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How to Find - Affordable Housing and Financial Help for Rent or Utilities
Site: Halton
|Record #: BTN1074
|Last Full Update: 24 Aug 2015
|Memos and Bulletins
|Public Comments
|This database also has records for: Emergency shelters, Income Programs and Financial Assistance, Free and low cost dental care, Free and low cost legal help
|Agency and Service Names
|Alternate Name
|Affordable housing (Low-Income / Subsidized / Nonprofit /non-profit / public / Ontario housing / social housing), How to Find ; Assistance / Help with Rent payment ; Assistance / Help with utility, gas, electricity, heating bills
|Agency Information
|Legal Status
|(50) Non Profit
|Service Information
|Description (Service)
|This topic record explains different types of housing and how to apply, and is an index to other housing-related records in this database.
1. Nonprofit Housing
* most (but not all) nonprofit housing providers centralize their applications for subsidized units through HATCH (Halton Access To Community Housing) at Halton Region 905-825-6000, and take their own applications for market rent units.
* for a list of ALL nonprofit housing in Halton, see here (how to apply is shown in details for each housing community)
* nonprofit housing provides subsidized (rent-geared-to-income or below-market-rent) units, for people who meet low-income criteria
* some also have market rent units, open to people of any income
* some are exclusively for seniors or people with disabilities, and some provide supportive services, such as meals, personal support, etc.
* some is owned by Halton Region government (what was formerly called public housing or Ontario Housing) and some is owned by other nonprofit organizations and charities
2. Housing in the private rental market
Halton Housing Help provides services for renters and landlords, contact at Halton Region 905-825-6000
* provides free help and support to find and keep rental housing
* its Halton Rent Connect listings (see here) may include some for house sharing, or reduced rent in exchange for household help, which may reduce the cost of housing in the private rental market
* for more details, see separate record here
Also see listings in local newspapers and commercial websites, such as www.gottarent.com, www.viewit.ca, Kijiji, etc.
3. Housing for youth 16 and older
Bridging the Gap program helps youth ages 16 to 24 find housing, also has Host Homes initiative to match youth with host homeowners who provide safe temporary housing and Bridge House program which provides transitional housing for up to two years in Burlington and Milton * also provides assistance in accessing Ontario Works, food, alternative education and work, for more information see full record here.
1. Rent deposit assistance
May be available from Halton Region 905-825-6000 for low-income people who qualify
* covers 'last month' portion only.
2. Help to pay rent or utilities
* Housing Stability Fund (see separate record here) provides one-time assistance for those who are qualified, to apply, call Halton Region Coordinated Intervention Services Team at 905-825-6000.
* Winter Warmth & LEAP programs (for details see separate record here).
* Ontario Electricity Support Program (OESP) provides a credit directly on each monthly hydro bill for those under the Low Income Measure cutoff (for details see separate record here).
3. Property tax rebates and deferral (for homeowners)
See separate record for Property Tax Deferral Program and Low Income Seniors Property Tax Rebate here.
Halton Community Legal Services provides free legal assistance to low income people for housing and landlord/tenant issues (see separate record here).
|Areas Served
|Halton Region
|Not applicable.
|Site Information
|Located In Community
|Halton Region
|Unknown - Accessibility varies by location
|Taxonomy and Classification
|Service Categories
|Housing Expense Assistance ; Housing Search and Information ; Low Income/Subsidized Rental Housing ; Utility Assistance


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If you've been asked to make a sworn statement about your finances a Financial Affidavit can be a simple solution. A court may require you to provide information about your assets, expenses, and investments - this is common in divorce cases but can happen in many legal or business situations. Regardless of how the need arose, your Financial Affidavit is your formal financial statement.
Use the Financial Affidavit document if:
- A court or business has request confirmation of your financial situation.
- You are addressing financial issues dealing with a divorce
A court may ask you for a statement about your expenses, income, assets and liabilities; fortunately, it's easy to create a Financial Affidavit. All you need is your financial information, a written statement, and a notary public. Just remember that you're making a sworn statement, so there's no room for exaggeration or modesty. While you might not be before a judge an affidavit carries a lot of weight. So gather your information, double check that it's accurate, and a Financial Affidavit will help make it official.
Other names for this document: Financial Affidavit Form, Financial Disclosure Affidavit, Financial Statement Affidavit
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subset: commoncrawl


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Previous Episode | Next Episode
For Whom The Bell Klangs, Part 1For Whom The Bell Klangs, Part 1 (1990) Season 1 Episode 45- TaleSpin Cartoon Episode Guide by Dave Koch
This page has been viewed 8 times this month, and 435 times total.
- TaleSpin Cartoon Episode GuideEpisode GuideTelevisionSeriesCartoon
- Traditional Animation
- Walt Disney Television Animation.
- Animation Studio: Walt Disney Animation France S.A.
- Distributed by: Buena Vista Television
- Cartoon Characters: Kit Cloudkicker, Baloo, Rebecca Cunningham, Molly Cunningham, Wildcat, King Louie, Don Karnage, Shere Khan, Usher, Thaddeos E. Klang, Katie Dodd, City Mayor, Girl with Map, Brutus, Trader Joe, Red Robe Thugs, Scarabs.
- Voice Actors: R. J. Williams, Ed Gilbert, Sally Struthers, Janna Michaels, Pat Fraley, Jim Cummings.
Additional Voices: Charles Adler; Full Voice Cast ...
- Directed By Ed Ghertner, Larry Latham, Jamie Mitchell, Robert Taylor, James T. Walker; more Directors ...
- Produced By Ed Ghertner, Larry Latham, Jamie Mitchell, Robert Taylor, James T. Walker, Jymn Magon, Mark Zaslove, Ken Tsumura.
- Animated By Jean Luc Balester, Moran Caduissin, Pierre Fassel, Bruno Gaumetou, Dina Gellert-Nielsen, Arnold Gransac, Peter Haunsner, Nicholas Marlet, Dominique Montfery, Claude Montfort; more Animators ...
- Written By Mark Zaslove, Duane Capizzi, Karl Geurs, Ken Koonce, Jymn Magon, Bruce Talkington, David Weimers, Len Uhley.
- Music: Christopher L. Stone.
- First Aired on November 27, 1990.
- Originally Released in Syndication.
- Running Time: 30 minutes.
- Episode Number: 45
- Season: 1
- Color
Cartoon Summary:
Tired of adventure, Baloo and Louie decide to relax, only to run into Katy, a foxy archaeologist, whose goal in life is to find the lost city of Tinabula.
Cartoon Production Information:
The animal inhabitants of Rudyard Kipling's beloved Jungle Book graduated from swinging in the trees to full-time professional careers and complicated emotional lives in the television spin-off Tale Spin. Part of the appeal of Disney's Tale Spin... (more)
Cartoon Video:
Sorry, we do not have a video of For Whom The Bell Klangs, Part 1. If you have one, or know of one on Youtube, Vimeo or any other site, Let Us Know
Submit Additional Information:
Do you have anything to add to this page? Have we made any mistakes... or do you have any additional information about For Whom The Bell Klangs, Part 1? If so, we would love to hear from you. Please send us a quick note with your additions or corrections to this page, and we will make the corrections as soon as possible!
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Do you love For Whom The Bell Klangs, Part 1, or do you think it is the worst cartoon ever? Let us know what you think! Surely you have an opinion... so share what you think. Take a minute and post your own comments about this cartoon here.


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Are you Paula Langenhoff?Claim your profile
Publications (2)0 Total impact
Article: "But we can't go back"[Show abstract] [Hide abstract]
ABSTRACT: In 2004, a provincial cancer agency in Canada developed and implemented a provincewide Leadership Development Initiative (LDI) to enhance organizational leadership and relationships. Research using a quasi-experimental survey design determined whether LDI implementation influenced the emotional health and leadership practices of LDI participants. An ethnographic approach (18 focus groups and 13 individual interviews) explored participants' perceptions of the LDI. This article presents qualitative findings that contribute to understanding the statistically significant findings of increasing levels of cynicism, emotional exhaustion, and burnout for most LDI participants. The LDI was regarded as a critical strategy for helping leaders grow and cope with change and help in changing organizational leadership culture to be more collaborative and inclusive. However, an organizational history of short-lived, flavor-of-the-month development initiatives and growing skepticism and disengagement by leaders represented in the themes of Catch-22 and "there is no going back" contributes to understanding why these quantitative measures increased. Few studies have explored the hypothesis that real organizational development happens through a series of planned stages. In this study, leaders experienced escalating frustration because change was not seen to occur fast enough in "others" and reported that this was necessary before they would alter their own behavior. Leadership development programs in general need to reflect the reality that it takes considerable time, patience, and effort to effect fundamental change in leadership culture.
- [Show abstract] [Hide abstract]
ABSTRACT: Purpose – The purpose of this paper is to illustrate the formation of the Leadership Development Initiative (LDI) and to demonstrate how the program was collaboratively tailored to meet the organizational and developmental needs of leaders in the organization, using a learning cohort approach for implementation. Design/methodology/approach – This paper describes how the LDI was designed, implemented, and assessed through its various stages of formation. Beginning with theory, a learning cohort approach was envisioned to not only bridge organizational departments by bringing leaders from all divisions to learn together, but would also be more sustainable in the long term. A participatory action research study was used to enhance program development and to ultimately explore the effectiveness of the LDI. Findings – The LDI was critical to developing leadership and management competencies/skills, organizational networking, relationship building, and fostering a philosophy of leadership as collaborative visionary practice toward a common goal. Research limitations/implications – The conceptual framework of the LDI using a learning cohort approach may provide an approach for further development of leadership programs in other healthcare organizations. Practical implications – The LDI demonstrated how internally developed leadership programs can be an effective approach, with evaluation and application of research findings to continually improve and enhance the program, when resources are limited but the desire to learn is not. Originality/value – The LDI program is a peer based, cohort approach established through a conceptual framework based on advanced leadership theories and practices.
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Alberta Health ServicesCalgary, Alberta, Canada


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As Willis Davis tells it, he's healthy as a mule. He eats what he wants, and does what he wants. He is free of the potentially deadly skin cancer that he was diagnosed with five years ago.
Davis, 75, was diagnosed with stage IIIc melanoma in September of 2009. It was just before he and his wife, Robbin, had finalized the purchase of a new home in the Virginia community of Ringgold. His cancer was spreading, said Frances Collichio, MD, a researcher with the UNC Lineberger Comprehensive Cancer Center and a clinical professor in the UNC School of Medicine Division of Hematology/Oncology. And Davis wanted more time.
"I said 'Lord, if you'll give me a few more years to live, to let me get squared away on this house, then you'll have your will and your way,' " he said.
In a month of the cancer diagnosis, Davis was in surgery at the N.C. Cancer Hospital. But his cancer continued to spread, so Collichio said he needed a treatment that would attack the cancer throughout the body. They turned to an investigational oncolytic immunotherapy available through a clinical trial at the N.C. Cancer Hospital and other medical centers.
The investigational treatment, talimogene laherparepvec, or T-VEC, uses a modified herpes simplex I virus to fight melanoma. The virus has been genetically engineered to be non-pathogenic, as well as to selectively replicate in cancer cells in order to kill them. It has also been modified to trigger the body's disease-fighting immune system against cancer by releasing a trigger called granulocyte macrophage colony-stimulating factor (GMCSF).
"We recognized that the surgery alone was not going to help, and we needed something we could give him that would treat his whole system," Collichio said. "We had seen some promising early data for this an investigational treatment for patients with in-transit melanoma like this."
The phase III trial, whose findings were published earlier this year in the Journal of Clinical Oncology, included 436 patients with stage IIIb to IV melanoma. UNC was one of the top five medical centers enrolling in the study, with 19 patients, according to the pharmaceutical company developing the drug, Amgen. The study found that T-VEC increased median overall survival by about four months compared with injections of GMCSF alone. Sixteen percent of patients had a durable response of six months or more, and 26 percent of patients showed an overall response. The study authors, which included Collichio, state that the treatment is the first oncolytic immunotherapy to show a benefit for patients in a phase III trial for melanoma.
Within several hours of receiving the T-VEC treatment, Davis experienced flu-like symptoms that lasted about two hours, and that then dissipated by the next morning. After four treatments with T-VEC, Davis was considered to be in cautious remission. He is now cancer-free, Collichio said, and they hope he is cured. He said he was told that if T-VEC hadn't worked, he likely would have had eight to nine months to live.
"The treatment worked wonders on me," he said. "It's a miracle."
Davis said he is grateful for the compassionate care he received from Dr. Collichio, and also advocated for U.S. Food and Drug Administration approval of the treatment to help other patients. The pharmaceutical company Amgen has submitted an application to the FDA for approval of T-VEC for treatment of injectable regionally or distantly metastatic melanoma.
"Dr. Collichio just showed that she cared for me, and did everything she could do for me, including getting me accepted in that program," he said. "If (T-VEC) is not approved, it would be a travesty to people with melanoma," he also said.
UNC Lineberger is participating in an additional clinical trial for T-VEC. A multi-center, Phase Ib/II, trial sponsored by Amgen will test T-VEC in combination with the immunotherapy treatment ipilimumab in patients with previously untreated, unresectable, advanced melanoma compared with ipilimumab alone.]]>
Nancy E. Thomas, MD, PhD, an associate professor of dermatology School of Medicine's dermatology and a member of UNC Lineberger Comprehensive Cancer Center, will lead the research project, called Image Analysis to Assess Melanoma Heterogeneity. The project will examine imagery from more than 1,300 melanoma patients worldwide, including 214 from North Carolina.
A $190,000 award from the University Cancer Research Fund will support the project. The North Carolina General Assembly created the fund in 2007 to accelerate the battle against cancer at UNC Chapel Hill's School of Medicine and its Lineberger Comprehensive Cancer Center.
RENCI specialists in bioinformatics, image analysis and data mining will work with Dr. Thomas and melanoma researchers at UNC-Chapel Hill to develop algorithms or computational methods that can identify cancerous and healthy tissue in high-resolution images. Once cells in the images are identified as cancerous or healthy, the researchers will collect information on physical details, such as cell size, shape, and color of melanoma cells. All these details will be used to develop evidence-based models of melanoma cell descriptions.
In addition, advanced computational methods will be used to identify the physical characteristics of the melanoma cells--features uncovered through image analysis--which are associated with tumor classification, based on known information about somatic genetic mutations in melanomas, and survival.
"What's exciting about our approach is that we may be able to uncover relationships between the physical qualities of melanoma cells, tumor genotype, and patient outcomes" said Charles Schmitt, manager of biological science programs at RENCI and a co-investigator on the project. "It's the kind of work that can only be done by bringing together expertise in multiple areas."
Nearly 60,000 new cases of melanoma were diagnosed in the U.S. in 2007, according to estimates from the American Cancer Society, and more than 8,000 patients died of the disease. Melanoma cases continue to increase and prognosis is poor for patients with advanced melanoma tumors.
"The objective of this proposal is to utilize image analysis to uncover associations between the physical characteristics of melanoma, somatic mutations in melanoma, and survival" said Thomas. "But ultimately, our long-term goal is to help patients. We want to use image analysis to improve melanoma classification, which we would expect to improve diagnosis and guide treatment recommendations."]]>
"We're now in an era where we have changing paradigms," Ollila said. Seven new melanoma therapies have emerged since 2011, including some targeting mutations of a gene called BRAF and others that work to trigger the body's own immune system to fight the disease.
The conference was highlighted by a presentation from Antoni Ribas, MD, PhD, a professor of medicine and surgery at the David Geffen School of Medicine at the University of California Los Angeles and director of the UCLA Jonsson Comprehensive Cancer Center Tumor Immunology Program, on research into a new type of immune modulating drugs. PD-1 inhibitors, the first two drugs were just FDA-approved last year, work by blocking a receptor to activate the body' immune system against metastatic melanoma cells.
The U.S. Food and Drug Administration approved the PD-1 inhibitor pembrolizumab in September for treatment of patients with advanced or un-resectable melanoma and who are no longer responding to other drugs. Ribas was the lead investigator for a phase I clinical trial for the drug. Another PD-1 inhibitor, or nivolumab, was approved in December.
Ribas said PD-1 inhibitors are going to mean "remarkable advances" in treatment.
Thursday's conference also included talks on outcomes for surgical treatment for stage IV cancer, melanoma prevention, as well as cancer-causing behaviors.
Dr. Puneet Jolly, MD, PhD, an assistant professor in the UNC School of Medicine Department of Dermatology, spoke on sunscreen and sun protective clothing in melanoma prevention. He described recent regulations that put emphasis on sunscreen protection against both ultraviolet A as well as ultraviolet B radiation.
Historically, there hasn't been as strong of an emphasis on protection against UVA radiation in sunscreen products, he said, as SPF is a direct measure of protection against UVB radiation alone.
New sunscreen labeling regulations have been put in-place to indicate protection against both. In 2012, the FDA established a test to determine which sunscreens could be labeled "broad spectrum," to indicate protection against UVA as well as UVA radiation.
"This is important because it is becoming increasingly clear that UVA radiation plays a big role in the development of melanoma in addition to UVB," Jolly said. "It is also becoming more apparent that sun protective clothing may be an even better way to protect against these harmful rays than sunscreen," he added.
Indoor tanning was the topic of a presentation by Seth Noar, a UNC Lineberger member and professor in the UNC School of Journalism and Mass Communication. He spoke on a 2014 study published in JAMA Dermatology that found that young women continue to use tanning beds, despite being aware of the health risks associated with indoor tanning. Of 706 university women surveyed, 45 percent indicated they had used tanning beds.
"The evidence is in: we know how bad this is, we know it's a carcinogen, but we have a lot of work to do in getting the word out, not only to young women who do this behavior, but to parents," Noar said.
Also at the conference, a presentation by Karyn Stitzenberg, MD, MPH, FACS, a UNC Lineberger member and assistant professor of surgery in the UNC School of Medicine Division of Surgical Oncology, focused on a more uncommon type of melanoma – gynecologic melanoma. Vulvar and vaginal melanomas represent less than 2 percent of all melanomas. Although uncommon, the mortality rate from these melanomas is very high because patients generally present with advanced disease. To improve early detection, more provider awareness and education is needed. She said any sign of pigmentation in the external female genital organs or in vaginal tissue should be biopsied.
The 10th annual UNC Multidisciplinary Conference is already in the planning stages for February 2016.]]>
The research, published today in the journal Nature Communications, provides evidence for how these particular melanoma cells help tumors resist drugs designed to block blood vessel formation.
"For a long time the hope has been that anti-angiogenic therapies would starve tumors of the nutrients they need to thrive, but these drugs haven't worked as well as we all had hoped," said Andrew C. Dudley, PhD, assistant professor in the Department of Cell Biology and Physiology, member of the UNC Lineberger Comprehensive Cancer Center, and senior author of the paper. "There are likely several reasons why these drugs haven't been effective; our research suggests that these previously uncharacterized cells could be one of the reasons."
Most of the drugs developed to disrupt tumor blood vessels target a protein called vascular endothelial growth factor, or VEGF, which is part of a major signaling pathway in the noncancerous endothelial cells that typically line blood vessels in tumors. But other research has suggested that tumors are able to resist anti-angiogenic therapies – particularly those targeting VEGF – through a variety of complex mechanisms. In one set of experiments, Dudley and graduate student James Dunleavey, used a known anti-angiogenic drug which blocks VEGF and found that this new subpopulation of melanoma cells was more prevalent in drug-resistant tumors in mouse tumor models. Moreover, tumors composed entirely by this new subpopulation in mouse models did not respond at all to anti-VEGF therapy.
This research further elucidates the complex nature of human tumors, which are not comprised solely of the same type of cancer cell but instead feature a mixed population of different cell types with different functions.
To make these discoveries, Dunleavey first isolated what he thought were noncancerous endothelial cells from melanoma tumors. Then he conducted a genetic analysis to reveal that these cells did not express most of the well-known biomarkers common to endothelial cells. For instance, the cells didn't express VEGF receptors. This could explain why the anti-VEGF therapy was ineffective at blocking tumor growth.
"These cells looked very different from normal endothelial cells in cultures," said Dudley, who is also a member of the UNC McAllister Heart Institute. "We didn't know what these cells were. For a while, we kind of scratched our heads until Jim conducted more experiments over the course of a year to find that these cells had several markers similar to melanoma cells." Further analysis revealed that these cells were in fact a new kind of melanoma cell, one that expressed a particular protein called PECAM1, which is very important to the function of endothelial cells.
PECAM1 is an adhesion molecule. Scientists have known that endothelial cells use it to stick together to form blood vessels. When Dudley's team looked at blood vessels in tumors made of PECAM1-positive tumors, they found melanoma cells alongside noncancerous endothelial cells on the inside of vessels. "We don't think these new melanoma cells are just passively filling in gaps between endothelial cells in the tumor vasculature," Dudley said. "How they come to form blood-filled channels seems to be an active process that involves PECAM1."
Dudley and Dunleavey then teamed up with other scientists, including UNC's Paul Dayton, PhD, a professor in the Department of Biomedical Engineering, member of the UNC Lineberger Comprehensive Cancer Center, and co-author on the Nature Communications paper. Dayton's lab conducted ultrasound imaging studies showing that PECAM1-positive tumor blood vessels in mice had twice the vascular density of PECAM1-negative vessels. And the blood volume of PECAM1-positive blood vessels was 4 ½ times greater than PECAM1-negative vessels. This showed the researchers that these newly discovered PECAM1-positive melanoma cells had a real effect on the function of tumor blood vessels.
Dunleavey added, "We think these cells help allow tumor cells to interact in specific ways with bona fide endothelial cells." And this interaction – plus the lack of VEGF responsiveness – could help blood vessels and blood-filled channels resist therapies designed to destroy them.
Dunleavey and Dudley said that this discovery is likely just one part of how some tumors manage to circumnavigate therapies designed to attack their blood vessels.
"Anti-angiogenic therapies are typically used in conjunction with another drug," Dunleavey said. "It could be that we'll need to develop a combination of anti-angiogenic drugs to attack the endothelial cells that form blood vessels and the tumor cells that might form blood-filled channels in tumors."
Other authors of the Nature Communications paper, include UNC graduate students Lin Xiao, David Irwin, Victoria Brings, and Sarah E. Shelton; UNC undergraduate student Joshua Thompson; lab technician Mi Mi Kim; Janiel M. Shields, PhD; David W. Ollila, MD, professor of surgery at UNC; Rolf A. Brekken, PhD, associate professor at the University of Texas Southwestern Medical Center; and Juan M. Melero-Martin, PhD, assistant professor of surgery at Harvard.
This research was funded by grants from the National Institutes of Health and the University Cancer Research Fund at UNC-Chapel Hill.]]>
"When melanoma is diagnosed early, the prognosis is good. However, once it spreads, it is very difficult to treat," noted David Ollila, MD, co-director of UNC's multidisciplinary melanoma program and a surgical oncologist.
That's why UNC Cancer Care and UNC Lineberger Comprehensive Cancer Center are sponsoring a program that reaches out to hair stylists and barbers to provide them with the information they need to help detect clients' skin cancers on their scalp or neck, and to counsel them about cancer prevention.
"I have personally cared for several patients with melanoma and other skin malignancies whose cancer on was first noted by their hair stylist or barber," Ollila says. "Stylists have a unique role and point of view from behind the chair and, armed with information, they can save lives."
The free program will be held at the N.C. Cancer Hospital's Conference Room #1, on the Ground Floor, on Monday, May 9, 2011 from 10 a.m. to 1 p.m.
The program includes information on melanoma and other skin cancers and demonstrations of how to recognize them, tips on prevention, and advice on how to care for clients who might be undergoing treatment for skin cancer.
To register, please call (919) 843-0680 or email Beth Fogel, RN . Lunch will be provided to program participants.]]>
The researchers found high levels of a particular enzyme in melanoma samples that they believe is a driver of the cancer's growth. The enzyme, called interleukin-2 inducible T-cell kinase, or ITK, has not previously been explored as a driver of solid tumors. Normally, it's expressed in a subset of the body's disease-fighting immune cells.
The researchers hope the findings, which were published today in the journal Clinical Cancer Research, could lead to new treatments for melanoma since, as the researchers state, one drug that can block ITK's activity has been approved for blood cancers and others are in the pipeline for other diseases.
"We have discovered that ITK is highly expressed in melanoma even though it was thought to be restricted to immune cells, and when you inhibit it, you decrease melanoma growth," said Nancy E. Thomas, MD, PhD, a UNC Lineberger member, the Irene and Robert Alan Briggaman Distinguished Professor in the UNC School of Medicine Department of Dermatology and the paper's senior author. "Therefore, we think it's a good potential drug target."
There is a need for new treatment targets for melanoma, a deadly disease once it's started to spread. Melanoma of the skin has a 98 percent five-year survival rate when the cancer is localized, according to data from the National Cancer Institute Surveillance, Epidemiology and End Results Program. But once the cancer has spread regionally, the five-year-survival rate falls to 64 percent. And the survival rate falls to 16 percent after the cancer has spread to more distant regions.
"New therapies are needed because of the high mortality rate for metastatic melanoma, and the ability of melanomas to become resistant to many of the current therapies," said Craig Carson, PhD, a research instructor in the UNC School of Medicine Department of Dermatology and the paper's first author. Carson said they hope their recent finding will lead to new treatments for melanoma.
In an analysis of normal skin tissue, non-cancerous moles, and melanoma samples, researchers found that ITK was expressed at greater levels in primary and metastatic melanomas than in non-cancerous moles. In the metastatic melanoma samples, 91 percent had higher expression levels than of the non-cancerous moles.
The finding was surprising to the researchers because the ITK enzyme is typically expressed only in certain cells in the body.
"It's only found in a subset of the immune cells," Carson said.
ITK helps with the development of certain immune cells, the researchers say, and is involved in immune cell activation, development and production.
"The cancerous cells were packed with that protein, and it was bizarre – that's not supposed to be there," Thomas said. "And so, the question is, well, what is it doing there?"
They found that the gene's expression in the melanoma cells was a driver of the cancer. When they manipulated cells in the test tube to have lower ITK expression, they found that the cells reproduced more slowly and with less movement. They also found that an experimental inhibitor of the ITK protein's activity had the same effect on cells and slowed tumor growth in mice with melanoma.
They hope their findings will lead to development of treatments for melanoma.
"ITK has been conceived of as a therapeutic target for inflammatory diseases such as chronic obstructive pulmonary disorder, but because ITK had not been noted in melanoma before, it has not been a target for its treatment," Carson said. "I expect ITK to become an important therapeutic target for melanoma because of the expected minimal side effects, and the fact that ITK is found in so many of the melanomas we have investigated."
Funded in part by the University Cancer Research Fund, the findings were the result of years of collaborative work involving multiple UNC Lineberger researchers and University of North Carolina School of Medicine departments.
The study was funded by the National Cancer Institute, the National Institute of Environmental Health Sciences, the University Cancer Research Fund, the Harry J. Lloyd Charitable Trust, an UNC LCCC Development Grant, The V Foundation, the Doris Duke Charitable Foundation Clinical Research Fellowship, the National Center for Advancing Transnational Sciences and The Irene and Alan Briggaman Distinguished Professorship. UCRF supported, in part, work in the Mouse Phase 1 Unit and the UNC Translational Pathology Laboratory.
Suggested citation for this article: Carson C.C., Moschos S.J.,Edmiston S.N., Darr D.B., Nikolaishvili-Feinberg N, Groben PA, Zhou X, Kuan PF, Pandey S, Chan KT, Jordan JL, Hao H, Frank JS, Hopkinson DA, Gibbs DC, Alldredge VD, Parrish E, Hanna SC, Berkowitz P, Rubenstein DS, Miller CR, Bear JE, Ollila DW, Sharpless NE, Conway K, Thomas NE. IL-2 Inducible T-cell Kinase, a Novel Therapeutic Target in Melanoma. Clinical Cancer Research.
Contact: Laura Oleniacz
This comprehensive characterization of the biological underpinnings of melanoma is the latest work by researchers involved in TCGA, a National Cancer Institute and National Human Genome Research Institute-sponsored effort to create an atlas of genetic and epigenetic changes that drive different cancers. The researchers collected samples from 331 patients and used several molecular methodologies to complete the study, the largest of its kind to-date for cutaneous melanoma. The findings were published online today in the journal Cell.
"This study explains some long-standing clinical observations that we could not entirely comprehend, in particular for stage III melanoma," said Stergios Moschos, MD, a UNC Lineberger member, a clinical associate professor of medicine at the University of North Carolina School of Medicine Division of Hematology/Oncology and a member of the data analysis and manuscript committee for the TCGA melanoma project. "This work can also serve as a reference map to assist in personalized prognostic and treatment decisions and future clinical trials for patients with cutaneous melanoma."
In the study, the researchers identified four genomic subtypes of melanoma based on mutations. Two subgroups were defined by mutations that have already been shown to be common in melanoma – mutations in the BRAF and RAS genes. But from a previously heterogeneous group of people who lacked those mutations, one potentially clinically significant subgroup emerged.
That new group was characterized by inactivating mutations in a gene called NF1. Patients in the NF1-mutant group – which made up about 14 percent of the entire patient population in the study-- were significantly older and their cancers harbored significantly more mutations. Moschos hopes this finding will trigger new research into targeted treatments for patients in that group, and perhaps into the use of treatments that are already FDA-approved.
"For example, BRAF and MEK inhibitor combinations are now used to treat patients with BRAF mutant melanomas, and MEK inhibitor combinations are being explored for RAS-mutant melanomas," said Ian Watson, PhD, an instructor of genomic medicine who was one of three analysis co-chairs for the project from The University of Texas MD Anderson Cancer Center. "Pre-clinical studies have already demonstrated that some NF1-mutant melanoma cell lines respond to MEK inhibitors, but more work is needed to identify responders and non-responders within this new melanoma subtype, as well as to determine strategies to treat (patients in the Triple Wild-type subgroup without BRAF, RAS, and NF1 mutations)."
The fourth subgroup was defined by patients who lacked BRAF, RAS, or NF1 mutations. They didn't have high incidence mutations, but had some low-frequency mutations in genes such as cKIT, and had a significantly higher number of gene copy alterations (gains or losses). Thirty percent of samples in that subgroup had ultraviolent light (UV)-type signature mutations, while more than 90 percent of samples in each of the other groups had UV-type signatures. The high overall incidence of UV signatures points to the important role of sun or tanning bed exposure in this disease, Moschos said. Overall, the researchers hope the subgroup findings can help personalize treatment decisions and guide new targeted treatment strategies.
The study also helped to reveal the importance of the body's immune response in melanoma, Moschos said. In an analysis of RNA expression data led by Katherine Hoadley, PhD, a UNC Lineberger member and research assistant professor of genetics, and Xiaobei Zhao, a postdoctoral research associate at UNC Lineberger, the study found that 51 percent of patients had high expression levels of genes predominately expressed by immune cell subsets. A pathologic analysis of tumors confirmed that genes thought to be immune-related did come from melanoma-infiltrating immune cells, suggesting an augmented immune response in that group. And patients in the immune-high group with regionally metastatic disease had better overall survival than patients of similar stage and without high expression of immune genes. That finding has implications for immunotherapy treatments that work by unlocking the brakes on the body's own immune response to the disease, Moschos said.
"Given that recent studies showed that immune checkpoint inhibitors may be more effective in patients whose tumors are already infiltrated by immune cells, it is not surprising that these immunotherapies are not effective for everybody," he said.
In addition to identifying cells with a higher immune response, the RNA analysis also identified a subgroup of patients with regionally metastatic melanoma who had a worse prognosis. That group exhibited high expression of genes associated with pigmentation and keratins, which are skin-toughening proteins usually found in epithelial skin cells. This keratin-expressing subtype of melanoma had been previously identified by UNC Lineberger Director Norman Sharpless, MD, the Wellcome Distinguished Professor in Cancer Research, and collaborators, but the worse prognosis of this group is a new finding.
Another immune-related finding was that a protein called PD-L1 that's been used to predict responses to immune checkpoint inhibitors can be overexpressed by melanoma cells for genetic reasons. They found amplification of the PD-L1 gene in people with BRAFV600 mutations in particular. The finding helps explain why the test the measures PD-L1 expression in tumors alone is not sufficient to predict responses to PD1/PD-L1 targeted therapies, Moschos said.
The study was funded by the National Institutes of Health.]]>
The grant will investigate a novel target in melanoma, MerTK, which was discovered in Dr. Shelley Earp's lab with a then-UNC medical student and doctoral candidate Doug Graham. Dr. Graham, now a professor of pediatric oncology at the University of Colorado, and Dr. Earp have been collaborating on this project for over a decade and were joined five years ago by Stephen Frye, PhD and Xaiodong Wang, PhD, UNC Lineberger members in UNC's Eshelman School of Pharmacy, who have worked with the team to develop a drug that targets MerTK activity.
Their recent publication showed that MerTK is elevated in metastatic melanoma and that the team's prototype drug could slow the growth of melanoma cells both alone and even more effectively in combination with some of the newly approved melanoma drugs. Approximately half of the funds will be used by the UNC Lineberger/Colorado team to develop their small molecule drug, while the other half will be used by team members in Israel who will concentrate on understanding how MerTK is activated from outside the melanoma cell and how that might be blocked to enhance therapy.
"Melanoma rates continue to increase worldwide, while the rates of other common cancers have been decreasing," said Debra Black, MRA Co-Founder and Chair. "Several new treatment options have been made available to melanoma patients in recent years, but there is still an urgent need for better treatments. It will take collaboration from around the globe and all sectors of the research industry to defeat this disease. MRA is incredibly grateful to the Saban Family Foundation for their generous commitment to melanoma research."
"We are tremendously excited to partner with MRA to fund research during this pivotal time in the battle against melanoma," said Dr. Cheryl Saban, President of the Saban Family Foundation. "The Foundation's gift will help fund promising research from world-class institutions in Israel and the U.S., speeding the development of therapies for this aggressive form of skin cancer."]]>
For more than 60 years, scientists have known that cancer cells undergo glycolysis, or metabolize glucose, at a much higher rate than normal cells. The observation, called the Warburg effect, demonstrated that the normal energy producing processes in the cell are disrupted in cancer cells, preventing them from using metabolic pathways in the cell's mitochondria (often called the cell's "power plants").
Recently, however, increasing evidence suggests that, in addition to glycolysis, other metabolic pathways may also play a role in cancer, with important therapeutic implications. A promising strategy for targeting cancer cells, while sparing normal cells, is to target these altered metabolic processes with drug therapies. Elesclomol has been shown to trigger cell death in metastatic melanoma cells, primarily by suppressing oxidative phosphorylation – the process that cells use to transform nutrients into energy.
Moschos and his team demonstrated in the lab that metastatic melanoma cells exhibit a higher rate of glycolysis compared to their normal counterpart cells, termed melanocytes, which would be expected due to the Warburg effect.
"But we also found, surprisingly, that these cells have higher rates of oxidative phosphorylation – they are producing energy through more than one pathway, which explains a lot about how the drug works," says Dr. Moschos.
He notes that this drug has an interesting history. In a 600-patient phase III clinical trial conducted almost 4 years ago, Elesclomol had clinical benefit in the subgroup of patients with normal serum LDH. However, the FDA discontinued the trial, because the Elesclomol in combination with another chemotherapeutic drug may have negative effects in patients with high serum LDH, which is associated with poorer patient outcomes in metastatic melanoma. At the time, very little was known about Elesclomol's mechanism of action – blocking oxidative phosphorylation.
"Our inability to show how Elesclomol worked through measurement of biomarkers was the major driver to conduct this laboratory study," said Moschos, whose team took the clinical trial results back to the lab to try to figure out why the drug worked.
"Our results suggest that targeting oxidative phosphorylation in melanoma is a promising strategy for early metastatic disease, before melanoma cells switch their primary metabolic source to glycolysis, as Otto Warburg showed 60 years ago" said Dr. Moschos.
"Second, we were able to demonstrate a mechanism of resistance to Elesclomol, where long-term exposure to the drug leads to the selection of melanoma cells with high levels of glycolysis. This suggests that a two-pronged strategy aimed at blocking both metabolic pathways may be called for."
The results of the study were published today in the journal Public Library of Science One.
Dr. Moschos conducted the research when he was a faculty member at the University of Pittsburgh Melanoma and Skin Cancer Program in collaboration with Dr. Bennett Van Houten, Richard M. Cyert Chair in Molecular Oncology, University of Pittsburgh. He joined UNC's division of hematology/oncology and UNC Lineberger Comprehensive Cancer Center in January. The research appears today in Proceedings of the Library of Science ONE.
Other members of the research team include scientists from the University of Pittsburgh, the Women's Health Integrated Research Center at Inova Health System in Annandale, VA, Carnegie Mellon University and the University of Heidelberg.
The project was funded by a Career Development Award of a SPORE in Skin Cancer at the University of Pittsburgh (National Cancer Institute grant P50CA121973) and a Pennsylvania Department of Health PA CURE award. Synta Pharmaceuticals Corporation provided the Elesclomol drug used in the laboratory research.]]>
Melanoma is one of the only forms of cancer that is still on the rise and is one of the most common forms of cancer in young adults. The incidence of melanoma in women under age 30 has increased more than 50 percent since 1980. Metastases are the major cause of death from melanoma.
The team found that mice lacking the P-Rex1 protein are resistant to melanoma metastases. When researchers tested human melanoma cells and tumor tissue for the protein, P-Rex1 was elevated in the majority of cases – a clue that the protein plays an important role in the cancer's spread. Their findings were published today in the journal Nature Communications.
"We know that mutations in a gene called BRAF are important for the development of melanoma and several years ago we published a collaborative paper listing 82 proteins that seem to be affected by this genetic pathway. From that list, we focused on P-Rex1 in collaboration with Dr. Nancy Thomas here at UNC and researchers in the United Kingdom," says Channing Der, PhD, a member of the UNC research team. Der is Kenan Professor of pharmacology at UNC-Chapel Hill and member of UNC Lineberger.
A drug approved this summer, vemurafenib, is the first treatment directed at the BRAF mutation. Clinical trials found that the treatment offers a significant survival benefit.
"We think that vemurafenib may work, in part, by blocking the up-regulation of P-Rex1," Der adds.
"As a physician and scientist, I know firsthand the frustration of having very limited therapeutic options to offer to patients with metastatic melanoma," says Nancy Thomas, MD, PhD, whose laboratory analyzed the protein's expression in human cells. "Pinpointing that P-Rex1 plays a key role in metastasis gives us a better understanding of how vemurafenib may work and a target for developing new treatments," she adds.
Thomas is a professor of dermatology and member of UNC Lineberger.
The work at UNC Lineberger was led by Katherine Pedone, PhD, a postdoctoral fellow in Der's laboratory. Other team members were Alexander Finn, MD, PhD, Pamela Groben, MD, Honglin Hao, and Craig Carson, PhD.
This study included Owen Sansom, PhD and collaborators at the Beatson Institute and other collaborators in the UK, France, Canada and Switzerland.
The research was supported by the Association of International Cancer, National Institutes of Health, American Cancer Society, Cancer Research UK and Target-Melanoma. Initial support at UNC was provided by the University Cancer Research Fund.]]>
Dr. Ollila is surgical director of the UNC Multidisciplinary Melanoma Program and of the UNC Breast Center. He serves as associate physician-in-chief of the North Carolina Cancer Hospital and is a member of UNC Lineberger Comprehensive Cancer Center.
He said, "I am honored to be appointed to this prestigious professorship. Bill Millis understands melanoma on a very personal level, and his support of collaborative research across disciplines to better understand melanoma will help UNC increase knowledge about this cancer."
Dr. Ollila recently spent six months as a visiting scholar at the University of Sydney in Australia and the Melanoma Institute Australia, working with the internationally renown melanoma surgeon Dr. John Thompson.
Dr. Ollila earned his undergraduate degree in chemistry from Miami University of Ohio. He earned his medical degree from the University of Cincinnati in Ohio. He completed his residency in surgery at Riverside Methodist Hospital in Columbus, Ohio and a fellowship in surgical oncology at the John Wayne Cancer Institute in Santa Monica, California before joining the UNC faculty in 1997.]]>
When removing melanomas from the skin, surgeons have to plan an excision 'margin' around thecancer to minimize the chance of a localized recurrence. However, larger excision margins often require a skin graft or a complex flap to close,, note Ollila and Thompson, citing one study where 46 percent of patients with four centimeter margins needed a skin graft compared with only 11 percent of patients with a two centimeter margin.
A recent meta-analysis – a technique where multiple trial results are compiled and compared to assess the evidence base – notes that current evidence from randomized clinical trials is not adequate to tell surgeons the best margin for common clinical presentations of melanoma. An article published today in the same issue of The Lancet adds to the evidence base with a trial that notes no significant difference in overall survival or recurrence-free survival for patients with a melanoma thicker than 2mm who were randomly assigned to a two centimeter or four centimeter resection margin.
The authors note that the next appropriate study would be to compare one centimeter and two centimeter margins in a randomized trial which could potentially further minimize the need for skin grafts and/or complex closure techniques. They also urge their colleagues in the field to advance the understanding of melanoma tumor biology to help ensure a safe excision margin using multidisciplinary team science. One possibility could be new techniques to evaluate the cells near the margins called comparative genomic hybridization and fluorescent in-situ hybridization. These techniques could be used to ensure that a smaller surgical margin around the tumor still has an adequate clearance of malignant melanocytic cells. If not this could be the possible explanation for a local recurrence.
Dr. Ollila is an associate professor in the division of surgical oncology at UNC-Chapel Hill. Currently he is a visiting scholar at the University of Sydney (Australia) and the Melanoma Institute Australia.]]>


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Lent arrives on February 10! Sign up today for a Lent devotional experience.
Christ having, in the former chapter, armed his disciples against the corrupt doctrines and opinions of the scribes and Pharisees, especially in their expositions of the law (that was called their leaven, Matt. 16:12), comes in this chapter to warn them against their corrupt practices, against the two sins which, though in their doctrine they did not justify, yet in their conversation they were notoriously guilty of, and so as even to recommend them to their admirers: these were hypocrisy and worldly-mindedness, sins which, of all others, the professors of religion need most to guard against, as sins that most easily beset those who have escaped the grosser pollutions that are in the world through lust, and which are therefore highly dangerous. We are here cautioned, I. Against hypocrisy; we must not be as the hypocrites are, nor do as the hypocrites do. 1. In the giving of alms, Matt. 6:1-4. 2. In prayer, Matt. 6:5-8. We are here taught what to pray for, and how to pray (Matt. 6:9-13); and to forgive in prayer, Matt. 6:14, 15. 3. In fasting, Matt. 6:16-18. II. Against worldly-mindedness, 1. In our choice, which is the destroying sin of hypocrites, Matt. 6:19-24. 2. In our cares, which is the disquieting sin of many good Christians, Matt. 6:25-34.


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UK – Comic Heroes Re-Launch Party
January 7, 2016 by Colin Solan
Filed under Comic Books, England, Signing and Appearance Profiles
Kieron Gillen, Jessica Martin, Paul Cornell, and Rachael Stott sign at Orbital Comics on on Friday January 15, 2016 at 7:00 PM to celebrate the return of Comic Heroes magazine!
Orbital Comics
8 Great Newport Street, London WC2H 7JA, United Kingdom
020 7240 0591
UK – Star Wars Day
November 23, 2015 by Colin Solan
Filed under Comic Books, England, Other, Science Fiction and Fantasy, Signing and Appearance Profiles
Gosh! Comics celebrates the release of Star Wars VII: The Force Awakens on the 12th December! Jedi Knight JAKe (How to Speak Droid / Wookiee) will run a workshop for kids from 11:00 AM till 1:00 PM. Writer Kieron Gillen (Phonogram, The Wicked and Divine, Young Avengers) will also be here for a Darth Vader Volume 1 signing from 2:00 – 3:00 PM.
Gosh Comics
1 Berwick St, SoHo, London W1F0DR
United Kingdom
CA – CBLDF's Comic-Con Welcome Party 2015
July 1, 2015 by Colin Solan
Filed under Comic Books, Comic-Con International, Horror, Other, Science Fiction and Fantasy, Signing and Appearance Profiles
Kick-off Comic-Con with comics' greatest creators at the Comic Book Legal Defense Fund's Comic-Con Welcome Party, sponsored by Image Comics and comiXology with a special gallery display from Black Phoenix Alchemy Lab. The fun starts at 8:00 p.m. PDT on Thursday, July 9, at the Westgate Hotel, where CBLDF welcomes you to Comic-Con for a night of amazing creators, astonishing artwork, and outstanding exclusives. RSVP here.
Meet great creators: Every year the greatest creators in comics drop in at the CBLDF Welcome Party. Confirmed attendees so far this year include Scott Snyder, Jock, Jeff Lemire, Kieron Gillen, Fábio Moon, Gabriel Bá, Tim Seeley, Ben Acker, Ben Blacker, Jonathan Hickman, Joshua Williamson, and more are expected to drop in over the course of the night.
Get the exclusive goods: The first 200 attendees will receive a free gift bag, with exclusive items from Image Comics, McFarlane Toys, comiXology, and CBLDF. RSVP here.
Smell awesome at the Black Phoenix Alchemy Lab/Trading Post: Black Phoenix Alchemy Lab will be debuting their Profanities series, with a selection of limited edition Expletives that will only be available at the CBLDF Welcome Party. Proceeds from every sale at the CBLDF Welcome Party benefit CBLDF.
Get first dibs on CBLDF exclusives: CBLDF has been working hard to put together an exclusive assortment for Comic-Con attendees. We have an all-new tote bag featuring art by the terrific Vanesa R. Del Rey (Hit); an embroidered Comic-Con souvenir patch and new CBLDF t-shirt, both designed by Brian Wood (Starve); and the CBLDF-exclusive variant of Star Trek/Green Lantern from IDW Publishing and DC Comics.
Preview the incredible items in CBLDF's Comic-Con auction: Get a first look at the amazing original art up for grabs at Saturday's CBLDF Comic-Con Auction, including pieces by Jim Lee, Kelley Jones, Jeff Smith, Matt Kindt, Gilbert Hernandez, J. Scott Campbell, Herb Trimpe, Jeffrey Brown, Greg Ruth, Ray Fawkes, Tyler Crook, and many more.
Get new Neil Gaiman art from Neverwear: Neverwear has an ever-growing line of items based on the works of author Neil Gaiman and is an ardent supporter of CBLDF. Neverwear will support the Fund at the SDCC Welcome Party by premiering "Hope," a new print by Chris Ridell, along with classic designs by David Mack, Jim Lee, Olivia, and Jouni Koponen. Proceeds from sales at the CBLDF Welcome Party benefit CBLDF.
Come support free speech and experience the best of Comic-Con at the CBLDF Comic-Con Welcome Party, Thursday, July 9, at the Westgate Hotel (1055 Second Avenue, San Diego, CA 92101), from 8:00 – 11:00 PM! This party is FREE for CBLDF Members. Non-members: Suggested $10 – $20 donation at the door, please. You can RSVP here.
Image Comics is a comic book and graphic novel publisher founded in 1992 by a collective of bestselling artists. Image has since gone on to become one of the largest comics publishers in the United States. Image currently has five partners: Robert Kirkman, Erik Larsen, Todd McFarlane, Marc Silvestri and Jim Valentino. It consists of five major houses: Todd McFarlane Productions, Top Cow Productions, Shadowline, Skybound and Image Central. Image publishes comics and graphic novels in nearly every genre, sub-genre, and style imaginable. It offers science fiction, fantasy, romance, horror, crime fiction, historical fiction, humor and more by the finest artists and writers working in the medium today. For more information, visit www.imagecomics.com.
ComiXology, an Amazon.com, Inc. subsidiary (NASDAQ:AMZN), has revolutionized the comic book and graphic novel industry by delivering a cloud-based digital comics platform that makes discovering, buying, and reading comics more fun than ever before. ComiXology's Guided View reading technology transforms the comic book medium into an immersive and cinematic experience, helping comiXology become a top ten grossing iPad app in 2011 and 2012 and the top grossing non-game iPad app in 2012 and 2013. Offering the broadest library of comic book content from over 75 publishers—and independent creators as well—comiXology will not stop until everyone on the face of the planet has become a comic book fan. ComiXology is based in New York City, with operations in Los Angeles and Paris.
We specialize in formulating body and household blends with a dark, romantic Gothic tone. Our scents run the aesthetic gamut of magickal, pagan and mythological blends, Renaissance, Medieval and Victorian formulas, and horror/Gothic-themed scents. By utilizing our knowledge of homeopathy and aromatherapy, the conceptual theories of hermetic alchemy, and the aesthetic artistry of perfumery, we have mastered the art of encapsulating allegorical ideas into singular olfactory experiences. We are the first of our kind, and have over fifteen years of practical experience in the field. Our expertise shows. We pride ourselves on the artistry of our products, and our skill in their creation. All of our products are hand-blended here in our laboratory. Integrity and dedication is vitally important to us, and we do our best to provide the best possible product and slavishly good service to all our clients.
Comic Book Legal Defense Fund is a non-profit organization protecting the freedom to read comics! Our work protects readers, creators, librarians, retailers, publishers, and educators who face the threat of censorship. We monitor legislation and challenge laws that would limit the First Amendment. We create resources that promote understanding of comics and the rights our community is guaranteed. Every day we publish news and information about censorship events as they happen. We are partners in the Kids' Right to Read Project and Banned Books Week. Our expert legal team is available at a moment's notice to respond to First Amendment emergencies. CBLDF is a lean organization that works hard to protect the rights that our community depends on. For more information, visit www.cbldf.org
The Westgate Hotel
1055 Second Avenue San Diego, CA 92101
UK – FCBD: Image Signings
April 10, 2015 by Colin Solan
Filed under Comic Books, England, Signing and Appearance Profiles
Duncan Fegredo (MPH), Kieron Gillen (The Wicked + The Divine), and Christian Ward (ODY-C) appear at Gosh Comics on Saturday May 2nd from 3-6pm for Free Comic Book Day!
Gosh Comics
1 Berwick St, SoHo, London W1F0DR
United Kingdom
Image Comics Schedule at Emerald City Comicon 2015
March 26, 2015 by Colin Solan
Filed under Comic Books, Convention News, Horror, Other, Science Fiction and Fantasy, Television, Washington
Press Release:
Image Comics is pleased to return to Seattle this year for Emerald City Comicon on Friday, March 27 through Sunday, March 29.
- LOW, VOL. 1 hardcover by Rick Remender and Greg Tocchini, $35
- THE WICKED + THE DIVINE #9 by Kieron Gillen and Jamie McKelvie, $5 (also available at creator table #II-06)
- DESCENDER #1 by Jeff Lemire and Dustin Nguyen, $5 (also available at creator table #Y-05)
- SEX CRIMINALS, VOL. 2 hardcover by Matt Fraction and Chip Zdarsky, $40 (Table #II-04)
- WAYWARD, VOL. 1 hardcover by Jim Zub and Steven Cummings, $30 (Table #HH-11)
- DESCENDER #1 by Jeff Lemire and Dustin Nguyen, $5 (#Y-05, also available at Image booth #312)
- INVISIBLE REPUBLIC #1 by Gabriel Hardman and Corinna Bechko, $10 (#HH-05)
- WAYWARD #6 variants by Jim Zub and Steven Cummings, starting at $5, blank sketch covers for $10 or $25 with sketch (Table #HH-11)
- THE WICKED + THE DIVINE #9 by Kieron Gillen and Jamie McKelvie, $5 (also available at Image booth #312)
Friday 3/27, Image Comics Presents: ART!
3:30 – 4:20 PM, Hall D (TCC 302)
Image Comics is proud to publish some of the best and brightest artists in comics. Join Benjamin Dewey (TOOTH & CLAW), Jamie McKelvie (THE WICKED + THE DIVINE), Leila Del Duca (SHUTTER), Nick Dragotta (EAST OF WEST), Wes Craig (DEADLY CLASS), Dustin Nguyen (DESCENDER), and James Harren (RUMBLE) as they discuss creating, influences, learning, and finding your voice.
Saturday 3/28, Image Comics Presents: Your New Favorite Comics
11 – 11:50 AM, Hall C (TCC 301)
Creator-owned comics work because YOU support them. Frank Barbiere (FIVE GHOSTS), Matt Fraction (SEX CRIMINALS), Kieron Gillen (THE WICKED + THE DIVINE), Brandon Graham (PROPHET), Joshua Williamson (BIRTHRIGHT), Kurtis Wiebe (RAT QUEENS), Rick Remender (BLACK SCIENCE), and Greg Rucka (LAZARUS) create some of your favorite comics. How? Why? There's only one way to find out.
Sunday 3/29, Image Comics Presents: Something For Everybody
2:30 – 3:20 PM, Hall D (TCC 302)
Whether you like crime, westerns, sci-fi, fantasy, or genre mash-ups, Ivan Brandon (DRIFTER), Kelly Sue DeConnick (BITCH PLANET), Jay Faerber (COPPERHEAD), Megan Levens (MADAME FRANKENSTEIN), Joe Keatinge (SHUTTER), Jeff Lemire (DESCENDER), Kurt Busiek (THE AUTUMNLANDS: TOOTH & CLAW), and Landry Walker (DANGER CLUB) know that genre is just a starting point for endless storytelling possibilities. Come pick their brains.
12 – 12: 45 PM: Landry Walker
1 – 1:45 PM: Jeff Lemire & Dustin Nguyen
1 – 1:45 PM: Paul Maybury
1 – 1:45 PM: Matt Fraction
2 – 2:45 PM: Brian Joines
2 – 2:45 PM: Justin Jordan
2 – 2:45 PM: Ryan Ottley
3 – 3:45 PM: Steve Orlando
3 – 3:45 PM: Kyle Higgins
3 – 3:45 PM: Kelly Sue DeConnick
4 – 4:45 PM: Jacob Semahn
4 – 4:45 PM: Megan Levens
4 – 4:45 PM: Joshua Williamson
5 – 5:45 PM: Otis Frampton
5 – 5:45 PM: Ed Brisson & Johnnie Christmas
5 – 5:45 PM: Rick Remender & Matteo Scalera
11 – 11:45 AM: Michael Moreci
11 – 11:45 AM: Chris Burnham
12 – 12:45 PM: John Layman
12 – 12:45 PM: Greg Rucka
12 – 12:45 PM: Landry Walker
1 – 1:45 PM: Nick Dragotta & Tom Fowler
1 – 1:45 PM: Anthony Johnston & Justin Greenwood
1 – 1:45 PM: Ryan Ottley
2 – 2:45 PM: Frank Barbiere & Chris Mooneyham
2 – 2:45 PM: Matt Fraction
2 – 2:45 PM: Joe Eisma
3 – 3:45 PM: Joshua Williamson
3 – 3:45 PM: Rick Remender & Wes Craig
4 – 4:45 PM: Joe Keatinge & Leila del Duca
4 – 4:45 PM: Jay Faerber & Brian Joines
5 – 5:45 PM: Jeff Lemire & Dustin Nguyen
5 – 5:45 PM: Corinna Bechko & Gabriel Hardman
6 – 6:45 PM: Ken Kristensen
6 – 6:45 PM: Riley Rossmo
11 – 11:45 AM: Kelly Sue DeConnick
11 – 11:45 AM: Landry Walker
11 – 11:45 AM: Joe Keatinge & Leila del Duca
12 – 12:45 PM: Kurtis Wiebe & Tyler Jenkins
12 – 12:45 PM: Brandon Graham & Simon Roy
1 – 1:45 PM: Kurt Busiek & Benjamin Dewey
1 – 1:45 PM: Ivan Brandon
1 – 1:45 PM: Matt Fraction
2 – 2:45 PM: Tim Seeley
2 – 2:45 PM: Stuart Moore & Gus Storms
3 – 3:45 PM: Nick Pitarra
Barbiere, Frank O-09
Bechko, Corinna HH-05
Brandon, Ivan H-05
Brisson, Ed HH-07
Burnham, Chris T-01
Busiek, Kurt HH-02
Canete, Eric Q-12
Christmas, Johnnie P-06
Craig, Wes CC-06
DeConnick, Kelly Sue II-03
Del Duca, Leila DD-11
Dewey, Benjamin 1214
Dodson, Terry C-19
Dragotta, Nick O-06
Eisma, Joe HH-06
Faerber, Jay GG-02
Fawkes, Ray W-06
Fowler, Tom HH-04
Fraction, Matt II-04
Gillen, Kieron II-06
Glass, Bryan J.L. Z-01
Graham, Brandon DD-12
Greenwood, Justin G-14
Hardman, Gabriel HH-05
Harren, James O-07
Jenkins, Tyler P-07
Joines, Brian GG-02
Jordan, Justin Q-09
Keatinge, Joe DD-11
Layman, John GG-01
Lemire, Jeff Y-05
Lenox, Emi Y-06
Levens, Megan E-12
Maybury, Paul A-13
McKelvie, Jamie II-05
McNeil, Carla Speed F-14
Mooneyham, Chris O-08
Moore, Stuart P-11
Moreci, Michael HH-06
Nguyen, Dustin Y-04
Ottley, Ryan Q-08
Pitarra, Nick O-05
Remender, Rick CC-05
Robertson, Darick R-03
Rossmo, Riley O-05
Roy, Simon DD-12
Rucka, Greg F-09
Scalera, Matteo Q-10
Seifert, Brandon II-11
Stewart, Dave A-10
Templesmith, Ben W-07
Wiebe, Kurtis J. P-06
Williamson, Joshua U-09
Wilson, Matt II-07
Zub, Jim HH-11
UK – Darth Vader #1 Signing
January 20, 2015 by Colin Solan
Filed under Comic Books, England, Signing and Appearance Profiles
Writer Kieron Gillen (Young Avengers, Thor, The Wicked & The Divine) appears at Orbital Comics on Saturday, February 14, 2015 at 2:00 PM to celebrate the release of the first issue of DARTH VADER from Marvel Comics!
Orbital Comics
8 Great Newport Street, London WC2H 7JA, United Kingdom
020 7240 0591
UK – The Wicked + The Divine Launch Party
October 24, 2014 by Colin Solan
Filed under Comic Books, England, Signing and Appearance Profiles
Kieron Gillen and Jamie McKelvie appear at Gosh Comics for a signing of THE WICKED + THE DIVINE on Wednesday, November 12th from 7:00 – 9:00 PM.
Gosh Comics
1 Berwick St, SoHo, London W1F0DR
United Kingdom
UK – The Wicked & The Divine Signing
June 6, 2014 by Colin Solan
Filed under Comic Books, England, Signing and Appearance Profiles
Writer Kieron Gillen and artist Jamie McKelvie launch their new comic, The Wicked & The Divine – with an exclusive Forbidden Planet variant cover, at the our London Megastore at 6:00pm on Wednesday 18th June.
Every ninety years, twelve gods incarnate as teenagers. They are loved. They are hated. In two years, they are dead.
The team behind critically thermonuclear floor-fillers Young Avengers and Phonogram reunite to start a new ongoing superhero fantasy with a beautiful oversized issue. Welcome to The Wicked & The Divine, where gods are the ultimate pop-stars. But remember: just because you're immortal, doesn't mean you're going to live forever.
Kieron Gillen came to attention as a comic writer with his collaboration with Jamie McKelvie, Phonogram. Since then, he's worked for publishers including Marvel, Image and Avatar, on books as varied as Iron Man, Uber, THREE, Thor, Journey Into Mystery, Uncanny X-Men and a load more. He reunited with Jamie for several projects, most notably Phonogram: The Singles Club and Young Avengers. His achievements include not being found out.
Jamie McKelvie came to attention as a comic artist with his collaboration with Kieron Gillen, Phonogram. Since then he's worked as a comic artist, illustrator and costume designer. The mind behind modern iconic designs like Captain Marvel, Ms. Marvel, and Miss America, his comic work includes a run on Defenders with Matt Fraction and the critically adored Young Avengers. His achievements include putting up with Kieron for over a decade.
Forbidden Planet London Megastore
179 Shaftesbury Avenue, London, WC2H 8JR


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Last year says Naz Long is pretty good at that.
If you can understand why they are, then you are right there with them.
The stupid is really showing on this board after the loss
It tells me that you are one dumb mother ******
All this ******** is comical.
The past few years we have been notorious for breaking down in physical games. Our players get caught up in emotions and it kills their focus. Hurts to say it but...
I nominate HoopsTournament
will you take a helicopter?
whats the spread?
heck of a dick measuring contest going on in here
He shouldn't be dancing, might re-injure himself.
You should probably rethink that one.
I dont care what higher level recruits it will bring in. I just want to be able to tell the tavernhawks off.
Well ive only seen 6 and 12 packs
Maybe he doesn't give a **** about what you think about his McKay comments.
who the **** drinks wine coolers? Of course this comes from a dude who normally posts about wrestling.
Funny thing is, I also heard from Pollard that Pauly Rhodes knows how to coach.
That ham-hock damn near killed ya
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Wow. Did you just read the internet or what? This was news days ago, and this article adds absolutely nothing.
not this absurd rumor AGAIN!!! btw, they recently debunked these rumors, it's now water under the bridge.
I thought the same thing, Forrest. How does this guy get to blog on WSJ.com of all sites?
The news has been out since yesterday that multiple reputable sources(one of the manufacturers themselves) are confirming there is no delay.
The original ESTIMATED delivery for launch date at the end of March was 1 million devices. Now they've confirmed 600k - 700k by 3/26. The rumor of only 300k was a false rumor or blatant lie.
iPad news and updates:
Your right Forrest, Think Equity is a little late with the news. I wrote last week that I didn't think Apple would launch the iPad until after March options stop trading (which is on the 19th). So the 26th sounds right. As to production being light, I'm not so sure that isn't intentional. Shortages get more coverage than abundant supply.
Glad you woke up Matt. 2 little 2 late
It is a lie to try to get Apple's stock price to drop for a "fast trade".
Looks like this might be a *new* rumor. DOH!
There were production delays when the iPhone and iPod Touch first came out. There is always high demand for new Apple products. Apple will have to put people on a waiting list with a down payment like what they did with past products.
"The news has been out since yesterday that multiple reputable sources(one of the manufacturers themselves) are confirming there is no delay."
Seriously, the writers here must be allergic to due diligence.
Hmmm, rushing to get the product out. I'll wait until October then get it for my birthday. 6 months should be enough to workout some of the bugs.
the market for apple ipad.. this product will be a hughe success i thinkthis article abt


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Tags: briana, banks, figured, while, , ass, being, stroked, babes, porn stars, solo girls
Pornstars: Briana Banks
Submited: 7 years old
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Briana Banks gets figured while her ass is being stroked!