Remember that we have our cells test coming up very soon. Organelle pamphletes are due November 8th and 9th. Here are some videos on cancer to help with this final section of our cells unit.

This first one is a brief overview of what cancer does and how it spreads.

The next video goes over how the process of growth regulation and cell death occurs before going into the process of cancer.

You might also want to check out the following video at YouTube (I can’t seem to embed it)

The Biology of Cancer

Cancer is a complicated disease…I wish I could say it was easy, but I think it is very important to start looking at and trying to impart as much understanding about the disease, how it works, and how it is treated, as possible. Some of the material here is beyond the scope of our class and the knowledge being taught and assessed in our class.

What is Cancer Animation

Understanding Cancer

An Academic Look At Cancer

Cancer Risk Factors

Factors Impacting Cancer Growth – The end of this video looks at one companies treatment of these factors and cancer (ignore the plug for the company)

Breast Cancer Cells Dividing

Camera on Cancer Research

Acute myeloid leukaemia genes’ role discovered

By James Gallagher
Health reporter, BBC News

Three groups of mutations which cause acute myeloid leukaemia, a cancer of the white blood cells, have been identified by scientists.

The researchers suggest their work on mice, published in Nature Genetics, could lead to new treatments.

Two thousand people in the UK are diagnosed with acute myeloid leukaemia each year.

The charity Leukaemia and Lymphoma Research said the study offered invaluable insight.

During the illness, the bone marrow, which produces blood cells, starts to churn out immature white blood cells.

This changes the balance of the blood.

The white blood cells are not properly developed so they cannot fight infection and there are too few red blood cells to carry oxygen around the body.

The disease can be fatal within weeks if left untreated.

The research group at the Wellcome Trust Sanger Institute investigated how this form of leukaemia arises because they say there had been little progress in developing new drugs.

Three groups
The most common mutation implicated in the cancer is to the Npm1 gene.

By switching this gene on in blood cells in mice, the researchers were able to show that it boosted the ability of cells to renew themselves, which is a sign of cancer. Yet only a third of mice went on to develop leukaemia.

The researchers concluded other mutations must also play a part.

They randomly mutated genes in mice, with a technique known as insertional mutagenesis. By looking at mice which developed cancer, they could then trace which mutations were involved.

They found two additional types of mutation. One affects cell division and growth, while the other modifies the cell’s environment.

Dr George Vassiliou, consultant haematologist from the Wellcome Trust Sanger Institute, said they had “found critical steps that take place when the cancer develops. Identifying the biological steps in turn means we can look for new drugs to reverse the process.”

He told the BBC: “Getting new drugs to patients could take decades, but what can happen sooner is using drugs which are already on the shelf, but in a more targeted way.”

Dr David Grant, scientific director at Leukaemia & Lymphoma Research, said: “New designer drugs which target specific genetic mutations are proving increasingly effective in the treatment of blood cancers.

“This is a very important study as it offers an invaluable insight into the role of the most common form of mutation found in acute myeloid leukaemia. It explains how it develops and the other genetic factors that drive the leukaemia’s growth.

“It offers a potential model for the development of new drugs for this terrible disease in the future.”

Chemical Guided Missile Could Be the Answer to Wiping out Cancer

RNA Aptamer

ScienceDaily (Feb. 18, 2011) — Deakin University medical scientists have created the world’s first cancer stem cell-targeting chemical missile, placing them a step closer to creating a medical ‘smart bomb’ that would seek out and eradicate the root of cancer cells.

The Deakin researchers have worked with scientists in India and Australia to create the world’s first RNA aptamer, a chemical antibody that acts like a guided missile to seek out and bind only to cancer stem cells. The aptamer has the potential to deliver drugs directly to the stem cells (the root of cancer cells) and also to be used to develop a more effective cancer imaging system for early detection of the disease. Their discoveries have been published recently in an international cancer research journal, Cancer Science.

The Director of Deakin Medical School’s Nanomedicine Program, Professor Wei Duan, said the development of the aptamer had huge implications for the way cancer is detected and treated.

“Despite technological and medical advances, the survival rates for many cancers remain poor, due partly to the inability to detect cancer early and then provide targeted treatment,” Professor Duan said.

“Current cancer treatments destroy the cells that form the bulk of the tumour, but are largely ineffective against the root of the cancer, the cancer stem cells. This suggests that in order to provide a cure for cancer we must accurately detect and eliminate the cancer stem cells.”

The aptamer is the first part of the ‘medical smart bomb’ the researchers have been developing.

“What we have created is the ‘guided missile’ part of the ‘smart bomb’,” Professor Duan explained.

“The aptamer acts like a guided missile, targeting the tumour and binding to the root of the cancer.

“The aim now is to combine the aptamer with the ‘bomb’ (a microscopic fat particle) that can carry anti-cancer drugs or diagnostic imaging agents directly to the cancer stem cells, creating the ultimate medical smart bomb.”

Professor Duan said the medical smart bomb opened up exciting possibilities for detection and treatment of cancer.

“The cancer stem cell-targeting missile and the smart bomb could revolutionise the way cancer is diagnosed,” he explained.

“The minute size of the aptamer means it could locate cancer cells in their very early stages. Attaching radioactive compounds to the aptamer could lead to the development of sensitive diagnostic scans for earlier detection, more accurate pinpointing of the location of cancer, better prediction of the chance of cure and improved monitoring of the response to treatment.

“More accurate identification of the type of cancer present would lead to more personalised treatment that is more successful and cost-effective.

“This could ultimately lead to better cancer survival rates and greatly improved quality of life for patients.”

More about the project

The project is a collaboration between Deakin University’s School of Medicine and Institute for Technology Research and Innovation and the Indian Institute of Science in Bangalore, Institute of Life Science along with Barwon Health’s Andrew Love Cancer Centre and ChemGenex Pharmaceuticals. It has received $700,000 funding from the Federal Government’s Australia-India Strategic Research Fund, with reciprocal support from the Indian Government.

Cancer cells are made up of many cells that have different characteristics. They are, for example, like a tree with some cells being the root system and the others the branches and leaves; if you cut off the branches and leaves, the root of the tree is still alive. Current cancer treatments are ineffective in eradicating the whole cancer cell because they only kill the branches and leaves. The root cells are particularly tough and resistant to drugs and radiotherapy. They possess drug pumps that pumps out the anti-cancer drugs. This means that, while most of the cancer cell is killed, the cancer root remains and can regenerate. This makes the root cells (cancer stem cells) an important target for new cancer treatments.

There are two parts to the project being undertaken by the Deakin and Indian scientists.

The first is building the guided missile, or aptamer. The aptamer is a chemical antibody, much smaller and cheaper and easier to make than conventional antibodies, designed to bind specifically to cancer cells. It has been designed to effectively penetrate a tumour and specifically target cancer stem cells. This missile will carry the ‘bomb’; the second part of the drug delivery system.

The ‘bomb’ will be a very smart lipid, or fat particle that will remain stable in the body, i.e. it will not break down. This particle will carry the anti-cancer drug as well as anti-cancer genes.

When combined, the ‘smart bomb’ will be injected into the body and find the cancer cell. It will then enter the cell through an endosome route — a small road within the cell. Once inside the cell, it will very quickly release its contents and kill the whole cancer cell.

A unique part of the system being developed is that the bomb is very stable outside of the cancer cell, but once inside it will very quickly release its contents and kill the cancer cell from within. This system is made by materials that are very human compatible and human degradable — it is not toxic to other cells in the body and would cause very limited side-effects.

Cellular Communicators for Cancer Virus Identified

ScienceDaily (Nov. 8, 2010)

A new discovery by UNC scientists describes how cells infected by the Epstein-Barr virus (EBV) produce small vesicles or sacs called exosomes, changing their cellular “cargo” of proteins and RNA. This altered exosome enters cells and can change the growth of recipient cells from benign to cancer-producing.

In this way, virus-infected cells can have wide-ranging effects and potentially manipulate other cells throughout the body. The findings are reported in the Nov. 8 early online edition of the Proceedings of the National Academy of Sciences.

Nancy Raab-Traub, PhD, professor of microbiology and Immunology, said, “Exosomes may be the Trojan Horse through which EBV gains control of cells that are not even infected. Importantly, the production of exosomes may provide a new therapeutic target that can be blocked to reduce cancer growth.” Raab-Traub is a Sarah Graham Kenan Professor and member of UNC Lineberger Comprehensive Cancer Center.

Epstein-Barr Virus (EBV) is perhaps the world’s most successful virus as almost everyone is infected with it for life. EBV cannot be eliminated by the immune system and is constantly secreted into saliva where it is effectively transmitted. Infection with the virus rarely causes disease; however, EBV is found in several major cancers, including lymphoma and cancer of the nose and throat, where its proteins hijack the cell’s growth regulatory mechanisms to induce uncontrolled cell growth characteristic of cancer.

Through exosomes, a protein called latent membrane protein 1, that is considered the EBV oncogene, can be delivered to uninfected cells. Significantly, EBV also changes the entire contents of the exosomes to deliver cellular proteins that are also activated in cancers. This surprising finding reveals that one infected cell can have wide-ranging effects and induce the unchecked growth of neighboring cells.

The immune system is constantly on guard to identify foreign viral proteins. Through exosomal uptake, cancer cells would be stimulated to grow without the expression of proteins that “announce” infection to the immune system, thus allowing unchecked growth. The study also showed that the cells that produce blood vessels, the process called angiogenesis, readily take in the altered exosomes and are potentially induced to grow.

“The next step,” explains David Meckes, PhD, postdoctoral fellow in the Raab-Traub lab and first author of the paper, “is to determine how the virus controls which proteins are sorted into exosomes and how this process could be inhibited.”

Other UNC Lineberger authors, all members of the Raab-Traub laboratory, are: Kathy Shair, PhD;Aron Marquitz, PhD; Patrick Kung, PhD ; and Rachel Edwards, BS. The research was supported by a grant from the National Cancer Institute.

Editor’s Note: This article is not intended to provide medical advice, diagnosis or treatment.

Soy May Stop Prostate Cancer Spread: Experimental Soy-Based Drug Shows Benefits in Men With Localized Prostate Cancer

ScienceDaily (Nov. 8, 2010)

Northwestern Medicine researchers at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University have found that a new, nontoxic drug made from a chemical in soy could prevent the movement of cancer cells from the prostate to the rest of the body.

These findings are being presented at the Ninth Annual American Association for Cancer Research Frontiers in Cancer Prevention Research Conference.

Genistein, a natural chemical found in soy, is being used in the lab of Raymond Bergan, M.D., the director of experimental therapeutics at the Lurie Cancer Center, to inhibit prostate cancer cells from becoming metastatic and spreading to other parts of the body. So far the cancer therapy drug has worked in preclinical animal studies and now shows benefits in humans with prostate cancer.

A recent phase II randomized study of 38 men with localized prostate cancer found that genistein, when given once a day as a pill, one month prior to surgery, had beneficial effects on prostate cancer cells.

Researchers examined the cancer cells from the subjects’ prostates after surgery and found that genistein increased the expression of genes that suppress the invasion of cancer cells and decreased the expression of genes that enhance invasion.

“The first step is to see if the drug has the effect that you want on the cells and the prostate, and the answer is ‘yes, it does,'” said Bergan, a professor of hematology and oncology at Northwestern University Feinberg School of Medicine and a physician at Northwestern Memorial Hospital.

The next step is to conduct another phase II study to see if the drug can stop the cancer cells from moving out of the prostate and into the rest of the body, Bergan said. If confirmed, Bergan said this could be the first therapy for any cancer that is non-toxic and targets and inhibits cancer cell movement.

“All therapies designed to stop cancer cell movement that have been tested to date in humans have basically failed have because they have been ineffective or toxic,” Bergan said. “If this drug can effectively stop prostate cancer from moving in the body, theoretically, a similar therapy could have the same effect on the cells of other cancers.”

Funding from the National Institutes of Health supported this research.

Editor’s Note: This article is not intended to provide medical advice, diagnosis or treatment.

Jellyfish Cells ‘Diagnose’ Cancer, York Scientists Say

01 November 2010

Luminous cells from jellyfish can be used to diagnose cancers deep inside the body, scientists have said.

The process uses the green fluorescent protein (GFP) enabling jellyfish to glow in the dark.

Researchers in North Yorkshire found it can be targeted at cancer cells allowing them to be spotted using a special camera.

A team from the Yorkshire Cancer Research Laboratory at York University has developed the procedure.

The team’s leader, Professor Norman Maitland, believes it will revolutionise the way some cancers are diagnosed.

He said: “Cancers deep within the body are difficult to spot at an early stage, and early diagnosis is critical for the successful treatment of any form of cancer.

“What we have developed is a process which involves inserting proteins derived from luminous jellyfish cells into human cancer cells.

“Then, when we illuminate the tissue, a special camera detects these proteins as they light up, indicating where the tumours are.”

The process is an extension of the work done by American chemist Dr Roger Y Tsien, who won a Nobel Prize in 2008 for taking luminous cells from the crystal jelly species of jellyfish and isolating the GFP.

Prof Maitland said: “When we heard about Dr Tsien’s work, we realised how that advance might be useful in the diagnosis of cancer.

‘Flare up’
“X-rays, for example, struggle to penetrate well deeply into tissues and bone, so diagnosing dangerous microscopic bone cancer is difficult.

“Our process should allow earlier diagnosis to take place.”

The York team’s process uses an altered form of the protein so that it shows up as red or blue, rather than its original green.

Viruses containing the proteins are targeted to home in on tiny bundles of cancer cells scattered throughout the body which are too small to be seen by conventional scanning techniques.

But the viruses grow and, while doing so, make more and more of the fluorescent proteins.

“When a specially-developed camera is switched on, the proteins just flare up and you can see where the cancer cells are.” said Prof Maitland.

“We call the process ‘Virimaging’.”

Deep in body
The team expects the procedure to be ready for clinical trials within five years, if the research continues to go to plan.

Prof Maitland said one problem, however, may be the availability of the specialised cameras needed for the process.

A United States company is the only one which has so far designed and built a camera system which allows the jellyfish proteins to be seen with the desired resolution so deep in the body.

This kit costs about £500,000 and Prof Maitland said he was currently raising the funds to buy one.

Taken from:

Anticancer protein might combat HIV

Anticancer protein might combat HIV

Tumor suppressor p21 found in abundance in people impervious to developing AIDS
Web edition : Thursday, October 21st, 2010

VANCOUVER — A protein best known as a cancer suppressor may enable some people infected with HIV to fend off the virus indefinitely, a new study shows. Copious production of this protein, called p21, shows up in a select group of HIV-positive people who rarely develop AIDS, scientists reported October 21 at a meeting of the Infectious Diseases Society of America.

Some HIV patients, dubbed long-term nonprogressors, get infected with HIV yet seem impervious to its effects. While research has suggested factors that could separate these lucky few from most HIV patients, the specifics underlying their resistance are still an area of keen interest. “This is a specific group of patients who are spontaneously able to control HIV and don’t get sick from it,” says infectious disease physician Mathias Lichterfeld of Harvard Medical School and Massachusetts General Hospital in Boston, who presented the new data.

In the new study, researchers compared four groups of people — 14 who were HIV negative, 16 with HIV that had progressed, 10 with HIV who were undergoing treatment and 15 whose HIV infection had totally stalled. This last group included nonprogressors so adept at halting an HIV infection that they didn’t even have any virus detectable by routine tests. (Researchers ascertained infection by testing for antibodies to HIV.) Scientists call this subset of patients elite controllers. “They comprise 1 percent or fewer of HIV-infected people,” Lichterfeld says.

The researchers obtained immune cells called CD4 T cells — the prime targets of HIV — from all the volunteers and subjected these cells to lab tests. The tests showed that elite controllers had CD4 T cells that made 10 to 100 times more p21 than did people in the other three groups. “It’s not a subtle difference. It’s quite striking,” Lichterfeld says.

When the researchers put these cells in lab dishes and subjected them to an HIV assault, the cells loaded with p21 held off the virus.

“These data suggest that this protein can inhibit HIV,” Lichterfeld says. But he notes that the mechanism by which p21 does this and even how these cells make extra amounts of the protein are not yet fully understood. There may be genetic variations involved, he says.

“It might offer an alternative way to control HIV if we can find a way to manipulate this p21 protein in patients,” he says. But using p21 as a tool probably won’t be as simple as giving the protein to people.

“The fact that it occurs in nature is encouraging — that you have a natural model,” says Joel Gallant, an infectious disease physician who specializes in HIV at Johns Hopkins University in Baltimore. Although many questions need to be answered before finding a way to use p21 clinically, he says, “this could be critical someday in getting better control of HIV.”