i ajd što se kancerozne stem ćelije (KSĆ) uspešno kriju u naslagama sala i onemogućavaju citostatike da prodru do njih, već KSĆ uspevaju da modulišu masno tkivo (u kom su se naselile) da radi u njihovu korist. hit!  :cry:


Quote
Fatty tissue may be ‘robbers cave’ for cancer stem cells, driving poor prognosis for obese patients

By Garth Sundem in Featured, Latest News, Research · July 20, 2016 ·

Across many cancer types, obese patients fare worse than leaner patients. Now a University of Colorado Cancer Center study published in the journal Cell Stem Cell offers a compelling hypothesis why: researchers found that leukemia stem cells “hide” in fatty tissue, even transforming this tissue in ways that support their survival when challenged with chemotherapy. It is as if leukemia stem cells not only use fatty tissue as a robbers’ cave to hide from therapy, but actively adapt this cave to their liking.

“It’s been increasingly appreciated that cancer can originate in stem cells and that failing to kill cancer stem cells can lead to relapse. Researchers have also come to appreciate the importance of surrounding tissues – the ‘niche’ or tumor microenvironment — in supporting cancer stem cells. In leukemia, the obvious niche is the bone marrow, but little attention has been paid to other sites in the body. This study is one of the first to evaluate adipose tissue, fat, as a possible tumor-supporting niche,” says Craig Jordan, PhD, investigator at the CU Cancer Center and Nancy Carroll Allen Professor of Hematology in the CU Department of Medicine.

Jordan describes how the “very original and insightful” line of reasoning of first author, Haobin Ye, PhD, was essential for the study. First, obese leukemia patients have poorer outcomes. Second, stem cells drive growth, resist therapy and can create relapse in leukemia. Third, the tumor microenvironment is important to cancer stem cells. At the intersection of obesity, stem cells and tumor microenvironment is adipose tissue – could stem cells in fatty tissue cause poorer prognosis in obese patients?

Robbers.CaveThe group started by examining cancer cells found in the adipose tissue of a mouse model of leukemia. Rather than the expected mix of regular cancer cells with cancer stem cells, the group found that this fatty tissue was enriched for cancer stem cells. No lowly sneak-thieves were these – it was the master thieves of cancer stem cells that exploited the robbers’ cave of fatty tissue. Not only was there a disproportionately high ratio of stem cells in adipose tissue, but these stem cells used a different energy source than stem cells in the bone marrow microenvironment – appropriately, these stem cells in fatty tissue powered their survival and growth with fatty acids, manufacturing energy by the process of fatty acid oxidization. In fact, these adipose tissue stem cells actively signal fat to undergo a process called lipolysis which releases fatty acids into the microenvironment.

“The basic biology was fascinating: the tumor adapted the local environment to suit itself,” Jordan says.

Finally, when the group challenged these cells with chemotherapy they discovered that stem cells in fatty tissue that had switched their energy source to fatty acids were more resistant than stem cells outside this tissue. When Ye, Jordan and colleagues examined samples of human leukemia, they found characteristics similar to the mouse models – cells specialized to use fatty acids as their energy source were more resistant to chemotherapy.

“Perhaps in the context of chemotherapy treatment, these stem cells in adipose tissue might be harder to kill than stem cells in the bone marrow,” Ye says.

If further work bears out this hypothesis, it could help to explain the fact of poorer outcomes in obese patients. The group plans to continue studies with mouse models of varying obesity, potentially shedding light on whether more adipose tissue provides either more energy or a larger robbers’ cave for cancer stem cells evading treatment.

evo ga i ceo rad: http://www.cell.com/cell-stem-cell/pdf/S1934-5909(16)30151-5.pdf

Some things you have to do yourself.

Meho Krljic

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Re: Lek protiv Raka i...nikom nista?
« Reply #20 on: 02-08-2016, 09:13:14 »
Možda nije trebalo da se ugojim ko svinja  :cry: :cry: :cry: :cry: :cry:

lilit

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Re: Lek protiv Raka i...nikom nista?
« Reply #21 on: 02-08-2016, 10:53:37 »
ne kukaj nego manje jedi!
ili bar to što jedeš slikaj i stavi na odgovarajući topik da se i mi ostali debljamo!!! (sad mi treba onaj smajli za plakanje od smeha al i ovaj će da posluži :lol: :lol: :lol:)
Some things you have to do yourself.

Pizzobatto

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Re: Lek protiv Raka i...nikom nista?
« Reply #22 on: 02-08-2016, 10:58:59 »
ovo istraživanje bi moglo da se provjeri u Rumuniji. Čaušesku je naredio da tokom osamdesetih svaki Rumun može da dobije 900 kalorija dnevno. Svi su bili šlang. Nađemo podatke o bolestima, i uporedimo ih sa današnjom Rumunijom, da vidimo kakvu statistiku bi dobili.

Ispašće da su ga džaba ubili.
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala

lilit

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Re: Lek protiv Raka i...nikom nista?
« Reply #23 on: 02-08-2016, 11:07:22 »
ne bi moglo pošto je prosečan rumun danas u mnogo (moj subjektivni osećaj) manjem stresu nego prosečan rumun u čaušesku doba a stres je gadan endogeni faktor koji na kancer utiče preko raznih mehanizama. na stranu što su tadašnji i današnji citostatici u rumuniji dva sveta.

ovo gore istraživanje samo govori da se ćelije raka nasele u masnom tkivu i da onda podrede to masno tkivo svojim potrebama a ne da su gojazni bolesniji od mršavih.
premda, ima i istraživanja da je obesity direktno proporcionalna generisanju nekih vrsta raka a naravno i da ta obesity-induced konstantna inflamacija ne vodi ničem dobrom al o tome u drugom poglavlju :lol:
Some things you have to do yourself.

zosko

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Re: Lek protiv Raka i...nikom nista?
« Reply #24 on: 02-08-2016, 11:42:31 »
ili bar to što jedeš slikaj i stavi na odgovarajući topik da se i mi ostali debljamo!!!

mlogo neukusno. protiv debljanja se ide mesom, ne salatom. meho da slika sta jedu macke!

Pizzobatto

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Re: Lek protiv Raka i...nikom nista?
« Reply #25 on: 02-08-2016, 11:49:29 »
ja jeo ovsene pahuljice, a vi vidite šta ćete
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala

lilit

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Re: Lek protiv Raka i...nikom nista?
« Reply #26 on: 02-08-2016, 12:25:58 »
dijeta?
Some things you have to do yourself.

Pizzobatto

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Re: Lek protiv Raka i...nikom nista?
« Reply #27 on: 02-08-2016, 13:25:14 »
poslije ovog horor članka razmišljam i da na neki drugi način unosim B vitamin
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala

lilit

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Re: Lek protiv Raka i...nikom nista?
« Reply #28 on: 30-08-2016, 17:40:40 »
kad se imaju resursi i dovoljan broj godina da modulacija imunskog sistema radi brže i efikasnije od razvoja kancera (a kancer bio IV stage kancer)

Quote
Jimmy Carter, rebuilding after cancer

http://edition.cnn.com/2016/08/25/health/jimmy-carter-cancer-anniversary-habitat-for-humanity/index.html

https://en.wikipedia.org/wiki/Pembrolizumab
Some things you have to do yourself.

Meho Krljic

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Re: Lek protiv Raka i...nikom nista?
« Reply #29 on: 23-09-2016, 08:16:46 »
Microsoft will ‘solve’ cancer within the next 10 years by treating it like a computer virus, says company



Quote
The human body will eventually be able to be ‘reprogrammed’ back into a healthy state, experts working for the tech company have claimed




Microsoft says it is going to “solve” cancer in the next 10 years.
The company is working at treating the disease like a computer virus, that invades and corrupts the body’s cells. Once it is able to do so, it will be able to monitor for them and even potentially reprogramme them to be healthy again, experts working for Microsoft have said.
The company has built a “biological computation” unit that says its ultimate aim is to make cells into living computers. As such, they could be programmed and reprogrammed to treat any diseases, such as cancer.


In the nearer term, the unit is using advanced computing research to try and set computers to work learning about drugs and diseases and suggesting new treatments to help cancer patients.
The team hopes to be able to use machine learning technologies – computers that can think and learn like humans – to read through the huge amounts of cancer research and come to understand the disease and the drugs that treat it.


At the moment, so much cancer research is published that it is impossible for any doctor to read it all. But since computers can read and understand so much more quickly, the systems will be able to read through all of the research and then put that to work on specific people’s situations.
It does that by bringing together biology, maths and computing. Those have long been treated as relatively distinct but are coming closer together in recent years, and have been spurred on by Microsoft’s investment.


“The field of biology and the field of computation might seem like chalk and cheese,” Chris Bishop, head of Microsoft Research’s Cambridge-based lab, told Fast Company. “But the complex processes that happen in cells have some similarity to those that happen in a standard desktop computer.”
As such, those complex processes can potentially be understood by a desktop computer, too. And those same computers could be used to understand how cells behave and to treat them.
If that were possible, then those computers wouldn’t only be able to understand why cells behave as they do and when they might be about to become cancerous. They’d also be able to trigger a response within a cell, reversing its decision and reprogramming it so that it is healthy again.


Microsoft says that solution could be with us within the next five or ten years.
Andrew Philips, who leads Microsoft’s biological computation group, told The Telegraph that in as little as five years it hopes to be able to develop a system for detecting problems. “It’s long term, but … I think it will be technically possible in five to ten years’ time to put in a smart molecular system that can detect disease.”
 

Pizzobatto

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Re: Lek protiv Raka i...nikom nista?
« Reply #30 on: 23-09-2016, 09:30:48 »
Тај Гејтс, сем што је укро ОС из неке гараже, ништа паметно није урадио у животу.
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala

ridiculus

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Re: Lek protiv Raka i...nikom nista?
« Reply #31 on: 23-09-2016, 09:39:05 »
A što se odavno povukao sa mesta CEO-a kompanije?

Doduše, još je "tehnološki savetnik"...
Znate... u početku beše Šala, i Šala beše...itd

Pizzobatto

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Re: Lek protiv Raka i...nikom nista?
« Reply #32 on: 23-09-2016, 10:01:08 »
Лик је написао књигу 1995. Пут напред, у којој предвиђа технолошки развој. Године 1996. је морао да је исправља, јер није разматрао интернет.

Сада ће да лијечи компјутерским програмима. Гад хелп ас ол.
šta će mi bogatstvo i svecka slava sva kada mora umreti lepa Nirdala

lilit

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Re: Lek protiv Raka i...nikom nista?
« Reply #33 on: 04-11-2016, 09:22:06 »
epigenetika u fokusu, al spasa pušačima nema.

Quote
Smoking-Linked Cancer Mutations Mapped

Researchers have uncovered the genomic mutations and DNA methylation patterns likely caused by tobacco smoke in 17 types of cancerous tumors. A comprehensive survey of mutations likely caused by carcinogens found in tobacco smoke by researchers at the Los Alamos National Laboratory in New Mexico, the Wellcome Trust Sanger Institute, and their colleagues was published today (November 3) in Science. The work provides a window into understanding the mechanisms by which tobacco smoke induces mutations that can lead to cancer in tissues that are directly or indirectly exposed to it.

“Comparing the mutations in cancers arising in smokers and non-smokers using genomic sequencing has never been done to this extent,” Gerd Pfeifer of the Van Andel Research Institute in Michigan, who was not involved in the work but penned an accompanying editorial, told The Scientist.

“This study highlights how important primary prevention remains for tobacco-related cancers and how much we still don’t know about the details of how tobacco causes cancer,” said Steve Rozen of the Duke-NUS Center for Computational Biology in Singapore who also was not involved in the study.

Ludmil Alexandrov of the Los Alamos National Lab, along with the Wellcome Trust’s Michael Stratton  and their colleagues, used whole-genome sequences of 610 tumors and the exomes of 4,633 additional tumors, together covering 17 smoking-associated forms of cancer. The researchers examined each tumor as a mixture of multiple genomic mutation signatures identified in a previous study, which spanned a wider range of tumor types.?? Of the 5,243 tumors the researchers examined in the present study, 2,490 were derived from tobacco smokers and 1,063 from never-smokers.

“The hypothesis is that chemicals in tobacco directly damage DNA in tissues like the lung that are directly exposed to tobacco smoke. But there is not an understanding of how tobacco smoke increases the risk of cancer in other tissues not directly exposed to smoke like the bladder, and kidneys,” Alexandrov told The Scientist. “We wanted to understand the mechanisms by which tobacco can increase the risk for cancer.”

The tumor types with the highest odds ratio for developing cancer in individuals who smoke an average of more than 30 cigarettes a day are those that occur in tissues directly exposed to tobacco smoke, the researchers showed (small cell lung cancer, squamous lung cancer, and lung adenocarcinomas). Tallying the number of mutations observed in lung tissue samples, the researchers estimated that approximately 150 mutations accumulate in a given lung cell in individuals who smoke a pack of cigarettes a day for a year.

The team also found a mutational signature characteristic of tumors of the lung and larynx in smokers. This guanine-to-thymine base-pair change is thought to occur as a result of DNA adducts on guanines and has been previously demonstrated as the mutational signature that occurs in cells exposed to a known tobacco-derived carcinogen.

For tissues indirectly exposed to tobacco smoke, the picture is more complicated.

The researchers uncovered a complex mutational pattern spanning all the cancer types examined. This cellular aging–related mutational pattern was found in tumors from smokers and nonsmokers, but was enriched among smokers. “What we think is happening in this case is that tobacco smoke is deregulating a molecular clock, and that is increasing the speed with which these mutations accumulate,” explained Alexandrov.  How these mutations occur is not yet clear.

“The tissues with direct tobacco exposure look different than tissues exposed indirectly,” said Rozen. “The ones affected indirectly are more mysterious, pointing out that we really don’t know the mechanism by which smoking causes tumors in these tissues.”

While different DNA methylation patterns in the blood cells of smokers compared to nonsmokers have been observed, in the present study, the researchers observed similar patterns of methylation in both groups.

Several tissues in which tobacco smoke–associated cancers develop are those involved in metabolism and waste filtration, such as stomach, liver, bladder, and kidney. “These tissues don’t see the tobacco smoke directly, so the tobacco is likely acting through a proxy,” Alexandrov told The Scientist.

“We thought that this study would confirm prior results about smoking and cancer-causing DNA mutations,” he continued. “But we found quite a few new mechanisms suggesting that there is a lot that we still don’t know.”

Pfeifer suggested that the approach should now be used to study the origins of other cancers for which the carcinogen is unknown. “We can look at the mutational signatures to give us good clues on the type of mutagen that could have caused the mutations,” he said.

Alexandrov, Stratton, and colleagues now plan to apply the same methodology to uncover the mutational patterns and potential mechanisms behind other factors, such as obesity and hormonal changes, known to increase the risk of certain cancers. “We know that tobacco causes cancer and have revealed a suite of potential mechanisms. But there are a host of other factors that cause cancer and yet we have no idea about the mechanisms,” Alexandrov said.

http://science.sciencemag.org/content/354/6312/618.full
Some things you have to do yourself.