This October, cyclists from throughout the Philadelphia area will be riding approximately 150 miles to raise money for cancer research at the Abramson Cancer Center through The Philadelphia Ride to Conquer Cancer.

Here are two stories of riders who are making an impact in The Ride to Conquer Cancer. 

“I’ve been given the opportunity to live.” – Eileen

In early 2013, Eileen Doyle went to the doctor concerned about inconsistencies in her menstrual cycle. That March, at the age of 26, she was diagnosed with an aggressive form of ovarian cancer. A large tumor was removed, and later she had both of her ovaries removed. Eileen endured six months of chemotherapy and radiation treatments, which took a huge toll on her and seriously affected the active lifestyle to which she was accustomed.

Facing a cancer diagnosis and managing treatment can be one of the most difficult times in a person’s life – the physical pain is terrible, but the emotional challenges that cancer brings can be even tougher. For Eileen, not only did she have to undergo aggressive treatments, but she was still grieving the loss of her 23-year old sister, who had passed away just one year earlier from stage IV metastatic nasopharyngeal cancer. Eileen found it helpful to participate in weekly support groups – finding strength in sharing experiences with others facing or having faced cancer.

Participating in The Ride to Conquer Cancer means everything to Eileen, not only to help her become more active again, but also to give back to her medical team at Penn Medicine’s Abramson Cancer Center who saved her life. “It means everything to be able to give back to The Abramson Cancer Center and to share with my friends and family the amazing support that the staff gave me to help me get better.”

Eileen will tell anyone how much easier her visits are because even though she’s going to the hospital, it is a great atmosphere with staff that are welcoming and supportive to each individual patient. “I have been given the opportunity to live and with this new perspective I am determined to keep going with as positive of an attitude as I possibly can.”

Read more of Eileen’s story on her participant page.

Kevin wants to raise money that stays local, to help local people with cancer

Kevin Kelly was diagnosed over 15 years ago with leukemia.

He was treated by David L. Porter, MD, at Penn Medicine’s Abramson Cancer Center, who is part of a comprehensive team of experts whose vision helped establish one of the oldest and largest Bone Marrow and Stem Cell Transplant Programs in the country. Fortunately, Kevin had a brother who was a match, which enabled him to undergo a successful bone marrow transplant and work towards recovery from his cancer.

About four years ago, during a routine bone marrow biopsy, Kevin’s doctors discovered that his cancer had returned. He is now on a daily medication that stabilizes his cancer, but it requires him to go to the hospital every 45 to 60 days for tests. It was during one of these checkups that he saw an advertisement for The Ride to Conquer Cancer and registered without hesitation. To be able to be part of supporting the research that helped provide Kevin with treatment options was all the motivation he needed.

“I’m happy to be a part of this ride so that I can share my own experiences at Penn and help raise money that stays local to help local people.”

Despite his treatments, Kevin feels great and is training regularly, now up to 65 miles in a single ride. Training helps him get through the psychological effects of his cancer by keeping him focused on positive health.

“Participating in The Ride is a goal. Not many people can ride 150 miles in a weekend, but with the training and support from The Ride guides, you will accomplish something great that will go towards a great cause.”

Read more of Kevin’s story on his participant page.

Join the Crew

Are you interested in getting involved in The Ride to Conquer Cancer, but don’t want to ride 150 miles? We still need you!

We are actively seeking people to join our crew team, volunteering to support the hundreds of riders along their route by:

• Providing snacks and meals on the route
• Setting up camp
• Providing medical care if you need it
• Marking the route with directional signage
• Driving our event vehicles
• Helping with route safety
• And much more!

Crew members are the backbone of the event. They are our bike mechanics, route guides and food distributors. Because of all their hard work and dedication, crew members experience the same perks as the riders such as access to a hot shower, catered meals and a cozy tent at Camp.

Join us today and be part of a great team!

Learn more about becoming a crew member, or contact Bridget at 215-323-5005 or [email protected].

The majority of causative variants in familial breast cancer remain unknown. Of the known risk variants, most are tumor cell autonomous, and little attention has been paid yet to germline variants that may affect the tumor microenvironment. In this study, we developed a system called the Consomic Xenograft Model (CXM) to map germline variants that affect only the tumor microenvironment. In CXM, human breast cancer cells are orthotopically implanted into immunodeficient consomic strains and tumor metrics are quantified (e.g., growth, vasculogenesis, and metastasis). Because the strain backgrounds vary, whereas the malignant tumor cells do not, any observed changes in tumor progression are due to genetic differences in the nonmalignant microenvironment. Using CXM, we defined genetic variants on rat chromosome 3 that reduced relative tumor growth and hematogenous metastasis in the SS.BN3IL2Rγ consomic model compared with the SSIL2Rγ parental strain. Paradoxically, these effects occurred despite an increase in the density of tumor-associated blood vessels. In contrast, lymphatic vasculature and lymphogenous metastasis were unaffected by the SS.BN3IL2Rγ background. Through comparative mapping and whole-genome sequence analysis, we narrowed candidate variants on rat chromosome 3 to six genes with a priority for future analysis. Collectively, our results establish the utility of CXM to localize genetic variants affecting the tumor microenvironment that underlie differences in breast cancer risk. Cancer Res; 74(22); 1–11. ©2014 AACR.

The majority of causative variants in familial breast cancer remain unknown. Of the known risk variants, most are tumor cell autonomous and little attention has been paid yet to germline variants that may affect the tumor microenvironment. In this study, we developed a system called the Consomic Xenograft Model (CXM) to map germline variants that impact only the tumor microenvironment. In CXM, human breast cancer cells are orthotopically implanted into immunodeficient consomic strains and tumor metrics are quantified (e.g., growth, vasculogenesis, and metastasis). Because the strain backgrounds vary, whereas the malignant tumor cells do not, any observed changes in tumor progression are due to genetic differences in the non-malignant microenvironment. Using CXM, we defined genetic variant(s) on rat chromosome 3 that reduced relative tumor growth and hematogenous metastasis in the SS.BN3IL2Rγ consomic model compared to the SSIL2Rγ parental strain. Paradoxically, these effects occurred despite an increase in the density of tumor-associated blood vessels. In contrast, lymphatic vasculature and lymphogenous metastasis were unaffected by the SS.BN3IL2Rγ background. Through comparative mapping and whole genome sequence analysis, we narrowed candidate variants on rat chromosome 3 to six genes with a priority for future analysis. Collectively, our results establish the utility of CXM to localize genetic variants affecting the tumor microenvironment which underlie differences in breast cancer risk.

Dysregulation of the Akt/PKB pathway has been associated with poor prognosis in several human carcinomas. Current approaches to assess Akt activation rely on intensity-based methods, which are limited by the subjectivity of manual scoring and poor specificity. Here, we report the development of a novel assay using amplified, time-resolved Förster resonance energy transfer (FRET), which is highly specific and sensitive and can be adapted to any protein. Using this approach to analyze primary breast tissue microarrays, we quantified levels of activated pAkt at a spatial resolution that revealed molecular heterogeneity within tumors. High pAkt status assessed by amplified FRET correlated with worse disease-free survival. Our findings support the use of amplified FRET to determine pAkt status in cancer tissues as candidate biomarker for the identification of high-risk patients. Cancer Res; 74(18); 1–13. ©2014 AACR.

Metadherin (MTDH) overexpression in diverse cancer types has been linked to poor clinical outcomes, but definitive genetic proof of its contributions to cancer remains incomplete. In particular, the degree to which MTDH may contribute to malignant progression in vivo is lacking. Here, we report that MTDH is amplified frequently in human prostate cancers where its expression levels are tightly correlated with prostate cancer progression and poor disease-free survival. Furthermore, we show that genetic ablation of MTDH in the transgenic adenomcarcinoma of mouse prostate (TRAMP) transgenic mouse model of prostate cancer blocks malignant progression without causing defects in the normal development of the prostate. Germline deletion of Mtdh in TRAMP mice prolonged tumor latency, reduced tumor burden, arrested progression of prostate cancer at well-differentiated stages, and inhibited systemic metastasis to distant organs, thereby decreasing cancer-related mortality ∼10-fold. Consistent with these findings, direct silencing of Mtdh in prostate cancer cells decreased proliferation in vitro and tumor growth in vivo, supporting an epithelial cell–intrinsic role of MTDH in prostate cancer. Together, our findings establish a pivotal role for MTDH in prostate cancer progression and metastasis and define MTDH as a therapeutic target in this setting. Cancer Res; 74(18); 1–12. ©2014 AACR.