On Tuesday, researchers announced that a three-drug cocktail may help women with HER2-positive breast cancer better than any other drug used on its own. About one quarter of women with breast cancer make up this HER2 category.

Tests on mice revealed using the three drugs along with breast cancer drug tamoxifen helped wipe out tumors altogether. And the tumors did not come back. This is the first time mice were cured of a very aggressive human breast tumor. Incidentally, when a single drug was used, tumors returned within several weeks.

The three wonder drugs used in this study -- all are monoclonal antibodies that precisely target certain aspects of tumors -- are the experimental drug pertuzumab; trastuzumab, also known as Herceptin; and gefitinib, or Iressa.

Published in the Journal of the National Cancer Institute, this study supports the notion that HER2-positive tumors eventually become resistant to one drug and attacking them on several fronts seems to work better.

Some scientists think that the reason cancer recurs is because we haven't gotten to the root of the disease. What they mean by the root is -- the cancer stem cells.

Stem cells can reproduce and make exact copies of themselves and can live longer than ordinary cells. Embryonic stem cells can have the potential to become many different types of cells, whereas adult stem cells are generally limited to becoming into the cell types of a specific organ.

The researchers gave the analogy of a dandelion that is growing in your backyard. You can cut the weed but if you don't kill the root the dandelion will grow back. It seems that our treatments today for cancer can kill the ordinary cancer cells but can leave the stem cells behind to grow into new tumors and spread.

So how do we kill the cancer stem cells? Well, they don't know yet. But it is promising research that I look forward to hearing more about in the future.

There's been much press lately about the cervical cancer vaccine, its merits, its implications, and the debate surrounding the issue of vaccinating young girls against the sexually transmitted virus HPV.

Enter a new vaccine -- the ovarian cancer vaccine.

Early clinical trial results are promising for this vaccine, intended to fight off ovarian cancer tumors with patients' own cells -- but without the toxicity of traditional chemotherapy.

Says Dr. Ed Staren of Cancer Treatment Centers of America, "We're able to identify the specific components of the tumor and target it for individual therapy for the patient."

Doctors would surgically remove a patient's tumor and then send it to a lab where tumor cells would be used to create a vaccine specifically for the patient.

A second round of clinical trials to study the effectiveness of this vaccine will begin this summer.

Researchers have found that when cells become cancerous, they become 100 times more likely to genetically mutate than non-cancerous cells. This explains why tumor cells have so many mutations. Good news on the research front. But bad news on the treatment front -- because therapies that target a certain gene may be largely ineffective in controlling cancer.

"This is very bad news, because it means that cancer cells in a tumor will have mutations that protect them from therapeutics," says lead researcher Dr. Lawrence Loeb, professor of pathology and biochemistry at the University of Washington School of Medicine in Seattle, who presented his findings February 18 at the meeting of the American Association for the Advancement of Science in San Francisco.

Loeb says chemotherapy drugs target specific oncogenes -- genes that affect the malignancy of a cell -- but if cancer cells are mutator cells, then a single tumor may have cells with all sorts of oncogenes. And while chemotherapy may kill some cancerous cells, millions of others will live on.

It's not all bad news, though, says Loeb who believes this research may help doctors determine the stage and malignancy of tumors by testing the number of mutations. It may also help researchers understand what makes a cancer cell a mutator and how to slow the rate of mutation.

"The idea is that if you might normally get exposed to something in the environment at 20 years old that would give you cancer by age 55, then if we cut the mutation rate in half, you might not get cancer until age 90, and you may even die of something else before that," Loeb explained.

Cancer drug Nexavar has made its point. It can help people with liver cancer survive longer.

Bayer Pharmaceuticals and Onyx Pharmaceuticals announced Monday that advanced stage clinical trials for this drug will end early. And now patients in the placebo arm of the study can begin treatment with the actual drug.

It's been a long road for researchers who have been searching for a liver cancer treatment that can target tumors with minimal side effects while extending life for months or even years.

It is estimated that 16,780 people in the United States will die from liver cancer in 2007 -- and it seems Nexavar, a drug initially predicted to fail when used for liver cancer -- may help save some of these lives.

Bayer and Onyx are planning to pursue FDA approval for this drug that has already been approved for kidney cancer.

Researchers have made a stem cell discovery that may help treat pancreatic cancer -- one of the deadliest forms of the disease.

University of Michigan scientists have found cancer stem cells in pancreatic tumors that appear to drive cell tumor growth and could lead to the development of drugs to target and kill these cells.

Pancreatic cancer kills 97 percent of people diagnosed with the disease within five years. Half of all diagnosed patients die within six months of diagnosis, and this cancer -- that spreads quickly and is rarely detected at an early state -- kills 33,000 each year in the United States alone. So any improvement in the study of this disease is a true gift.

"The clinical implications of this work are significant," said Dr. Diane Simeone, director of the Gastrointestinal Oncology Program at the University of Michigan Comprehensive Cancer Centre and lead author of the study, published in the journal Cancer Research.

"We've made baby steps in improving the survival in these patients -- on the order of a few months (longer to live) -- over the past decade or so. But we really haven't had a major breakthrough in coming up with something that has the potential to provide a cure," she said.

Simeone says killing these cancer stem cells is like pulling out the root of a weed. And she says the best way to pull out the root is to target these stem cells instead of the traditional approach of shrinking tumors by killing as many cells as possible -- an approach that may be flawed because cancer stem cells tend to resist standard therapies.

Kidney transplants can save lives. They can also increase the risk of developing a variety of cancers, according to Australian researchers who report a risk 300 percent higher than in the general population.

Most cancers developed in kidney transplant patients have a known or suspected viral origin, suggesting the weakened immune systems in these patients limit protection against cancer.

"The immunosuppressive drugs transplant patients take lower their ability to fight off infections that can trigger malignancy", the lead researcher said. "We believe the increased incidence of infection leads to the infection that results in cancer." She also notes there is probably an even greater risk of cancer among heart and lung transplant patients because these patients receive more powerful immunosuppressive drugs.

Researchers gathered their findings by comparing the incidence of cancer in 29,000 patients with end-stage kidney disease who received kidney transplants. Data was collected beginning five years prior to transplantation, during dialysis, and after transplantation. Researchers then consulted an Australian registry to identify cancers occurring between the years of 1982-2003. They compared the statistics with the number of cancers seen among transplant patients.

These cancers included melanoma, Kaposi's sarcoma, non-Hodgkin's lymphoma, Hodgkin's disease, leukemia and cancers of the lip, tongue, mouth, salivary gland, esophagus, stomach, colon, anus, liver, gallbladder, lung, connective and other soft tissue, vulva, cervix, penis, eye and thyroid. There was also an increase in nasal cavity and vaginal cancers.

This study has important implications for future immosuppression. Patients should give considerable thought to quality-of-life transplants -- such as face transplants and hand transplants -- and should carefully weigh the risks of weakened immunity. On a brighter note, this study might help prompt research on medication that can selectively target the part of the body responsible for rejecting a transplant. Because right now, medications affect the entire immune system -- and this is what makes patients more prone to developing cancer.

If you plan to send out photo holiday cards this season, consider supporting the youngest of cancer patients at the same time.

St. Jude Children's Research Hospital and Target have teamed up and are offering customers the chance to order from four 4X8 holiday card options. Each option was designed by one of four patients currently receiving treatment at St. Jude's -- the only children's hospital treating patients regardless of their ability to pay.

Designers include Christina, 11, who is busy fighting acute myeloid leukemia; Genesis, 8, and Samantha, 14, who are both battling osteosarcoma; and Jake, 4, who is trying to conquer heptoblastoma. One-hundred percent of all profits go directly to St. Jude.

This St. Jude and Target partnership was formed to support St. Jude's Thanks and Giving program -- a national endeavor that encourages customers to honor the healthy children in their lives by giving to those who are not.

You can place your St. Jude holiday card order through Yahoo! Photos.

All cells in our body are programmed to die. They have a limited lifespan and they die when they are damaged, worn out or no longer needed by the body. This is a normal process called apoptosis, programmed cell death, that the body depends on to be healthy. When cells die they are replaced by new ones.

In cancer cells the process of apoptosis fails and the damaged cells live on and multiply indefinitely and uncontrollably. Most chemotherapy drugs that are given to cancer patients are aimed at killing fast dividing cells, this is sometimes successful at halting the disease but these drugs damage many normal tissues.

Researchers look to find smarter drugs that do not have severe side effects but target only the cancer cell itself. A new drug being studied in the lab suggests that it may prove to be more effective and less toxic than current chemotherapy drugs. The drug called ABT-737 has a different strategy for attacking cancer. Instead of poisoning the cancer cells, the new drug attempts to reactivate the cell death program that had failed.

The leader of the project, Dr. David Huang says "Much more remains to be done to assess the drug's safety and effectiveness in patients, but early results from the laboratory are promising. Our hope is that the new drug will prove to be more effective while having fewer side effects".

Photographer Sharon Seligman's images are inspired by her personal journeys. She photographs people and birds and residential communities. She also captures the journeys of women enduring breast cancer. Her work speaks of the human experience. It speaks of her own experience. It speaks volumes.

Bearing Witness: Beyond the Surface of Breast Cancer is one of Seligman's portfolios. It's a photographic trip down memory lane, depicting self-portraits of courageous breast cancer survivors. Seligman tells her own story in words that border the left side of each portrait. Captions to the right of each black and white photograph offer a glimpse into the life of each woman whose being is displayed in raw form, for all to see, for all to contemplate, for all to appreciate.

And then in another portfolio, Seligman offers more photographs, more visions of the breast cancer experience.

Seligman aims to share the physical changes that come from breast cancer, to project the inner truths. Clearly, she is right on target.

Last night I watched the first of the two-part series Breaking the Cancer Code with Katie Couric. Current chemotherapy and radiation treatments for cancer are, as Couric called it, "a scorched body approach" for cancer patients. "They throw everything against the wall to see what sticks."

It is frustrating for the cancer patient, for the oncologist, for the cancer community. Why haven't we made more advancements, why don't we understand cancer any better than we do, why must we endure treatments that attack healthy cells in order to kill off cancerous ones with generalized treatments that might or might not stick? Because, right now, that's all there is to offer in the fight against cancer.

Which makes Couric's news feature all that more compelling -- and hopeful. The scientific community is beginning to make progress in discovering what cancer cells are made of and how they work. As a result, an emerging class of cancer treatment drugs, called targeted therapies, are beginning to show promise. Drugs that target the cancer cell without causing any collateral damage to healthy cells, like Herceptin, Gleevec and Avastin. Herceptin targets proteins on the surface of the cell, Gleevec works inside the cell to block cancer's growth and Avastin shuts down the blood vessels that feed the tumor.

Johns Hopkins University's Dr. Bert Vogelstein has spent 30 years unraveling the secret codes to cancer, and when referring to cancer he is quoted as saying, "It was a total mystery, a black box. It was like some plague from outer space."

Tonight, Couric takes a look at super computers that can take cancer cells and test which treatments work and which ones remain ineffective in treating an individual cancer -- before the cancer patient begins treatment. To watch an off camera discussion between Couric and CBS News medical correspondent Dr. Jon LaPook regarding targeted cancer therapies and super computers, watch this video.

Kim Taylor is a 45-year-old single mother who lives in Suwannee County, Florida and is proud to have successfully raised one daughter -- a graduate of the University of Florida. Kim enjoys outdoor activities like camping as well as sewing, crafting, and carpentry projects. She is most at peace spending time with her family, working as a youth volunteer -- and raising awareness for breast cancer. It's a interest she acquired just two years ago, compliments of a personal encounter with the disease that has taught her to let the little things go, to appreciate every sunrise, to make every moment matter.

In laboratory testing, by targeting the FoxM1 gene, a little-known antibiotic has been proven effective as an anti-cancer treatment, according to University of Illinois researchers.

As the researchers explain, the FoxM1 gene is responsible for turning on genes needed for cell proliferation and turning off genes that block proliferation. Uncontrolled proliferation is characteristic of cancer cells. The antibiotic, siomycin A, appears to suppress the activity of the FoxM1 gene.

During the research, the antibiotic was found to be non-toxic and prompted cancer cells into a process called apoptosis, or cancer cell suicide, without damaging surrounding cells. More testing with need to be done before the drug can reach the clinical trial phase. The study will be published in the October issue of Cancer Research.

Yesterday the Food and Drug Administration approved the drug Vectibix for patients who have metastatic colon cancer. Vectibix is to be given by IV following standard chemotherapy treatments. The FDA approved the drug after it showed effectiveness in slowing tumor growth and, in some cases, reduced tumor size.

Steven Galson, MD,MPH, the director of the FDA's Center for Drug Evaluation and Research said "This approval adds a treatment option for patients with an advanced stage of a disease that can be life threatening".

Vectibix is a monoclonal antibody, scientists can make monoclonal antibodies that react with specific antigens on certain types of cancer cells. As researchers discover more cancer associated antigens, they will be able to direct monoclonal antibodies against more and more cancers.

A review was done by an international panel of experts of literature concerning chronic myeloid leukemia (CML) for the recommendation of treatment options. The panel included ten members that reviewed 194 papers on CML written since 1998.

The article was recently published in the journal Blood. Gleevec (imatinib mesylate) has become a standard treatment for Philadelphia chromosome-positive CML. Specific guidelines for the use of Gleevec in the treatment of CML have recently been compiled.

• All newly diagnosed patients should be treated with 400 mg of Gleevec per day.
• Patients who do not respond to Gleevec should be treated with higher doses, an allogeneic stem cell transplantation, or experimental therapy. This experimental therapy could include agents designed to over come resistance to Gleevec.

Responses to treatment can be determined by several laboratory tests. Talk to your physician about specific details regarding responses to Gleevec.