A horrible story of a mother passing melanoma on to her baby has come to the attention of ABC News. Briana Cox, who had melanoma removed in 2006, was assured that her cancer had not spread. This made her assume that it was safe for her to have a child. However, two months after having her baby it was found that an advanced stage of the cancer had traveled all over her body. Furthermore, it was found that her child, Addison, had stage IV melanoma.

Obviously this is an extremely heartbreaking story for anyone to hear. Briana Cox passed away in February, and it was her wish that this story be shared. She wanted others to understand how truly dangerous this cancer is. How did the baby contract melanoma? Doctors were initially baffled, but found that, “Cox’s cancer cells had metastasized during her pregnancy and crossed the placenta to her developing fetus”.

James Cox, Briana’s husband, compares the ordeal to “running into a brick wall”. Clearly the couple were taken aback by the events. In fact, this has only been recorded a few number of times. Dr. Pooja Hingorani points out however that, “All cancer can happen in pregnancy…But melanoma is the most common cancer to pass through the placenta from the mother”. Hingorani says that 30% of cancers passed from a mother to a fetus is melanoma, but that she had only seen four to five cases of this happen.

The prognosis for the now 9-month-old is dire. At best, Addison’s life expectancy is about two years. Her cancer is similar to her mother’s — in the brain, shoulder, lungs, kidney, liver, leg, and even the back of her tongue, according to the Arizona Republic, which first reported the story.

The Cox family is hoping for a miracle with little Addison, who is undergoing chemotherapy. She is using the same therapy which was created for her mother, and at the moment she is responding. “Her medication has to constantly be changed for her size as she grows. The cancer cells also constantly mutate, so the chemotherapy is constantly changing”, said the family correspondent.

Doctors are hoping that Briana and Addison’s case will allow them to discover how this could have been prevented. We here at MoleSafe hope that they do, and we wish the Cox family the best of luck!

Patrys Limited, an Australian company, has completed phase I of  its trial for PAT-SM6 anti-cancer antibody. The trial used the highest dosages that were found to be safe, Proactive Investors Australia reports. The purpose of this phase was to establish how tolerable and safe the drug is for human use. Fortunately, no significant safety issues were discovered.

“PAT-SM6 is a natural human antibody that has shown promise as a potential treatment for multiple types of cancer including melanoma”, the article states. It targets the protein GRP78, which controls cancer growth and survival. The other goal of the trial was to look at secondary endpoints. These endpoints measured the antitumor activity of PAT-SM6.

In August 2011, the company reported that analysis of tumour samples from two patients treated with PAT-SM6 found that the antibody had penetrated into the tumour biopsies, even though the doses were substantially below the anticipated therapeutic levels.

The drug is also being looked at to treat myeloma, a blood cancer. Studies showed that PAT-SM6 was also able to target bone marrow cells. The treatment of these cells with this anti-cancer antibody led to a significant amount of cell death. Scientists are clearly hoping that this will apply to melanoma cells as well.

Here at MoleSafe, we certainly hope they’re right! What do YOU think? Comment below and let us know.

A large advance happened in the melanoma world this week. Researchers were able to identify the molecular switch which controls transcription factor ATF2. ATF2 can progress melanoma, but also act as a suppressor in non-melanoma skin cancers. Teams based at the Sanford-Burnham Medical Research Institute, the University of California: San Diego, Ajou University School of Medicine in Korea, and Yale University found that the function of ATF2 depends on whether it’s held in the nucleus or within the cytoplasm, GEN News reported. The location of the transcription factor depends on the protein Kinase Cε.

Describing their work in cultured cells, Sanford-Burnham’s Ze’ev A. Ronai , Ph.D., and colleagues subsequently confirmed that in primary human melanoma, high levels of PKCε are associated the most with aggressive tumors and poorer patient survival. Reporting in Cell, the team claims its findings could provide the foundation for the development of prognostic tests and new approaches to rendering melanoma less resistant to therapy. Their published paper is titled “PKCε Promotes Oncogenic Functions of ATF2 in the Nucleus while Blocking Its Apoptotic Function at Mitochondria.”

Activating ATF2 plays a role in the development and growth of cells. It also plays a role in a cells’ response to DNA damage. ATF2 plays these roles when located in the nucleus of a cell. What scientists are trying to figure out is what is ATF2′s role when located in cytoplasm. Why does ATF2 have dual locations?

Prior research had found that squamous cell carcinoma (SSC) accumulates ATF2 in the cytosol, so the team started their work in an SSC cell line. They initially confirmed that whereas nonstressed cells exhibited predominantly nuclear ATF2, when the cells were put under genotoxic stress through treatment with etoposide (ETO), ultraviolet C, or ionizing radiation, ATF2 trafficked to the cytoplasm and associated with proteins at the mitochondrial outer membrane (MOM).

This mitochondrial localization of ATF2 following genotoxic stimuli was similarly exhibited in other cell types including normal human fibroblasts (HSF), primary human keratinocytes (NHEK), and melanocytes (HEM) as well as other SCC cell lines. In contrast, while some melanoma cell lines exhibited partial ATF2 accumulation at mitochondria in response to genotoxic stimuli, in a number of melanoma lines the transcription factor simply didn’t translocate to mitochondria.

Subsequent work using the SSC cells demonstrated that localization of ATF2 at the MOM directly blocked the formation of HK1/VDAC1 complexes that normally form in response to various forms of stress and disrupted MOM integrity, leading to mitochondrial leakage as a precursor to cell death.

What the studies also confirmed, was that Kinase Cε regulated the activity of ATF2. What was found was that patients with a decreased rate of survival had high Kinase Cε levels. This means that the protein is directly responsible for whether a tumor is malignant or not. The researchers are now trying to figure out how to release ATF2 from Kinase Cε’s control. If they can do that, scientists will be able to stop tumors from being malignant.

This is extremely exciting news, and we at MoleSafe wish them the best of luck!

What do YOU think about this news? Comment below and let us know.