Understanding Your Melanoma Pathology Report...
Suzanne McGettigan, MSN, CRNPAffiliation: The Abramson Cancer Center of the University of PennsylvaniaLast Modified: May 9, 2008
Definition of terms
Cellular Description (the type of melanoma):
Superficial Spreading Melanoma
Nodular Melanoma
Acral Lentiginous
Lentigo Melanoma
Other: mucosal melanoma
Breslow Thickness: depth a melanoma lesion extends below the skin surface, measured in millimeters
Clark's Level: depth a melanoma lesion extends below the skin surface, based on involved skin layer (the larger the level number, the deeper into the tissue it extends)
Clark's Level I—lesion involves the dermis
Clark's Level II—lesion involves the papillary dermis
Clark's Level III—lesion invades and fills the papillary dermis
Clark's Level IV—lesion invades reticular dermis
Clark's Level V—lesion invades sub-cutaneous tissue
(Depending upon where the melanoma is located on the body, the millimeters of depth for each Clark level can vary widely, so one person's Clark's III may be 1 mm, while another person's is 2 mm.)
Radial Growth Phase (RGP): The melanoma lesion is described as either having RGP present or absent. If present, RGP indicates that the melanoma is growing horizontally, or radially, within a single plane of skin layer.
Vertical Growth Phase (VGP): The melanoma is described as either having VGP present or absent. If present, it is an indication that the melanoma is growing vertically, or deeper, into the tissues.
Tumor-Infiltrating Lymphocytes (TILs): TILs describes the patient's immune response to the melanoma. When the pathologist examines the melanoma under the microscope, he/she looks for the number of lymphocytes within the lesion. This response, or TILs, is usually described as brisk, non-brisk, or absent, although occasionally can be described as mild or moderate. TILs indicate the immune system's ability to recognize the melanoma cells as
abnormal.
Ulceration: Ulceration is the sloughing of dead tissue. This can sometimes occur in the center of a melanoma lesion. The presence of ulceration may alter the stage classification of a melanoma. Ulceration is thought to reflect rapid tumor growth, leading to the death of cells in the center of the melanoma.
Regression: Regression is described as being present or absent. If it is present, the extent of regression is identified. Regression describes an area within the melanoma where there is absence of melanocytic growth. When regression is present, the total size of the melanoma is hard to characterize.
Mitotic Rate: This term describes the frequency of division within the melanoma. Higher mitotic rates are associated with more rapidly dividing cells, and therefore larger lesions with greater potential for metastasis.
Satellites: Satellite lesions are nodules of tumor/melanoma located more than 0.05 mm from the primary lesion. Satellites are described as being present or absent.
Blood Vessel/Lymphatic Invasion: Blood vessel invasion, aka angioinvasion, as well as lymphatic invasion are described as being present or absent. If present, it means that the melanoma has invaded the blood or lymph system, respectively.
Other words you may encounter
Types of biopsies
Shave Biopsy: a superficial area of the lesion is taken off, often with a razor-type blade.
Punch Biopsy: the removal of a circular area of skin with an instrument known as a punch, which comes in various sizes- sort of like a miniature round cookie cutter.
Incisional Biopsy: the removal of a portion of the affected tissue, for examination, using a knife.
Excisional Biopsy: the removal of the entire affected area and often some healthy tissue for examination using a knife.
Necrosis - the death of tissue: may also indicate the rapidity with which the tumor is growing
Tuesday, December 30, 2008
Jump starting your Immune system with CTLA-4 & Interlukin-2 Therapy for Melanoma ---James Breitfeller
11/06/08 ---This is my Theory
Posted Nov 6, 2008 9:59am on Carepages
This is my Theory
The Interlukin-2IL-2, which works by stimulating killer T-cells to attack melanoma. In some cases with the right body chemistry, helps communicate that message to the killer T-cells and the body begins to fight off the Beast.
In other cases, your body chemistry is different than mine and may lack some sort protein/? or what ever. So in this case, the communication is lost like a drop signal from your cell phone. What you need is another Cell Tower to transmit that signal. That is where CTLA-4 coming in to play. It builds the tower to help with the communication. I may be over simplifying the biochemistry but I am not in the lab to do the right experiments. So, I have to take an educated guess.
As you can see, Dr. Kirkwood and I wanted to induce tumor regression by using my own immune system. If we could get my immune system to recognize the tumors as foreign, then we might have a fighting chance. So we decide to try the CTLA-4 Therapy,
Antitumor response with prolonged time to progression has been seen in patients with melanoma who have received either of the CTLA-4 antibodies and durable antitumor responses have been observed with ipilimumab in patients with melanoma ovarian cancer, prostate cancer, and renal cell carcinoma It has been seen, antitumor responses may be characterized by short-term progression followed by delayed regression.
An important, possibly unique, clinical characteristic of anti-CTLA-4 antibodies is that the duration of clinical response -- and even stable disease -- is often quite prolonged.
This is what I believe is going on in my case but I have no proof.
So lets combine the two clinical trials and that was done by Dr. Rosenberg at the National Cancer Institute.
So I took it apon myself to to a little research and this is what I came up with. I believe it all makes sense. I still may be over simplifying the actual process but I am not a biochemist. So Here goes:
Dendritic cells (DCs) are immune cells and form part of the our immune system. Their main function is to process antigen material and present it on the surface to other cells of the immune system, thus functioning as Antigen-Presenting Cells (APC).
The dendritic cells are constantly in communication with other cells in the body. This communication can take the form of direct cell-to-cell contact based on the interaction of cell-surface proteins. An example of this includes the interaction of the receptor B7 of the dendritic cell with CD28 present on the lymphocyte. However, the cell-cell interaction can also take place at a distance via cytokines. These components of the immune system communicate with one another by exchanging chemical messengers. These proteins are secreted by cells and act on other cells to coordinate an appropriate immune response.
Cytokines include a diverse assortment of interleukins, interferons, and growth factors.One cytokine, interleukin 2 (IL-2), triggers the immune system to produce T cells. IL-2’s immunity-boosting properties have traditionally made it a promising treatment for several illnesses which include Hepatitis C and Melanoma.
There are several steps to activation of the immune system against a foreign molecule. The T cell receptor must first interact with the MHC molecule. The T cell receptor or TCR is a molecule found on the surface of T lymphocytes (or T cells) that is, in general, responsible for recognizing antigens bound to Major Histocompatibility Complex (MHC) molecules. MHC the most gene-dense region of the Human genome and plays an important role in the immune system, autoimmunity.
This first interaction involves the CD4 or CD8 proteins which form a complex with the CD3 protein to bind to the MHC molecule of the (APC). Antigen-presenting cell This is also called "Signal 1" and its main purpose is T cell activation.
However, this is insufficient for producing a T cell response by itself. In fact, lack of further stimulatory signals sends the T cell into anergy. Anergy is a term in immunobiology that describes a lack of reaction by the body's defense mechanisms to foreign substances.
The Second costimulatory signal necessary to continue the immune response can come from B7-CD28 and CD40-CD40L interactions. The primary role of the B7 proteins is to give a second signal to the T cell. The B7 protein/receptor is present on the Antigen-presenting cell and is able to interact with the CD28 receptor on the T cell surface; this is also known as "Signal 2". There are other activation signals which play a role in immune responses.
On these T cells there is are family receptors whose job is downregulate the T cell activation so the immune system maintains metabolic equilibrium so the immune system doesn’t start an autoimmune response and cause it to attack itself. One of these receptors is Cytotoxic T lymphocyte-associated antigen (CTLA4).
It was hypothesized back in the 1980’s that if you replaced the CTLA4 with Anti-CTLA4 that it might block the B7 receptor causing an enhancement of the T-cell activation, leading to a more robust antitumor immune response.
It was shown in mice with a disrupted CTLA-4 genes that their immune response ran unabated causing autoimmunity which was fatal.
It was also shown that the anti-CTLA-4 antibodies had a greater affinity to CTLA-4 than the B7 receptor. So by doing the CTLA-4 Therapy, it allowed signal 1 to become active.
So in the presents of the CTLA-4 antibody Therapy, I my case, we may have extended the antitumor response of the T-cells. This left Signal 1 active.
We then, hit the immune system with High dose of IL-2. This must have stimulated the cell to cell communication (Signal 2) causing the immune response to kick in against the foreign molecule (The Tumor)
AS YOU GUESSED IT, I MUST HAVE JUMP STARTED MY IMMUNE SYSTEM!!!!!!
Just don't know how long it will last.
Jimmy B
Posted Nov 6, 2008 9:59am on Carepages
This is my Theory
The Interlukin-2IL-2, which works by stimulating killer T-cells to attack melanoma. In some cases with the right body chemistry, helps communicate that message to the killer T-cells and the body begins to fight off the Beast.
In other cases, your body chemistry is different than mine and may lack some sort protein/? or what ever. So in this case, the communication is lost like a drop signal from your cell phone. What you need is another Cell Tower to transmit that signal. That is where CTLA-4 coming in to play. It builds the tower to help with the communication. I may be over simplifying the biochemistry but I am not in the lab to do the right experiments. So, I have to take an educated guess.
As you can see, Dr. Kirkwood and I wanted to induce tumor regression by using my own immune system. If we could get my immune system to recognize the tumors as foreign, then we might have a fighting chance. So we decide to try the CTLA-4 Therapy,
Antitumor response with prolonged time to progression has been seen in patients with melanoma who have received either of the CTLA-4 antibodies and durable antitumor responses have been observed with ipilimumab in patients with melanoma ovarian cancer, prostate cancer, and renal cell carcinoma It has been seen, antitumor responses may be characterized by short-term progression followed by delayed regression.
An important, possibly unique, clinical characteristic of anti-CTLA-4 antibodies is that the duration of clinical response -- and even stable disease -- is often quite prolonged.
This is what I believe is going on in my case but I have no proof.
So lets combine the two clinical trials and that was done by Dr. Rosenberg at the National Cancer Institute.
So I took it apon myself to to a little research and this is what I came up with. I believe it all makes sense. I still may be over simplifying the actual process but I am not a biochemist. So Here goes:
Dendritic cells (DCs) are immune cells and form part of the our immune system. Their main function is to process antigen material and present it on the surface to other cells of the immune system, thus functioning as Antigen-Presenting Cells (APC).
The dendritic cells are constantly in communication with other cells in the body. This communication can take the form of direct cell-to-cell contact based on the interaction of cell-surface proteins. An example of this includes the interaction of the receptor B7 of the dendritic cell with CD28 present on the lymphocyte. However, the cell-cell interaction can also take place at a distance via cytokines. These components of the immune system communicate with one another by exchanging chemical messengers. These proteins are secreted by cells and act on other cells to coordinate an appropriate immune response.
Cytokines include a diverse assortment of interleukins, interferons, and growth factors.One cytokine, interleukin 2 (IL-2), triggers the immune system to produce T cells. IL-2’s immunity-boosting properties have traditionally made it a promising treatment for several illnesses which include Hepatitis C and Melanoma.
There are several steps to activation of the immune system against a foreign molecule. The T cell receptor must first interact with the MHC molecule. The T cell receptor or TCR is a molecule found on the surface of T lymphocytes (or T cells) that is, in general, responsible for recognizing antigens bound to Major Histocompatibility Complex (MHC) molecules. MHC the most gene-dense region of the Human genome and plays an important role in the immune system, autoimmunity.
This first interaction involves the CD4 or CD8 proteins which form a complex with the CD3 protein to bind to the MHC molecule of the (APC). Antigen-presenting cell This is also called "Signal 1" and its main purpose is T cell activation.
However, this is insufficient for producing a T cell response by itself. In fact, lack of further stimulatory signals sends the T cell into anergy. Anergy is a term in immunobiology that describes a lack of reaction by the body's defense mechanisms to foreign substances.
The Second costimulatory signal necessary to continue the immune response can come from B7-CD28 and CD40-CD40L interactions. The primary role of the B7 proteins is to give a second signal to the T cell. The B7 protein/receptor is present on the Antigen-presenting cell and is able to interact with the CD28 receptor on the T cell surface; this is also known as "Signal 2". There are other activation signals which play a role in immune responses.
On these T cells there is are family receptors whose job is downregulate the T cell activation so the immune system maintains metabolic equilibrium so the immune system doesn’t start an autoimmune response and cause it to attack itself. One of these receptors is Cytotoxic T lymphocyte-associated antigen (CTLA4).
It was hypothesized back in the 1980’s that if you replaced the CTLA4 with Anti-CTLA4 that it might block the B7 receptor causing an enhancement of the T-cell activation, leading to a more robust antitumor immune response.
It was shown in mice with a disrupted CTLA-4 genes that their immune response ran unabated causing autoimmunity which was fatal.
It was also shown that the anti-CTLA-4 antibodies had a greater affinity to CTLA-4 than the B7 receptor. So by doing the CTLA-4 Therapy, it allowed signal 1 to become active.
So in the presents of the CTLA-4 antibody Therapy, I my case, we may have extended the antitumor response of the T-cells. This left Signal 1 active.
We then, hit the immune system with High dose of IL-2. This must have stimulated the cell to cell communication (Signal 2) causing the immune response to kick in against the foreign molecule (The Tumor)
AS YOU GUESSED IT, I MUST HAVE JUMP STARTED MY IMMUNE SYSTEM!!!!!!
Just don't know how long it will last.
Jimmy B
Sunday, December 28, 2008
Overcoming immunologic tolerance to melanoma: targeting CTLA-4 with ipilimumab (MDX-010).
Overcoming immunologic tolerance to melanoma: targeting CTLA-4 with ipilimumab (MDX-010).
Weber J.
H. Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, SRB-2, Tampa, Florida 33612, USA. Jeffrey.Weber@moffitt.org
Targeted biologic therapies such as anti-cytotoxic T lymphocyte antigen (CTLA-4) monoclonal antibodies, either as monotherapy or in combination with chemotherapy or vaccines, have shown great promise in late-stage melanoma, which has a very poor prognosis. Melanoma is relatively resistant to both chemotherapy and radiotherapy. Blockade of CTLA-4, which inhibits T-cell proliferation, promotes stimulation of adaptive immunity and T-cell activation, resulting in eradication of tumor cells. Two human monoclonal antibodies are under investigation in melanoma. Phase II and III clinical trials are currently evaluating the efficacy and safety of ipilimumab (MDX-010, Medarex, Inc., Princeton, NJ, and Bristol-Myers Squibb, Princeton, NJ) and tremelimumab (CP-675,206; Pfizer Pharmaceuticals, New York) in melanoma. Data are available on ipilimumab, which has been explored as monotherapy and in combination with vaccines, other immunotherapies such as interleukin-2, and chemotherapies such as dacarbazine. Overall response rates range from 13% with ipilimumab plus vaccine in patients with stage IV disease to 17% and 22% with ipilimumab plus dacarbazine or interleukin-2, respectively, in patients with metastatic disease. Responses have been durable, and among those experiencing grade 3 or 4 autoimmune toxicities, even higher response rates have been seen--up to 36%. While the optimal dose of ipilimumab has yet to be established, studies also indicate that higher doses may be more effective. Importantly, the lack of an initial clinical response may not predict ultimate treatment failure, because the onset of a response may follow progressive disease or stable disease. Pending results from registration studies with ipilimumab and lessons learned from registration studies conducted with tremelimumab will help to define the role of anti-CTLA-4 blockade in the treatment of metastatic melanoma.
PMID: 19001147 [PubMed - in process]
Related Articles
ReviewAnti-CTLA4 monoclonal antibody Ipilimumab in the treatment of metastatic melanoma: recent findings. [Recent Patents Anticancer Drug Discov. 2008]
ReviewReview: anti-CTLA-4 antibody ipilimumab: case studies of clinical response and immune-related adverse events. [Oncologist. 2007]
CTLA-4 blockade with monoclonal antibodies in patients with metastatic cancer: surgical issues. [Ann Surg Oncol. 2008]
The heterogeneity of the kinetics of response to ipilimumab in metastatic melanoma: patient cases. [Cancer Immun. 2008]
Overcoming immunologic tolerance to melanoma: targeting CTLA-4 with tremelimumab (CP-675,206). [Oncologist. 2008]
» See Reviews... » See All...
Patient Drug Information
Dacarbazine (DTIC-Dome®) Your doctor has ordered the drug dacarbazine to help treat your illness. The drug is given by injection into a vein.
» read more ...
Weber J.
H. Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, SRB-2, Tampa, Florida 33612, USA. Jeffrey.Weber@moffitt.org
Targeted biologic therapies such as anti-cytotoxic T lymphocyte antigen (CTLA-4) monoclonal antibodies, either as monotherapy or in combination with chemotherapy or vaccines, have shown great promise in late-stage melanoma, which has a very poor prognosis. Melanoma is relatively resistant to both chemotherapy and radiotherapy. Blockade of CTLA-4, which inhibits T-cell proliferation, promotes stimulation of adaptive immunity and T-cell activation, resulting in eradication of tumor cells. Two human monoclonal antibodies are under investigation in melanoma. Phase II and III clinical trials are currently evaluating the efficacy and safety of ipilimumab (MDX-010, Medarex, Inc., Princeton, NJ, and Bristol-Myers Squibb, Princeton, NJ) and tremelimumab (CP-675,206; Pfizer Pharmaceuticals, New York) in melanoma. Data are available on ipilimumab, which has been explored as monotherapy and in combination with vaccines, other immunotherapies such as interleukin-2, and chemotherapies such as dacarbazine. Overall response rates range from 13% with ipilimumab plus vaccine in patients with stage IV disease to 17% and 22% with ipilimumab plus dacarbazine or interleukin-2, respectively, in patients with metastatic disease. Responses have been durable, and among those experiencing grade 3 or 4 autoimmune toxicities, even higher response rates have been seen--up to 36%. While the optimal dose of ipilimumab has yet to be established, studies also indicate that higher doses may be more effective. Importantly, the lack of an initial clinical response may not predict ultimate treatment failure, because the onset of a response may follow progressive disease or stable disease. Pending results from registration studies with ipilimumab and lessons learned from registration studies conducted with tremelimumab will help to define the role of anti-CTLA-4 blockade in the treatment of metastatic melanoma.
PMID: 19001147 [PubMed - in process]
Related Articles
ReviewAnti-CTLA4 monoclonal antibody Ipilimumab in the treatment of metastatic melanoma: recent findings. [Recent Patents Anticancer Drug Discov. 2008]
ReviewReview: anti-CTLA-4 antibody ipilimumab: case studies of clinical response and immune-related adverse events. [Oncologist. 2007]
CTLA-4 blockade with monoclonal antibodies in patients with metastatic cancer: surgical issues. [Ann Surg Oncol. 2008]
The heterogeneity of the kinetics of response to ipilimumab in metastatic melanoma: patient cases. [Cancer Immun. 2008]
Overcoming immunologic tolerance to melanoma: targeting CTLA-4 with tremelimumab (CP-675,206). [Oncologist. 2008]
» See Reviews... » See All...
Patient Drug Information
Dacarbazine (DTIC-Dome®) Your doctor has ordered the drug dacarbazine to help treat your illness. The drug is given by injection into a vein.
» read more ...
Thursday, December 25, 2008
To my Support Team, Friends, Family and Carepage Friends & Followers:
Dee and I would like to extend our warm wishes this Holiday Season. This past year has many things to ponder over. I for one, am grateful to be able to share with you my journey against the Beast and at the same time able to help others in their fight too. I am also so saddened that we lost so many Carepage friends in the battle.
I read somewhere that 68000 will be diagnosed with Melanoma this year and 8400 will die as a result. Even One is way too many. I have dedicated my time and efforts to educate myself and others on this subject matter so we can find the PATH. It is not easy, but it gives me purpose in life other than my Family and friends.
WE TOGATHER CAN HELP FIND A CURE.
To all the Patients that are trying clinical trials, I would like to take my hat off to you. In time of need, you are the sacrificial lambs that are thrown into the Cave of the Beast. You are on the front line willing to fight for another day. In my book, you are all Heroes.And we can’t forget the caregivers. They are in the trenches with us, holding our heads up so we can take aim at the Beast. For they are unsung Heroes that are never mentioned but dissevered better.
I guess I am starting to ramble on.
So on that note, I would like to say “Merry Christmas and a Happy New year.”
This could be the year of the Cure!!!
Take Care
Your Friends
I read somewhere that 68000 will be diagnosed with Melanoma this year and 8400 will die as a result. Even One is way too many. I have dedicated my time and efforts to educate myself and others on this subject matter so we can find the PATH. It is not easy, but it gives me purpose in life other than my Family and friends.
WE TOGATHER CAN HELP FIND A CURE.
To all the Patients that are trying clinical trials, I would like to take my hat off to you. In time of need, you are the sacrificial lambs that are thrown into the Cave of the Beast. You are on the front line willing to fight for another day. In my book, you are all Heroes.And we can’t forget the caregivers. They are in the trenches with us, holding our heads up so we can take aim at the Beast. For they are unsung Heroes that are never mentioned but dissevered better.
I guess I am starting to ramble on.
So on that note, I would like to say “Merry Christmas and a Happy New year.”
This could be the year of the Cure!!!
Take Care
Your Friends
Wednesday, December 17, 2008
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Greetings to One and All
This Blog is dedicated My Brother Kenny B. who passed away in the late 1970's with Cancer before the Internet.
It was he, who showed me How to live and give back. He was wise beyond his years.
Jimmy and Dee
Carepage: Jimmybreitfeller
Jimmy Breitfeller
It was he, who showed me How to live and give back. He was wise beyond his years.
Jimmy and Dee
Carepage: Jimmybreitfeller
Jimmy Breitfeller
My Profile as of 2009
- jimmy_B
- Last July (2005)I was riding my bicycle to work at the Eastman Kodak Research Labs about 3 miles from home. I was wearing a knapsack to carry my things to and from the labs. I started noticing an ache on my back. So I decide to go to the dermatologist. To make the long story short, it was cancer. I knew from my research that I would be needing adjuvant therapy. So I started communicating with Sloan Kettering, University of Pittsburgh Cancer Center, and a couple of others including the Wilmot Cancer Center at Strong. I realized that by telling my story, I might help someone else out there in a similar situation. So to all who are linked by diagnosis or by relation to someone with melanoma, I wish you well. Stay positive, read as much as you can (information helps to eliminate the fear associated with the unknown), and live for today, as no one can predict what tomorrow may bring. Jimmy B. posted 12/15/08
Public Service Announcement
A call for Melanoma Patients by Dr. Steven A Rosenberg
"We continue to see a high rate of clinical responses in our cell transfer immunotherapy treatments for patients with metastatic melanoma", Dr. Rosenberg said.
"We are actively seeking patients for these trials and any note of that on a patient-directed web site would be appreciated."
If you would like to apply for his trials, here is the website and information.
Dr. Rosenberg's information
Dr. Rosenberg's Clinical Trials
The Melanoma Research Alliance has partnered with Bruce Springsteen, the E Street Band, and the Federici family to alleviate suffering and death from melanoma. Please view Bruce Springsteen’s public service announcement inspired by Danny Federici. Danny was the E Street Band’s organist and keyboard player. He died on April 17, 2008 at Memorial Sloan-Kettering Cancer Center in New York City after a three year battle with melanoma.
http://www.melanomaresearchalliance.org/news/PSA/
Source Fastcures blog
"We continue to see a high rate of clinical responses in our cell transfer immunotherapy treatments for patients with metastatic melanoma", Dr. Rosenberg said.
"We are actively seeking patients for these trials and any note of that on a patient-directed web site would be appreciated."
If you would like to apply for his trials, here is the website and information.
Dr. Rosenberg's information
Dr. Rosenberg's Clinical Trials
The Melanoma Research Alliance has partnered with Bruce Springsteen, the E Street Band, and the Federici family to alleviate suffering and death from melanoma. Please view Bruce Springsteen’s public service announcement inspired by Danny Federici. Danny was the E Street Band’s organist and keyboard player. He died on April 17, 2008 at Memorial Sloan-Kettering Cancer Center in New York City after a three year battle with melanoma.
http://www.melanomaresearchalliance.org/news/PSA/
Source Fastcures blog
Join the Relay for Life!!!
Dear Family and Friends,
I’ve decided to take a stand and fight back against cancer by participating in the American Cancer Society Relay For Life® event right here in my community! Please support me in this important cause by making a secure, tax-deductible donation online using the link below.
To donate on line now, click here to visit my personal page.
Jimmy B AKA Melanoma_Missionary
Relay For Life® is a life-changing event that brings together more than 3.5 million people worldwide to:
CELEBRATE the lives of those who have battled cancer. The strength of survivors inspires others to continue to fight.
REMEMBER loved ones lost to the disease. At Relay, people who have walked alongside people battling cancer can grieve and find healing.
FIGHT BACK. We Relay because we have been touched by cancer and desperately want to put an end to the disease.
Whatever you can give will help - it all adds up! I greatly appreciate your support and will keep you posted on my progress.
Keep the Fire Burning!!!
Sincerely,
Jimmy Breitfeller