This is a photomicrograph at 1000x magnification of malignant lymphoma tumor, which displays large, loosely cohesive lymphoid cells. You can particularly see the difference in size between the lymphoma cells and the endothelial cells towards the center. (via)

This is a photomicrograph at 1000x magnification of malignant lymphoma tumor, which displays large, loosely cohesive lymphoid cells. You can particularly see the difference in size between the lymphoma cells and the endothelial cells towards the center. (via)

The Body’s Countdown to Death or Cancer
Described by some as a “doomsday clock”, every cell within the human body has a limit to the number of times it is able to safely divide, due to the telomeres on the ends of each chromosome. These telomeres act as caps on the tops of the chromosomes to protect the precious genetic material from fraying, but with every cell division these telomeres are shortened. 
Upon shrinking to a certain point, the telomere’s function is critically impaired. Technically, at this point the cell is supposed to die; however, when it continues to live, it proceeds as a cancerous cell. Now, based on recent research, scientists are hypothesizing that a drug could be developed to control the telomeres, effectively treating both cancer and aging diseases.
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The Body’s Countdown to Death or Cancer

Described by some as a “doomsday clock”, every cell within the human body has a limit to the number of times it is able to safely divide, due to the telomeres on the ends of each chromosome. These telomeres act as caps on the tops of the chromosomes to protect the precious genetic material from fraying, but with every cell division these telomeres are shortened. 

Upon shrinking to a certain point, the telomere’s function is critically impaired. Technically, at this point the cell is supposed to die; however, when it continues to live, it proceeds as a cancerous cell. Now, based on recent research, scientists are hypothesizing that a drug could be developed to control the telomeres, effectively treating both cancer and aging diseases.

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Silver as a Chemotherapy Drug
The value of silver has long been known for its beauty in jewelry, utensils, and its conductive properties. But a new property in making the headlines. Researchers have now found that the metal is just as effective as leading chemotherapy treatments, yet greatly reduces the side effects. 
Currently, cisplatin is the main drug used in the treatment of a wide range of cancers. The drug contains platinum with groups of molecules attached, creating a complex that reacts with DNA in cancer cells. These molecules that surround the platinum atom are the determining factor in how reactive and effective the treatment is. However, platinum is toxic to our systems, causing the many of the chemotherapy side-effects.
Basing her hypothesis off of previous studies indicating that silver compounds could be effective in killing cancer cells, Charlotte Willans from the Univerity of Leeds, along with her colleagues, created compound with silver atoms replacing platinum atoms. Upon attaching different types of carbene ligands to the silver atoms, the team incubated the compound with breast and colon cancer cells for almost a week, testing different concentrations of the substance.
The new compound based off of silver was concluded to be just as effective as cisplatin when it came to effectively attacking both types of cancer cells. Silver complexes which contained a ligand with two bonds proved more effective than those with a single bond, probably because they are more stable.
When implicated in biological functions, silver is far less toxic to healthy cells than platinum, making this study an important step in finding effective, non-toxic cancer treatments.

Silver as a Chemotherapy Drug

The value of silver has long been known for its beauty in jewelry, utensils, and its conductive properties. But a new property in making the headlines. Researchers have now found that the metal is just as effective as leading chemotherapy treatments, yet greatly reduces the side effects. 

Currently, cisplatin is the main drug used in the treatment of a wide range of cancers. The drug contains platinum with groups of molecules attached, creating a complex that reacts with DNA in cancer cells. These molecules that surround the platinum atom are the determining factor in how reactive and effective the treatment is. However, platinum is toxic to our systems, causing the many of the chemotherapy side-effects.

Basing her hypothesis off of previous studies indicating that silver compounds could be effective in killing cancer cells, Charlotte Willans from the Univerity of Leeds, along with her colleagues, created compound with silver atoms replacing platinum atoms. Upon attaching different types of carbene ligands to the silver atoms, the team incubated the compound with breast and colon cancer cells for almost a week, testing different concentrations of the substance.

The new compound based off of silver was concluded to be just as effective as cisplatin when it came to effectively attacking both types of cancer cells. Silver complexes which contained a ligand with two bonds proved more effective than those with a single bond, probably because they are more stable.

When implicated in biological functions, silver is far less toxic to healthy cells than platinum, making this study an important step in finding effective, non-toxic cancer treatments.


Test tubes surround a doctor doing cancer research in 1950.

Test tubes surround a doctor doing cancer research in 1950.

Melanoma Drug’s Link to Other Skin Cancers
The recently approved drug vemurafenib (Zelboraf) has been hailed as a breakthrough in the treatment of melanoma, the deadliest form of skin cancer. But roughly one-quarter of patients who take the medication develop a troublesome side effect: secondary skin cancers called squamous cell carcinomas.
Now, a new study by researchers at the Jonsson Comprehensive Cancer Center at the University of California, Los Angeles, and colleagues identifies the specific genetic mechanism that causes this side effect.
"What we found is that vemurafenib blocks the mutation that makes the melanoma grow, but when patients have skin cells with another mutation that’s probably induced from sun exposure, there the drug has the exact opposite effect and causes these squamous cell cancers to grow," said Dr. Antoni Ribas, co-senior author of the study and an associate professor of hematology/oncology at UCLA.
What’s more, the findings suggest that combining vemurafenib, a BRAF inhibitor, with a drug called an MEK inhibitor — which blocks the other mutation — may not only prevent this side effect, but may also lead to an even more effective melanoma treatment, Ribas said.
"It needs to be demonstrated in clinical trials, but the theory is that if we give these two medications together up front, we will be punching the melanoma where it really hurts twice, and also preventing the growth of secondary skin cancers," Ribas said.

Melanoma Drug’s Link to Other Skin Cancers

The recently approved drug vemurafenib (Zelboraf) has been hailed as a breakthrough in the treatment of melanoma, the deadliest form of skin cancer. But roughly one-quarter of patients who take the medication develop a troublesome side effect: secondary skin cancers called squamous cell carcinomas.

Now, a new study by researchers at the Jonsson Comprehensive Cancer Center at the University of California, Los Angeles, and colleagues identifies the specific genetic mechanism that causes this side effect.

"What we found is that vemurafenib blocks the mutation that makes the melanoma grow, but when patients have skin cells with another mutation that’s probably induced from sun exposure, there the drug has the exact opposite effect and causes these squamous cell cancers to grow," said Dr. Antoni Ribas, co-senior author of the study and an associate professor of hematology/oncology at UCLA.

What’s more, the findings suggest that combining vemurafenib, a BRAF inhibitor, with a drug called an MEK inhibitor — which blocks the other mutation — may not only prevent this side effect, but may also lead to an even more effective melanoma treatment, Ribas said.

"It needs to be demonstrated in clinical trials, but the theory is that if we give these two medications together up front, we will be punching the melanoma where it really hurts twice, and also preventing the growth of secondary skin cancers," Ribas said.

 
Great Science Frauds: Roger Poisson
Sometimes fraud can be driven by good, but misguided intentions. Poisson, a professor of surgery at the University of Montreal, was a member of the prestigious National Surgical Adjuvant Breast and Bowel Project (NSABP), a joint U.S. and Canadian research effort that since 1958 has conducted studies on some of the most effective treatments for breast cancer. In 1994, the U.S. Office of Research Integrity found that for nearly a decade, Poisson had enrolled patients who were not eligible for trials and then falsified or fabricated their medical records to cover up their ineligibility, in an effort to involve as many women as possible in the studies. Investigators found two sets of patient books in Poisson’s lab, one marked ‘true’ and another labelled ‘false.’ The women were part of trials that established that lumpectomy plus radiation was as effective as mastectomy in lowering risk of recurrent breast cancer.
Other studies have since confirmed the benefits of lumpectomy combined with radiation, but the misrepresentation caused many who underwent the procedure to question whether they had made the right decision. “People who are not on the front line of the battle have no idea how frustrating it can be to prepare an eligible patient for a trial, with several pep talks and a great deal of discussion, explanation for the informed consent and to convince the patient to participate and — at the last moment — to realize the patient [is ineligible],” he wrote to the investigators in his defense. Poisson was banned from receiving U.S. government research funding for eight years.

Great Science Frauds: Roger Poisson

Sometimes fraud can be driven by good, but misguided intentions. Poisson, a professor of surgery at the University of Montreal, was a member of the prestigious National Surgical Adjuvant Breast and Bowel Project (NSABP), a joint U.S. and Canadian research effort that since 1958 has conducted studies on some of the most effective treatments for breast cancer. In 1994, the U.S. Office of Research Integrity found that for nearly a decade, Poisson had enrolled patients who were not eligible for trials and then falsified or fabricated their medical records to cover up their ineligibility, in an effort to involve as many women as possible in the studies. Investigators found two sets of patient books in Poisson’s lab, one marked ‘true’ and another labelled ‘false.’ The women were part of trials that established that lumpectomy plus radiation was as effective as mastectomy in lowering risk of recurrent breast cancer.

Other studies have since confirmed the benefits of lumpectomy combined with radiation, but the misrepresentation caused many who underwent the procedure to question whether they had made the right decision. “People who are not on the front line of the battle have no idea how frustrating it can be to prepare an eligible patient for a trial, with several pep talks and a great deal of discussion, explanation for the informed consent and to convince the patient to participate and — at the last moment — to realize the patient [is ineligible],” he wrote to the investigators in his defense. Poisson was banned from receiving U.S. government research funding for eight years.

Could the US Have Given Chavez Cancer? 
Five South American presidents and former presidents, including Venezuela’s Hugo Chavez, have been recently diagnosed with cancer. Chavez speculated that US agents may be inducing the disease in South American leaders by feeding them or injecting them with an unspecified substance. The state department has rejected Chavez’s insinuation.
Can you give someone cancer? Not reliably. Injecting cancerous cells into a person isn’t enough to give him the disease. The abnormal tissue has to penetrate and grow in other areas of the body. If you injected someone with live cancer cells, their immune system would almost certainly attack and destroy the foreign tissue. In theory, secret agents might be able to induce cancer in a leftist South American president with a severely weakened immune system. Or perhaps they could harvest tissue from him, expose it to a carcinogen, and then reintroduce it into his body. As far as we know, however, these techniques have never successfully caused cancer in a human.
While it’s tough to induce cancer in an enemy, it’s certainly possible to increase his chances of developing the disease. The most effective option would be radiation. Oncologists implant radiation-emitting devices the size of a seed into some patients to combat existing cancers. It’s hard to say just how much the device would increase a healthy individual’s risk of cancer, but leaving a high-intensity model inside the body for weeks or months would result in a significant dose of radiation. The victim would likely notice the implant, though. They’re too big for an ordinary needle, and need to be inserted through a catheter.
You could, alternatively, contaminate the victim’s diet with high levels ofaflatoxin, which is associated with liver cancer. Or you could infect her or him with any of a number of cancer-causing biological agents. Helicobacter pyloricontributes to the development of gastric cancer, and human papillomaviruses can cause cervical, anal and a few other forms of cancer. But these tactics probably wouldn’t produce cancer in the short term and aren’t guaranteed to have any effect at all. In countries with high aflatoxin exposure, like China and parts of Africa, fewer than 1 in 1000 people develop liver cancer.
Most of the research on infusing cancer into humans is decades old. In the 1950s, Chester Southam gained notoriety by injecting hundreds of cancer patients and healthy prison inmates with live cancer cells. Southam wasn’t trying to give his subjects cancer. Rather, he was testing the efficiency with which the patients’ immune systems would reject the cells. He was so confident that the patients would fight off the invaders that he thought it unnecessary to tell them what he was doing. None of Southam’s patients seems to have developed metastatic cancer from his injections, and most modern oncologists believe the experiment posed little risk to the subjects. (One of the patients showed signs of a potentially spreading disease before dying of a separate illness.) Southam was sanctioned for fraudulent practices, however, and the case helped establish modern informed consent standards.
Southam’s experiments were abandoned in the 1950s, but he wasn’t the last doctor to inject a patient with live cancer cells. In 2009, a Taiwanese doctor was accused of implanting cancerous uterine cells into healthy patients as part of an insurance scam. While the insurance companies were out more than $660,000, none of the victims developed cancer.
Today, ethical physicians inject live cancer cells only into laboratory animals such as mice and rats. In most cases, the animals’ immune systems are compromised, or the rodents have been genetically engineered to rapidly spread mutant cells.

Could the US Have Given Chavez Cancer?

Five South American presidents and former presidents, including Venezuela’s Hugo Chavez, have been recently diagnosed with cancer. Chavez speculated that US agents may be inducing the disease in South American leaders by feeding them or injecting them with an unspecified substance. The state department has rejected Chavez’s insinuation.

Can you give someone cancer? Not reliably. Injecting cancerous cells into a person isn’t enough to give him the disease. The abnormal tissue has to penetrate and grow in other areas of the body. If you injected someone with live cancer cells, their immune system would almost certainly attack and destroy the foreign tissue. In theory, secret agents might be able to induce cancer in a leftist South American president with a severely weakened immune system. Or perhaps they could harvest tissue from him, expose it to a carcinogen, and then reintroduce it into his body. As far as we know, however, these techniques have never successfully caused cancer in a human.

While it’s tough to induce cancer in an enemy, it’s certainly possible to increase his chances of developing the disease. The most effective option would be radiation. Oncologists implant radiation-emitting devices the size of a seed into some patients to combat existing cancers. It’s hard to say just how much the device would increase a healthy individual’s risk of cancer, but leaving a high-intensity model inside the body for weeks or months would result in a significant dose of radiation. The victim would likely notice the implant, though. They’re too big for an ordinary needle, and need to be inserted through a catheter.

You could, alternatively, contaminate the victim’s diet with high levels ofaflatoxin, which is associated with liver cancer. Or you could infect her or him with any of a number of cancer-causing biological agents. Helicobacter pyloricontributes to the development of gastric cancer, and human papillomaviruses can cause cervical, anal and a few other forms of cancer. But these tactics probably wouldn’t produce cancer in the short term and aren’t guaranteed to have any effect at all. In countries with high aflatoxin exposure, like China and parts of Africa, fewer than 1 in 1000 people develop liver cancer.

Most of the research on infusing cancer into humans is decades old. In the 1950s, Chester Southam gained notoriety by injecting hundreds of cancer patients and healthy prison inmates with live cancer cells. Southam wasn’t trying to give his subjects cancer. Rather, he was testing the efficiency with which the patients’ immune systems would reject the cells. He was so confident that the patients would fight off the invaders that he thought it unnecessary to tell them what he was doing. None of Southam’s patients seems to have developed metastatic cancer from his injections, and most modern oncologists believe the experiment posed little risk to the subjects. (One of the patients showed signs of a potentially spreading disease before dying of a separate illness.) Southam was sanctioned for fraudulent practices, however, and the case helped establish modern informed consent standards.

Southam’s experiments were abandoned in the 1950s, but he wasn’t the last doctor to inject a patient with live cancer cells. In 2009, a Taiwanese doctor was accused of implanting cancerous uterine cells into healthy patients as part of an insurance scam. While the insurance companies were out more than $660,000, none of the victims developed cancer.

Today, ethical physicians inject live cancer cells only into laboratory animals such as mice and rats. In most cases, the animals’ immune systems are compromised, or the rodents have been genetically engineered to rapidly spread mutant cells.

Argentine President Cristina Fernandez de Kirchner has been diagnosed with cancer and will have an operation on 4 January, her government has announced.
The cancer is in her thyroid gland but has not spread to other parts of her body, a spokesman said.
 
Ms Fernandez, 58, recently began her second term as president after a landslide election victory. She will step aside as president for 20 days until January 24, with Vice-President Amado Boudou taking over.
The cancer was discovered on 22 December during routine medical tests, spokesman Alfredo Scoccimarro said.
 
The cancer - a papillary thyroid carcinoma - had not metastasised or affected her lymph nodes, he added, and the prognosis was very good. Specialists say this type of thyroid cancer has a high survival rate if treated early.

Argentine President Cristina Fernandez de Kirchner has been diagnosed with cancer and will have an operation on 4 January, her government has announced.

The cancer is in her thyroid gland but has not spread to other parts of her body, a spokesman said.

Ms Fernandez, 58, recently began her second term as president after a landslide election victory. She will step aside as president for 20 days until January 24, with Vice-President Amado Boudou taking over.

The cancer was discovered on 22 December during routine medical tests, spokesman Alfredo Scoccimarro said.

The cancer - a papillary thyroid carcinoma - had not metastasised or affected her lymph nodes, he added, and the prognosis was very good. Specialists say this type of thyroid cancer has a high survival rate if treated early.

Nine Mutated Genes Identified in Leukemia Patients
Chronic lymphocytic leukemia, or CLL, is the most common form of leukemia found in adults in North America. Yet the disease remains poorly understood, according to authors of a new study published in the New England Journal of Medicine.
Dr. Catherine Wu, one of the study authors and an assistant professor at Harvard Medical School, said all CLL cells look the same under the microscope. Yet patients with the cancer can have different outcomes – some live for 5 to 15 years with little or no treatment, others succumb to the disease within two years.
This unpredictability is one of the reasons Wu and her colleagues are attempting to identify mutated genes in the tumors of CLL patients. For this study they collected DNA samples from the leukemia cells of 91 patients and compared the gene sequences, or DNA order, to normal cells. The researchers reaffirmed two mutated genes that were already known to be involved in CLL, and confirmed two genes that had been suspected to be significant. Most importantly, they say they identified five new genes that were not known to have established roles in the disease. The most interesting, Wu said, was gene SF3B1.
The significance of SF3B1 is a bit tricky. SF3B1 plays a role in mRNA splicing. mRNA, or messenger RNA, carries instructions from DNA for making proteins. Splicing occurs when the mRNA is being prepared to produce the proteins that help your body function.
Mutations of the SF3B1 gene were found in 15% of the study’s patients, the second most-frequently mutated gene. These mutations were found primarily in patients with a poor cancer prognosis.
This means that if the gene could be identified, we would know which patients might not respond in the long-term to conventional chemotherapy, Wu said.
"It gives us new targets to go after in order to treat CLL," she said. "It provides us tools to help us predict more reliably how patients will fare. We may want to consider alternate therapies or think about other ways to treat it more effectively."

Nine Mutated Genes Identified in Leukemia Patients

Chronic lymphocytic leukemia, or CLL, is the most common form of leukemia found in adults in North America. Yet the disease remains poorly understood, according to authors of a new study published in the New England Journal of Medicine.

Dr. Catherine Wu, one of the study authors and an assistant professor at Harvard Medical School, said all CLL cells look the same under the microscope. Yet patients with the cancer can have different outcomes – some live for 5 to 15 years with little or no treatment, others succumb to the disease within two years.

This unpredictability is one of the reasons Wu and her colleagues are attempting to identify mutated genes in the tumors of CLL patients. For this study they collected DNA samples from the leukemia cells of 91 patients and compared the gene sequences, or DNA order, to normal cells.
 
The researchers reaffirmed two mutated genes that were already known to be involved in CLL, and confirmed two genes that had been suspected to be significant. Most importantly, they say they identified five new genes that were not known to have established roles in the disease. The most interesting, Wu said, was gene SF3B1.

The significance of SF3B1 is a bit tricky. SF3B1 plays a role in mRNA splicing. mRNA, or messenger RNA, carries instructions from DNA for making proteins. Splicing occurs when the mRNA is being prepared to produce the proteins that help your body function.

Mutations of the SF3B1 gene were found in 15% of the study’s patients, the second most-frequently mutated gene. These mutations were found primarily in patients with a poor cancer prognosis.

This means that if the gene could be identified, we would know which patients might not respond in the long-term to conventional chemotherapy, Wu said.

"It gives us new targets to go after in order to treat CLL," she said. "It provides us tools to help us predict more reliably how patients will fare. We may want to consider alternate therapies or think about other ways to treat it more effectively."

Drug Duo Kills Chemotherapy-Resistant Ovarian Cancer Cells

The use of two drugs never tried in combination before in ovarian cancer resulted in a 70 percent destruction of cancer cells already resistant to commonly used chemotherapy agents, say researchers at Mayo Clinic in Florida. Their report, published online in Gynecologic Oncology, suggests that this combination (ixabepilone and sunitinib), might offer a much needed treatment option for women with advanced ovarian cancer. When caught at late stages, ovarian cancer is often fatal because it progressively stops responding to the chemotherapy drugs used to treat it.

"Women die from ovarian cancer because their tumors become resistant to chemotherapy, so a drug that might be able to reduce that resistance — which may be what this combination of agents is doing — would be a boon to treatment of this difficult cancer," says study co-author Gerardo Colon-Otero, M.D., a hematologist-oncologist who cares for ovarian cancer patients.

The finding also highlights the importance of the role of a molecule, RhoB, that the researchers say is activated by the drug duo. The study’s senior investigator, cancer biologist John Copland, Ph.D., has identified RhoB as a key modulator for drug response in other tumor types, but says its role in ovarian cancer was unknown before this study.

"Now we find that with this combination of drugs, RhoB is increased and cells die," he says.

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sciencecenter:

Q: What’s the best way to make sure you remove every bit of a tumor during surgery?
A: You make the tumor glow in the dark. 

sciencecenter:

Q: What’s the best way to make sure you remove every bit of a tumor during surgery?

A: You make the tumor glow in the dark