About Ovarian Cancer

About Ovarian Cancer

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Treatment

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Further Information

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Cancer Information and links for other Wiki Cancer Pages

Message Board - Cancer with an Ostomy Section∞.
A place for those whose cancer results in an an ostomy to ask questions, seek support, discuss treatments etc etc.

A list of Websites, Message Boards etc for those cancers which can lead to ostomies∞

Latest Research

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Ovarian Cancer Research
PET-CT Highly Accurate For Detecting Ovarian Cancer Recurrence

Ovarian Cancer May Mimic Fallopian Tube Formation

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10 Mar 2007

A new study suggests that ovarian cancer cells form by hijacking a developmental genetic process normally used to form fallopian tubes. Scientists at the Georgia Institute of Technology and the Ovarian Cancer Institute discovered that the protein, PAX8, is involved in the development of fallopian tubes and is present in ovarian cancer cells, but not in normal ovarian tissue. The discovery not only provides a new target for diagnostic and therapeutic interventions, but also opens new avenues for basic research in ovarian cancer pathology. The research appears in Volume 104, Issue 3 of the journal Gynceologic Oncology.

"Our finding sustains the promise of a molecular genetic understanding of different cancers and emphasizes the importance of describing cancer in the context of normal human development that has gone awry due to genetic and epigenetic alterations," said Nathan Bowen, Georgia Cancer Coalition Distinguished Cancer Scientist at Georgia Tech and the Ovarian Cancer Institute (OCI).

Using cancerous and non-cancerous tissue straight from the operating room, Bowen and fellow OCI researchers are engaged in investigating the molecular profile of ovarian cancer tissue in order to discover the causes of ovarian cancer, develop a reliable diagnostic blood test and understand the genetic basis of resistance to chemotherapy.

In 2003, a group from Stanford University researching breast cancer discovered that paired box gene 8 is expressed in ovarian cancer tissue, but not in breast cancer. Taking note of the Stanford group's results, OCI researchers began to investigate the possibility that the gene and its products may be an important biomarker for detecting and researching the causes of ovarian cancer. They began to look for evidence of PAX8, the protein made by paired box gene 8, which was the next step in establishing the gene as a biomarker. Not only did they find PAX8 in the ovarian cancer cells, but they also found it in the cells that form fallopian tubes, the secretory cells. In addition, they discovered that the protein is not expressed in the normal ovarian surface epithelium.

Bowen proposes that ovarian cancer begins by using PAX8 to direct an adult stem cell population found on the ovarian surface to proliferate and ultimately form ovarian cancer. When this gene is turned on in an embryo, it leads to the development of fallopian tubes. When the gene is expressed in healthy adult ovarian cells that migrate into the body of the ovary, it leads to the development of ovarian inclusion cysts. Normally, the growth of cysts is kept in check by the cells' feedback mechanisms that turn off cell growth. But in cancer, when these feedback mechanisms are mutated, the cysts grow out of control until they metastasize.

"It's a way of molecularly characterizing tumors that may lead to designing specific therapies based on the molecular profile," said Bowen. "Biology is basically an information processing system to generate end products, and there are a lot of decisions that have to be made by the regulatory genes, like pax8, before the end products can be made.

Bowen's next steps are to find out why paired box gene 8 gets turned on and to discover its targets in order to find out of it turns on another decision-making gene or an endpoint gene.

"That's the daunting task of cancer biologists," he said. "Now that we've sequenced the human genome, we have to make sense out of the thousands of genes that are expressed in cancer at the same time."
http://www.medilexicon.com/medicalnews.php?newsid=64696∞

Women Without Regular Medical Care At Increased Risk Of Ovarian Cancer

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29 Mar 2007

In North America, ovarian cancer is the second most common gynecological cancer and is the leading cause of death among women with gynecological cancer. The high mortality is in part due to the difficulty of detecting and diagnosing this condition at an early stage.

In this case-control study, Abenhaim and colleagues examined whether the frequency of medical visits and pelvic examinations and the type of health care provider visited had an effect on the risk of ovarian cancer. They found that women who did not have an annual medical visit or pelvic examination and who had no regular health care provider were at an increased risk of ovarian cancer. This risk was most pronounced among postmenopausal women. Although the study could not determine whether women who sought regular health care and had a regular physician were at a decreased risk of ovarian cancer, the most prudent recommendation is that women, especially those who are postmenopausal, should be encouraged to maintain regular health care.
http://www.medilexicon.com/medicalnews.php?newsid=66227∞

Lessons From Ovarian Cells Migration: The Three "Ws" Of Ovarian Cancer Spreading

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15 May 2007

Who must go? When to go? Where to go? During development ovarian cells migrate in a spacial-temporal coordinated way, responding to specific signals that determine which cells have to move, when they have to move, and where they have to go. The same types of signals stimulate migration of ovarian cancer cells, which follow specific signals to move from the female genital tract towards the peritoneum and stroma, where they form metastases. These findings were presented today (May 13th) by Denise Montell, Professor of Biological Chemistry at the Johns Hopkins University School of Medicine in Baltimore (Maryland), at the Workshop on Cell Migration: From Molecules to Organisms and Diseases promoted by the European School of Molecular Medicine (SEMM) and the University of Milan, in collaboration with IFOM The FIRC Institute for Molecular Oncology of the Italian Foundation for Cancer Research, and IEO European Institute of Oncology. Venue of the Workshop is the IFOM-IEO Campus (via Adamello, 16, Milan) that was recently opened and represents the biggest area dedicated to the oncological research in Europe.

Epithelial ovarian cancer (EOC) develops in the ovary, especially in the cells that cover the outer surface of this organ. As it scores 190,000 new cases each year worldwide (61,000 in Europe), it has fuelled intensive investigations all over the world. Denise Montell and her group have been studying cell migration for years, in the attempt to elucidate the key elements that govern their movement. To this purpose the scientists have set up a system called "border cells model", employing fruit fly (Drosophila melanogaster) cells, which has led to the identification of specific regulatory signals that cells respond to. "Epithelial cells migrate in a way that is reminiscent of the migratory behavior of cancer cells - explains the scientists and this moving is highly coordinated as it responds to extracellular signals present in the surrounding microenvironment. Using our experimental model we were able to identify three kinds of signals."

They are:

- When: steroid hormones dictate the time when cells must start moving;

- Where: Growth Factors show them the right direction;

- Who: compounds called cytokines determine which cells will acquire mobility.

"Each of these signals continues Montell must work together in order for the cells to proceed to their correct destination. But they are not the only ones". Further investigations into the signaling pathway of ovarian cells, in fact, led Montell to identify Par-1 as a key gene that controls cells migration. "We found says Montell that Par-1 regulates the detachment of cells from the epithelium and a critical step in releasing the cells from the original tissue". Along these lines, future goal of the scientists will be to determine whether Par-1 contributes to ovarian cancer metastasis, or that of other carcinomas.

"Basic science results such as Montell's have great value points out Marina Mione, head of the IFOM program Genetic control of cell migration in zebrafish, and member of the Workshop's Scientific Committee as they pave the way for future clinical application. Devising new therapeutic approaches implies previous acquisition of solid scientific baseline information. Moving from observations acquired in physiological conditions Montell opens a number of new avenues that will promote our understanding of pathological conditions".

IFOM - THE FIRC INSTITUTE OF MOLECULAR ONCOLOGY FOUNDATION
Via Adamello 16
20139 Milano
http://www.ifom-ieo-campus.it∞
http://www.medilexicon.com/medicalnews.php?newsid=70879∞

Researchers Identify Genetic Mutation That May Alter Patients' Response To Cancer Therapeutics

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Article Date: 09 Jul 2007 - 0:00 PDT

Researchers from Eli Lilly & Company and the Phoenix-based Translational Genomics Research Institute (TGen) today announced finding a novel recurring mutation of the gene AKT1 in breast, colorectal and ovarian cancers. The altered form of AKT1 appears to cause tumor cell proliferation and may play a role in making cells resistant to certain types of therapies. The findings are reported in an advance online publication (AOP) of the journal Nature.

The PI3-Kinase/AKT pathway is among the most commonly activated cellular pathways in human cancers and members of this pathway are among the most frequently targeted for new cancer drug discovery efforts. Activation of this pathway results in cancer cell growth and cell survival. Although AKT1 is central to pathway activation, its role in cancer has been that of an intermediary between mutated upstream regulatory proteins and downstream survival signaling proteins. This is the first evidence of direct mutation of AKT1 in human cancer tumors: it was discovered in clinical samples from cancer patients, yet has never been detected in cancer cell lines.

"This discovery is a seminal finding in cancer biology that confirms AKT1 as an oncogene in breast, colorectal and ovarian cancer. The mutation alters the electrostatics of binding pocket in the pleckstrin homology domain, the portion of the enzyme that docks with phospholipids on the cell membrane," said Kerry L. Blanchard, PhD, MD, Executive Director, Discovery Biology Research, Eli Lilly & Company.

To identify the AKT1 mutation, the researchers analyzed 150 tumor samples from patients with either breast, colorectal or ovarian cancer (50 samples from each tumor type). Analysis of the data showed that 8 percent of breast, 6 percent of colorectal and 2 percent of ovarian tumors had the AKT1 mutation in the samples that were screened in their study.

"Recently, molecular features such as the AKT1 mutation are beginning to change drug development efforts. This discovery adds to the short but growing list of molecular features that may help guide both current and future cancer drug development," said John Carpten, PhD, Senior Investigator and Director of TGen's Integrated Cancer Genomics Division and the study's lead author. "The next step is to determine the prevalence of the AKT1 mutation in different populations and, hopefully, use the information gained to stratify patients going into clinical trials for AKT inhibitors."

If validated by further studies, the identification of this recurring mutation has the potential to impact cancer treatment and drug development.

"This is a gorgeous study that used a variety of sophisticated techniques to provide new insights into the tumorigenic process," said Bert Vogelstein, MD, Director of the Ludwig Center for Cancer Genetics & Therapeutics at The Johns Hopkins Kimmel Cancer Center.

James E. Thomas, PhD, of Lilly's Cancer Discovery Research division, ex- plained, "AKT1 is a protein kinase or enzyme that plays a key role in activating survival, proliferation and metabolic pathways. Interestingly, other cellular proteins that regulate this network have also been shown to be mutated in a variety of cancers including lung, breast ovary, prostate, colorectal and brain cancers. This mutation in AKT1 is striking direct evidence for the role of AKT1 in cancer formation."

The identification of the AKT1 mutation was a collaborative effort between Eli Lilly & Company and TGen. "This discovery demonstrates the importance of studying the genetic make up of cancers at the clinical level rather than re- lying on model systems," adds Jeffrey Trent, PhD, Scientific Director of TGen.

"This is a key study highlighting Lilly's commitment to translational re- search approaches in cancer drug discovery and development. Furthermore, this work is a great example of a successful public-private partnership at a global level that involves Lilly Research Laboratories in Indianapolis, TGen in Phoenix, Lilly Singapore Centre for Drug Discovery, and the Economic Development Board of Singapore," adds Richard Gaynor, MD, Vice President of Oncology Discovery at Eli Lilly & Company. He added, "This mutation further validates AKT1 as an attractive drug target, and it also will be a valuable tool for the stratification of patients for targeted therapies. This paradigm of identifying specific defects in cancer cells to successfully develop innovative therapies has been validated with oncology drugs such as Gleevec in leukemia and Herceptin in breast cancer."
http://www.medicalnewstoday.com/articles/76253.php∞

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