Rector's Reflections
Here it is, it's Lent. I don't believe that it's a coincidence that it begins at a time of year that is unstable. The coming of Spring is a season that seems to be trying to give birth to itself The days are cold one day, hot the next, wet one week, dry the next, cloudy, sunny - you get the picture. In a way, it's not unlike our spiritual lives at times, our relationship with God. Actually, Spring is the perfect time to jump into the season of Lent for exactly that reason. It matches us.
The goal, the plan for Spring is to produce beauty. So is the heart of Lent. When all the turmoil and vacillations of Spring and Lent are over, hopefully, something of joy and beauty will have arisen in us. the important thing to remember here is that all this takes intentional effort. Nature, God's skilled gardener, knows just what to do each year in preparing the soil, softening up the seeds, awakening the trees and flowers; each plant responds in its own way to the prodding of life with a steady and determined growth.
Our Lenten disciplines are much like the hand of that skilled gardener shaping and coaxing our souls to respond to what God has already planted in our souls and is now hoping will grow. It is a real time of discovery. It is a time of becoming who we were created to be.
Faithfully,
Fr. Reese+
ABOUT LENT
Lent is the 40-day period of repentance and renewal preceding Easter. It begins on Ash Wednesday and ends at Easter. Holy Week, the week before Easter, is commemoration of the last days in the life of Jesus on earth. Lent is the time set aside for meditation, prayer, fasting, self-denial, seeking forgiveness and holy works in God's Name. Lent is several weeks in the church year for increased understanding of the life of Jesus of Nazareth -- his ministry, sacrifice, and death. Lent is a special opportunity in which baptismal vows may be renewed and a new commitment may be made in one's faith and life. Lent is a liturgical season that can help one prepare and experience the full joy of the resurrection of Jesus Christ on Easter Day.
Thank you for taking the time to read the Advent E-pistle. If you have any comments or suggestions or would like to submit an article, please contact the church office at 542-4123 or secretary@adventbrownsville.org.
Tuesday, February 28, 2012
Side effects are really kicking in this week and its been painful for mom
I think mom is having a stronger mix of emotions this week. I think we all are. Mom is starting her 4th week of this new trial drug tomorrow and the side effects have started and are taking a toll. She has been in even more pain and is struggling more with keeping upbeat. She is doing her best and trying so hard. It is difficult to go about each day with the pain and changes. She is so wonderful to be around and is always helping others, but I see her trying to hide what she is really feeling and overall we just feel like crying.We, also, lost a good friend and a great man of God this last week who has been an ispiration for all humanity. He prayed with mom and was comforting, but he has returned home. He left behind a wonderful family and we are praying for them and know they will get through this and honor him.
There are just so many questions and confusion. There is depression and lonliness. There is a loss of identity. We all suffer in some way or another, but this by far the most difficult we are facing.
Mom will answer texts if you have her number and she will check email. Thank you all so much for your continued support and prayers.
-Vanessa
There are just so many questions and confusion. There is depression and lonliness. There is a loss of identity. We all suffer in some way or another, but this by far the most difficult we are facing.
Mom will answer texts if you have her number and she will check email. Thank you all so much for your continued support and prayers.
-Vanessa
Sunday, February 26, 2012
Sunday, February 12, 2012
God's message is clear and understood. Thank you.
This week went by really fast and I am thankful for that because mom starts her next treatment on tuesday. She goes in tomorrow just to give blood and then Valentine's day we will just be there in the morning. I really hope this one works.
I know God is working and is healing her. She is faithful, humbled, trusts in the Lord and is waiting patiently. Today we went to church at Oak Hills Church with Max Locado and is really wonderful. It was a little emotional for us because the theme was accepting, dealing with, and getting through trouble times and that here in this life we are in God's "waiting room". We must all be patient and trust in Him, and that He is working while we wait.
It was perfect and it was a perfect example of God's work. We needed to hear this message. Even though we believe and trust in His work, it was the icing on the cake just to hear the message through Locado and be comforted by his message.
So even though we are all waiting, we must accept the things we cannot change, have courage to change the things we can, and have faith in God's wisdom that he will guide us and direct our path.
Have a wonderful Sunday! Thank you.
-Vanessa
I know God is working and is healing her. She is faithful, humbled, trusts in the Lord and is waiting patiently. Today we went to church at Oak Hills Church with Max Locado and is really wonderful. It was a little emotional for us because the theme was accepting, dealing with, and getting through trouble times and that here in this life we are in God's "waiting room". We must all be patient and trust in Him, and that He is working while we wait.
It was perfect and it was a perfect example of God's work. We needed to hear this message. Even though we believe and trust in His work, it was the icing on the cake just to hear the message through Locado and be comforted by his message.
So even though we are all waiting, we must accept the things we cannot change, have courage to change the things we can, and have faith in God's wisdom that he will guide us and direct our path.
Have a wonderful Sunday! Thank you.
-Vanessa
Thursday, February 9, 2012
New Information on ALK resistant NSCLC
New Research in Resistance to Xalkori (crizotinib) for ALK-driven NSCLC
- By CraiginPA · Today at 1:34 am · 8 replies
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[Note: This is not a professional opinion, but a report of some very interesting research I read.]
There’s valuable information on resistance to Xalkori (crizotinib) in a newly-published article by Katayama & Shaw (as lead co-authors) and their colleagues in their article titled “Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers” in the research journal Science Translational Medicine: http://www.ncbi.nlm.nih.gov/pubmed/22277784
(Yes, that’s Alice Shaw, MD, PhD again, my oncologist at the Harvard-affiliated MGH in Boston.)
The research looked at just 18 patients with crizotinib-resistant cancer, but that’s enough to gain a lot of insight because of the deep lab analysis work done on those cancers. Although the odds of an individual having the different kinds of resistance won’t be reliable across all crizotinib patients, the value comes from being directionally insightful, not numerically precise.
For starters, only 28% (5/18) had either a resistant ALK mutation or an amplification of the ALK-fusion mutation. These are cases we’d hope would benefit from a 2nd generation ALK inhibitor. We don’t know if this percentage is representative of all crizotinib-resistant patients, but if it were it would imply only a “fair to good chance,” not a “likely chance,” that a 2nd generation ALK inhibitor would be helpful for crizotinib-resistant cancer.
The insights don’t end there, though. For example, the 2nd generation ALK inhibitors were found to vary in their effectiveness against the various resistant ALK mutations and might be less effective on the resistant cancer than crizotinib had been before resistance. And a couple of cases (2/18) developed an additional simultaneous route to bypass ALK inhibition via a gene called KIT.
Hmmm . . . That doesn’t sound so good. Is that all there is? Um, . . .
“There's one more thing” . . . (said in my best understated Steve Jobs / Detective Columbo voice*): . . .
If I’m reading the study correctly, most crizotinib-resistant ALK-driven cancer may have something you didn’t expect, and it might offer hope of being somewhat co-treatable with an additional inhibitor drug: EGFR! Not an EGFR mutation, but an over-active *normal* EGFR gene, pushing the cancer along. And it looks like this was found to some degree in almost every case they could test.
*(BTW, if you don’t understand the Steve Jobs / Detective Columbo reference, see: http://en.wikipedia.org/wiki/Stevenote#.22One_more_thing....22)
=== Resistant ALK Mutation Variants ===
The first form of resistance is the emergence (in survival-of-the-fittest style) of drug-resistant variants of the ALK mutation (4/18 cases) and “amplification” of the ALK fusion mutation (1/18).
The four crizotinib-resistant ALK variant sequences in these patients are named L1196M (an important ‘gateway’ mutation), S1206Y, G1202R, and “1151T insertion”. (These would be in addition to some previously-reported ones named C1156Y and L1152R.) In the lab, S1206Y wasn’t as resistant as the other three, suggesting crizotinib might still slow some weakly resistant variants even if unable to stop them.
The team lab-tested three 2nd generation ALK inhibitor drugs (TAE684, CH5424802, and ASP3026) against some ALK mutations. I might be misinterpreting the data, but against the original ALK these three drugs and crizotinib looked comparably effective. Against the four resistant ALK mutations, their effectiveness varied and the best wasn’t always the same. None were as effective against the resistant mutations as crizotinib had been against the original ALK mutation (and none was very effective against 1151T ins).
At first glance this might suggest shrinkage might be less common when treating resistant mutations with 2nd generation ALK inhibitors, but neither LDK 378 nor Ariad AP26113 were tested or mentioned and only a few mutations were tested. So for now, I’ll remain hopefully optimistic that at least one drug will be found effective enough to do the job for a particular resistant ALK mutation for a while.
(BTW, the marketing material from Ariad on their own early lab work for AP26113 suggested it might work on many ALK variants, including T1151, L1152, C1156, I1171, F1174, V1180, R1181, L1196, L1198, G1202, E1210, E1241, F1245, I1268, G1269, Y1278, and S1206 [that last one requiring a very high dose]. I think most of these were synthetically mutated using lab techniques rather than naturally occurring in patients, but clearly some show up in patients and any of them potentially could.)
=== Amplified ALK Mutation ===
One patient had resistance from amplification of the original “ALK fusion” mutation. (I think this might be what some studies refer to as gene “copy number gain” (CNG).) Basically, it’s the same original ALK mutation, but just more of it, too much for the crizotinib to block it all.
Hypothetically, I’d guess this might mean that a higher dose of crizotinib might help a little more for a while if the patient’s health can tolerate the side-effects and the FDA allowed it, or maybe a 2nd generation ALK inhibitor might help for a while (if one is more potent or more narrowly targeted to the ALK mutation, e.g., maybe the TAE684 column in article’s graph 1E ). Your oncologist should be able to discuss whether something like this could be testable or treatable in an ALK-targeted way.
=== HSP90 Inhibitor ===
With that as context, the research team’s lab work also found that a different kind of inhibitor might sometimes be more effective than the ALK inhibitors they were testing. HSP90 (heat shock protein 90) assists ALK fusion proteins. HSP90 inhibitors are being tested in clinical trials. The research team tested the HSP90 inhibitor 17-AAG (a derivative of natural geldanamycin) and found it was highly effective against the ALK mutations they tested. At the concentration they used, it seemed more potent than all the other drugs they tested, but it also was potent against the normal non-mutated ALK gene, which could mean stronger side effects, too. Other clinical research studies will have to determine the right HSP90 inhibitor and dose level to balance effectiveness vs. tolerable level of side effects.
=== KIT Amplification ===
Two of the 18 ALK resistance cases also had a second simultaneous resistance mechanism: amplification (e.g., copy number gain) of the KIT gene which led to over-expression of both KIT protein and a KIT-assisting ligand called “stem cell factor” (SCF). In engineered cells this combination made the cells resistant to crizotinib, yet sensitive to crizotinib if KIT were inhibited using Gleevec (imatinib).
So apparently there can be multiple simultaneous mechanisms of resistance in crizotinib-resistant cancer cells. For patients whose resistance is known to involve KIT/SCF, it sounds promising that an existing drug might eventually be available to help control the KIT route.
=== EGFR Activation (Phosphorylation) ===
The big surprise was phosphorylated EGFR (pEGFR) mediated resistance, detected in all but one of the cases that could be tested. This is not an EGFR mutation, nor EGFR amplification (e.g., copy number gain), but EGFR activation (phosphorylation, i.e., charged up and working). FWIW, according the article this might possibly be caused by up-regulation of the EGFR receptor itself and two ligands (EGFR ligand amphiregulin and ErbB3 ligand NRG1).
From that data presented, it seems the EGFR activation is usually present even before starting crizotinib and might limit response to crizotinib. In an experiment on a patient’s pre-crizotinib cells which were sensitive to crizotinib but less than normal, treatment with both Xalkori (crizotinib) and Iressa (gefitinib) suppressed cell growth more potently and induced significant apoptosis. In another experiment, it appeared an improved response might be possible by inhibiting both ALK and EGFR, even though the effect wasn’t as potent as crizotinib alone had been on cells that didn’t have EGFR activation. (This suggests there’s more going on here than just these two tyrosine kinases.)
=== It’s So Complicated ===
Yes, it’s complicated. Some ALK inhibitor resistance is due to a resistant ALK mutation, some is due to amplification … amplification … amplification (yes, I’m repeating myself more times than you can handle), some is due to KIT amplification, some is due to EGFR activation, and sometimes inhibiting multiple resistance routes still isn’t enough to lock down the cancer. (We obviously don’t know all the biochemical players in the cancer orchestra yet.)
This sounds like an example of how amazingly adaptable the human body is. You can inhibit or break a gene and you’re your body will try to compensate; you inhibit something more, and it tries to compensate again. That makes it hard to stop cancer, but research like this gives me hope that someday science will learn all the things we’ll need to do to control this beast for many years (most of the time).
=== So What Do We Do? ===
So what should we do when we develop crizotinib resistance?
Ask your oncologist (once they’ve had a chance to read the article). If they have questions, they can contact one of the authors.
For myself, I’d ask my oncologist if it’s possible to have a fresh biopsy of my resistant cancer tested for resistant or amplified ALK mutations, phosphorylated EGFR, and other possible mutations (e.g., KIT), and then treat the resistance accordingly.
Even without testing, I might ask my oncologist if he/she would consider giving ALK+EGFR combo inhibition a try (if the FDA would allow it), especially if my initial response to crizotinib was less than good. If not, I’d hunt for a combo-drug trial of it if one exists. Maybe one of us will find that answer and share it.
Sooner or later, a jump from the ALK inhibitor track to another track will be needed. In this research article, the HSP90 inhibitor experimental trial track seemed promising for crizotinib-resistant ALK-driven lung cancer. Your oncologist may be able to suggest which HSP90’s look most promising. (Other possible tracks: surgery, radiation, chemo, other chemo, immunotherapy, or other experimental things, if time permits.)
This summary and the abstract at http://www.ncbi.nlm.nih.gov/pubmed/22277784 may suffice for most, but your oncologist and some of you will want to buy and read the full article. It’s available by just following the below-the-abstract “LinkOuts” expandable-menu to the publication. (And if you find errors in my summary, please let me know so I can fix it promptly.)
Best hopes
There’s valuable information on resistance to Xalkori (crizotinib) in a newly-published article by Katayama & Shaw (as lead co-authors) and their colleagues in their article titled “Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers” in the research journal Science Translational Medicine: http://www.ncbi.nlm.nih.gov/pubmed/22277784
(Yes, that’s Alice Shaw, MD, PhD again, my oncologist at the Harvard-affiliated MGH in Boston.)
The research looked at just 18 patients with crizotinib-resistant cancer, but that’s enough to gain a lot of insight because of the deep lab analysis work done on those cancers. Although the odds of an individual having the different kinds of resistance won’t be reliable across all crizotinib patients, the value comes from being directionally insightful, not numerically precise.
For starters, only 28% (5/18) had either a resistant ALK mutation or an amplification of the ALK-fusion mutation. These are cases we’d hope would benefit from a 2nd generation ALK inhibitor. We don’t know if this percentage is representative of all crizotinib-resistant patients, but if it were it would imply only a “fair to good chance,” not a “likely chance,” that a 2nd generation ALK inhibitor would be helpful for crizotinib-resistant cancer.
The insights don’t end there, though. For example, the 2nd generation ALK inhibitors were found to vary in their effectiveness against the various resistant ALK mutations and might be less effective on the resistant cancer than crizotinib had been before resistance. And a couple of cases (2/18) developed an additional simultaneous route to bypass ALK inhibition via a gene called KIT.
Hmmm . . . That doesn’t sound so good. Is that all there is? Um, . . .
“There's one more thing” . . . (said in my best understated Steve Jobs / Detective Columbo voice*): . . .
If I’m reading the study correctly, most crizotinib-resistant ALK-driven cancer may have something you didn’t expect, and it might offer hope of being somewhat co-treatable with an additional inhibitor drug: EGFR! Not an EGFR mutation, but an over-active *normal* EGFR gene, pushing the cancer along. And it looks like this was found to some degree in almost every case they could test.
*(BTW, if you don’t understand the Steve Jobs / Detective Columbo reference, see: http://en.wikipedia.org/wiki/Stevenote#.22One_more_thing....22)
=== Resistant ALK Mutation Variants ===
The first form of resistance is the emergence (in survival-of-the-fittest style) of drug-resistant variants of the ALK mutation (4/18 cases) and “amplification” of the ALK fusion mutation (1/18).
The four crizotinib-resistant ALK variant sequences in these patients are named L1196M (an important ‘gateway’ mutation), S1206Y, G1202R, and “1151T insertion”. (These would be in addition to some previously-reported ones named C1156Y and L1152R.) In the lab, S1206Y wasn’t as resistant as the other three, suggesting crizotinib might still slow some weakly resistant variants even if unable to stop them.
The team lab-tested three 2nd generation ALK inhibitor drugs (TAE684, CH5424802, and ASP3026) against some ALK mutations. I might be misinterpreting the data, but against the original ALK these three drugs and crizotinib looked comparably effective. Against the four resistant ALK mutations, their effectiveness varied and the best wasn’t always the same. None were as effective against the resistant mutations as crizotinib had been against the original ALK mutation (and none was very effective against 1151T ins).
At first glance this might suggest shrinkage might be less common when treating resistant mutations with 2nd generation ALK inhibitors, but neither LDK 378 nor Ariad AP26113 were tested or mentioned and only a few mutations were tested. So for now, I’ll remain hopefully optimistic that at least one drug will be found effective enough to do the job for a particular resistant ALK mutation for a while.
(BTW, the marketing material from Ariad on their own early lab work for AP26113 suggested it might work on many ALK variants, including T1151, L1152, C1156, I1171, F1174, V1180, R1181, L1196, L1198, G1202, E1210, E1241, F1245, I1268, G1269, Y1278, and S1206 [that last one requiring a very high dose]. I think most of these were synthetically mutated using lab techniques rather than naturally occurring in patients, but clearly some show up in patients and any of them potentially could.)
=== Amplified ALK Mutation ===
One patient had resistance from amplification of the original “ALK fusion” mutation. (I think this might be what some studies refer to as gene “copy number gain” (CNG).) Basically, it’s the same original ALK mutation, but just more of it, too much for the crizotinib to block it all.
Hypothetically, I’d guess this might mean that a higher dose of crizotinib might help a little more for a while if the patient’s health can tolerate the side-effects and the FDA allowed it, or maybe a 2nd generation ALK inhibitor might help for a while (if one is more potent or more narrowly targeted to the ALK mutation, e.g., maybe the TAE684 column in article’s graph 1E ). Your oncologist should be able to discuss whether something like this could be testable or treatable in an ALK-targeted way.
=== HSP90 Inhibitor ===
With that as context, the research team’s lab work also found that a different kind of inhibitor might sometimes be more effective than the ALK inhibitors they were testing. HSP90 (heat shock protein 90) assists ALK fusion proteins. HSP90 inhibitors are being tested in clinical trials. The research team tested the HSP90 inhibitor 17-AAG (a derivative of natural geldanamycin) and found it was highly effective against the ALK mutations they tested. At the concentration they used, it seemed more potent than all the other drugs they tested, but it also was potent against the normal non-mutated ALK gene, which could mean stronger side effects, too. Other clinical research studies will have to determine the right HSP90 inhibitor and dose level to balance effectiveness vs. tolerable level of side effects.
=== KIT Amplification ===
Two of the 18 ALK resistance cases also had a second simultaneous resistance mechanism: amplification (e.g., copy number gain) of the KIT gene which led to over-expression of both KIT protein and a KIT-assisting ligand called “stem cell factor” (SCF). In engineered cells this combination made the cells resistant to crizotinib, yet sensitive to crizotinib if KIT were inhibited using Gleevec (imatinib).
So apparently there can be multiple simultaneous mechanisms of resistance in crizotinib-resistant cancer cells. For patients whose resistance is known to involve KIT/SCF, it sounds promising that an existing drug might eventually be available to help control the KIT route.
=== EGFR Activation (Phosphorylation) ===
The big surprise was phosphorylated EGFR (pEGFR) mediated resistance, detected in all but one of the cases that could be tested. This is not an EGFR mutation, nor EGFR amplification (e.g., copy number gain), but EGFR activation (phosphorylation, i.e., charged up and working). FWIW, according the article this might possibly be caused by up-regulation of the EGFR receptor itself and two ligands (EGFR ligand amphiregulin and ErbB3 ligand NRG1).
From that data presented, it seems the EGFR activation is usually present even before starting crizotinib and might limit response to crizotinib. In an experiment on a patient’s pre-crizotinib cells which were sensitive to crizotinib but less than normal, treatment with both Xalkori (crizotinib) and Iressa (gefitinib) suppressed cell growth more potently and induced significant apoptosis. In another experiment, it appeared an improved response might be possible by inhibiting both ALK and EGFR, even though the effect wasn’t as potent as crizotinib alone had been on cells that didn’t have EGFR activation. (This suggests there’s more going on here than just these two tyrosine kinases.)
=== It’s So Complicated ===
Yes, it’s complicated. Some ALK inhibitor resistance is due to a resistant ALK mutation, some is due to amplification … amplification … amplification (yes, I’m repeating myself more times than you can handle), some is due to KIT amplification, some is due to EGFR activation, and sometimes inhibiting multiple resistance routes still isn’t enough to lock down the cancer. (We obviously don’t know all the biochemical players in the cancer orchestra yet.)
This sounds like an example of how amazingly adaptable the human body is. You can inhibit or break a gene and you’re your body will try to compensate; you inhibit something more, and it tries to compensate again. That makes it hard to stop cancer, but research like this gives me hope that someday science will learn all the things we’ll need to do to control this beast for many years (most of the time).
=== So What Do We Do? ===
So what should we do when we develop crizotinib resistance?
Ask your oncologist (once they’ve had a chance to read the article). If they have questions, they can contact one of the authors.
For myself, I’d ask my oncologist if it’s possible to have a fresh biopsy of my resistant cancer tested for resistant or amplified ALK mutations, phosphorylated EGFR, and other possible mutations (e.g., KIT), and then treat the resistance accordingly.
Even without testing, I might ask my oncologist if he/she would consider giving ALK+EGFR combo inhibition a try (if the FDA would allow it), especially if my initial response to crizotinib was less than good. If not, I’d hunt for a combo-drug trial of it if one exists. Maybe one of us will find that answer and share it.
Sooner or later, a jump from the ALK inhibitor track to another track will be needed. In this research article, the HSP90 inhibitor experimental trial track seemed promising for crizotinib-resistant ALK-driven lung cancer. Your oncologist may be able to suggest which HSP90’s look most promising. (Other possible tracks: surgery, radiation, chemo, other chemo, immunotherapy, or other experimental things, if time permits.)
This summary and the abstract at http://www.ncbi.nlm.nih.gov/pubmed/22277784 may suffice for most, but your oncologist and some of you will want to buy and read the full article. It’s available by just following the below-the-abstract “LinkOuts” expandable-menu to the publication. (And if you find errors in my summary, please let me know so I can fix it promptly.)
Best hopes
Thursday, February 2, 2012
The History of Cancer
The History of Cancer
By Lisa Fayed, About.com Guide
Updated July 08, 2009
About.com Health's Disease and Condition content is reviewed by our Medical Review Board
See More About:
hippocrates
cancer causes
cancer treatment
diagnosing cancer
"The History of Cancer"
The History of Cancer: How Cancer was First Discovered and Treated
Believe it or not, cancer has afflicted people for several centuries. It is not a new disease. It is because of the early research that we hold a greater knowledge of cancer today.
Origin of the Word "Cancer"
The word cancer came from the father of medicine, Hippocrates, a Greek physician. Hippocrates used the Greek words, carcinos and carcinoma to describe tumors, thus calling cancer "karkinos." The Greek terms actually were words to describe a crab, which Hippocrates thought a tumor resembled. Although Hippocrates may have named "Cancer," he was certainly not the first to discover the disease. The history of cancer actually begins much earlier.
The First Documented Case of Cancer
The world's oldest documented case of cancer hails from ancient Egypt, in 1500 b.c. The details were recorded on a papyrus, documenting 8 cases of tumors occurring on the breast. It was treated by cauterization, a method to destroy tissue with a hot instrument called "the fire drill." It was also recorded that there was no treatment for the disease, only palliative treatment.
There is evidence that the ancient Egyptians were able to tell the difference between malignant and benign tumors. According to inscriptions, surface tumors were surgically removed in a similar manner as they are removed today.
What Early Physicians Thought Caused Cancer
Today, we know so much about the human body; however early Greek physicians weren't so fortunate. Hippocrates believed that the body was composed of four fluids: blood, phlegm, yellow bile and black bile. He believed that an excess of black bile in any given site in the body caused cancer. This was the general thought of the cause of cancer for the next 1400 years.
In ancient Egypt, it was believed cancer was caused by the Gods.
The Birth of the Pathological Autopsy
Autopsies done by Harvey in 1628 paved the way to learning more about human anatomy and physiology. Blood circulation was discovered, opening the doors for more research on diseases. It wasn't until 1761 that autopsies were performed to research cause of death in ill patients. Giovanni Morgagni of Padua was the first to do such autopsies.
More Theories on the Causes of Cancer
The lymph theory developed in the 17th century, replacing Hippocrates' black bile theory on the cause of cancer. The discovery of the lymphatic system gave new insight to what may cause cancer. It was believed that abnormalities in the lymphatic system was the cause.
It wasn't until the late 19th century that Rudolph Virchow recognized that cells, even cancerous cells, derived from other cells.
Other theories surfaced, such as cancer being cause by trauma, parasites, and it was thought that cancer may spread "like a liquid." It was later concluded that cancer spread through malignant cells by German surgeon, Karl Thiersch.
In 1926 a Nobel Prize was wrongfully awarded for the discovery of the cause of stomach cancer a worm.
The 20th century saw the greatest progression in cancer research. Research identifying carcinogens, chemotherapy, radiation therapy and better means of diagnosis were discovered.
Today, we are able to cure some types of cancer, and research is ongoing. Clinical trials and research studies are our key to finding a cure, or a definitive method of prevention.
Sources:
American Cancer Society - History of Cancer.
The Chemical Heritage Foundation -Chemotherapy Timeline.
National Cancer Institute - Closing in on Cancer: Solving a 5000-Year-Old Mystery).
http://cancer.about.com/od/historyofcancer/a/cancerhistory.htm
By Lisa Fayed, About.com Guide
Updated July 08, 2009
About.com Health's Disease and Condition content is reviewed by our Medical Review Board
See More About:
hippocrates
cancer causes
cancer treatment
diagnosing cancer
"The History of Cancer"
The History of Cancer: How Cancer was First Discovered and Treated
Believe it or not, cancer has afflicted people for several centuries. It is not a new disease. It is because of the early research that we hold a greater knowledge of cancer today.
Origin of the Word "Cancer"
The word cancer came from the father of medicine, Hippocrates, a Greek physician. Hippocrates used the Greek words, carcinos and carcinoma to describe tumors, thus calling cancer "karkinos." The Greek terms actually were words to describe a crab, which Hippocrates thought a tumor resembled. Although Hippocrates may have named "Cancer," he was certainly not the first to discover the disease. The history of cancer actually begins much earlier.
The First Documented Case of Cancer
The world's oldest documented case of cancer hails from ancient Egypt, in 1500 b.c. The details were recorded on a papyrus, documenting 8 cases of tumors occurring on the breast. It was treated by cauterization, a method to destroy tissue with a hot instrument called "the fire drill." It was also recorded that there was no treatment for the disease, only palliative treatment.
There is evidence that the ancient Egyptians were able to tell the difference between malignant and benign tumors. According to inscriptions, surface tumors were surgically removed in a similar manner as they are removed today.
What Early Physicians Thought Caused Cancer
Today, we know so much about the human body; however early Greek physicians weren't so fortunate. Hippocrates believed that the body was composed of four fluids: blood, phlegm, yellow bile and black bile. He believed that an excess of black bile in any given site in the body caused cancer. This was the general thought of the cause of cancer for the next 1400 years.
In ancient Egypt, it was believed cancer was caused by the Gods.
The Birth of the Pathological Autopsy
Autopsies done by Harvey in 1628 paved the way to learning more about human anatomy and physiology. Blood circulation was discovered, opening the doors for more research on diseases. It wasn't until 1761 that autopsies were performed to research cause of death in ill patients. Giovanni Morgagni of Padua was the first to do such autopsies.
More Theories on the Causes of Cancer
The lymph theory developed in the 17th century, replacing Hippocrates' black bile theory on the cause of cancer. The discovery of the lymphatic system gave new insight to what may cause cancer. It was believed that abnormalities in the lymphatic system was the cause.
It wasn't until the late 19th century that Rudolph Virchow recognized that cells, even cancerous cells, derived from other cells.
Other theories surfaced, such as cancer being cause by trauma, parasites, and it was thought that cancer may spread "like a liquid." It was later concluded that cancer spread through malignant cells by German surgeon, Karl Thiersch.
In 1926 a Nobel Prize was wrongfully awarded for the discovery of the cause of stomach cancer a worm.
The 20th century saw the greatest progression in cancer research. Research identifying carcinogens, chemotherapy, radiation therapy and better means of diagnosis were discovered.
Today, we are able to cure some types of cancer, and research is ongoing. Clinical trials and research studies are our key to finding a cure, or a definitive method of prevention.
Sources:
American Cancer Society - History of Cancer.
The Chemical Heritage Foundation -Chemotherapy Timeline.
National Cancer Institute - Closing in on Cancer: Solving a 5000-Year-Old Mystery).
http://cancer.about.com/od/historyofcancer/a/cancerhistory.htm
Prostate Cancer Found in Egyptian Mummy
This is an interesting article. Of course, some cancers are genetic and some cancers are due to environmental impressions. My mom's cancer is not genetic, but we don't know what environmental factor or factors have mutated her genetic DNA causing this to happen. We may never know. It is in God's hands.
-Vanessa
Prostate Cancer Found in Egyptian Mummy
Posted by Caitlin Bronson on January 30, 2012 9:08AM Boomer Health and Lifestyle.
A 2,200-year-old mummy was found to have prostate cancer, leading scientists to question whether genetics played a role.
The world’s second oldest case of prostate cancer was found in a 2,200-year-old mummy, the Canadian Press reports. According to American University in Cairo professor Salima Ikram, extensive testing of the mummy revealed that the disease was not caused by environmental influences, but rather by genetics.
“Living conditions in ancient times were very different,” Ikram explained. “There were no pollutants or modified foods, which leads up to believe that the disease is not necessarily only linked to industrial factors.”
Whether prostate cancer is caused by genetics or environmental factors is a big question in the field of cancer research, the Canadian Press said. While scientists often link cancer to diet and industrial toxins, older cases of cancer suggest that genetics may play a role as well.
Ikram and her team have been studying the ancient Egyptian mummy in Portugal for the past two years. The prostate cancer was discovered by using a high-resolution computerized tomography (CT) scan, which revealed lesions on the mummy’s lumbar spine.
The man died in his forties, researchers say. The mummy is kept at the National Archaeology Museum of Lisbon.
The oldest known case of prostate cancer was found in a 2,700-year-old skeleton of a Scythian king in Russia, AUC said in a statement. His skeleton was found in a steppe in Southern Siberia.
http://www.thirdage.com/news/prostate-cancer-found-in-egyptian-mummy_01-30-2012
-Vanessa
Prostate Cancer Found in Egyptian Mummy
Posted by Caitlin Bronson on January 30, 2012 9:08AM Boomer Health and Lifestyle.
A 2,200-year-old mummy was found to have prostate cancer, leading scientists to question whether genetics played a role.
The world’s second oldest case of prostate cancer was found in a 2,200-year-old mummy, the Canadian Press reports. According to American University in Cairo professor Salima Ikram, extensive testing of the mummy revealed that the disease was not caused by environmental influences, but rather by genetics.
“Living conditions in ancient times were very different,” Ikram explained. “There were no pollutants or modified foods, which leads up to believe that the disease is not necessarily only linked to industrial factors.”
Whether prostate cancer is caused by genetics or environmental factors is a big question in the field of cancer research, the Canadian Press said. While scientists often link cancer to diet and industrial toxins, older cases of cancer suggest that genetics may play a role as well.
Ikram and her team have been studying the ancient Egyptian mummy in Portugal for the past two years. The prostate cancer was discovered by using a high-resolution computerized tomography (CT) scan, which revealed lesions on the mummy’s lumbar spine.
The man died in his forties, researchers say. The mummy is kept at the National Archaeology Museum of Lisbon.
The oldest known case of prostate cancer was found in a 2,700-year-old skeleton of a Scythian king in Russia, AUC said in a statement. His skeleton was found in a steppe in Southern Siberia.
http://www.thirdage.com/news/prostate-cancer-found-in-egyptian-mummy_01-30-2012
Ups and downs, ups and downs... but always end up : )
Okay, so this week has been a bit of a roller coaster, but mom is staying strong and taking one day at a time. Last weekend was good. Saturday mom went over to my older brother John's house for salmon burgers. Mom said they were very good and she had a nice time. Sunday we went to a wonderful new church on the Southeast side of town for a really nice Healing service. We had a good time and everyone there was so kind and loving and expressed their faith and belief in God. It was a beautiful experience and mom really felt great afterwards. So did I. It was really comforting and was a good release. On Monday, the pain in mom's back subsided and it felt miraculous. It was amazing because it was the first day that mom had no constant discomfort or pain for at least 2 weeks. Tuesday the pain came back and was pretty strong by evening. It really scared me and affected me to hear her in that much pain. It was difficult that night emotionally. Wednesday, mom was up and out and trying to do everything she can and did very well for most the day, but after a while the pain can get to be too much and its hard on her. Oh then she got a flat tire that afternoon. Nice. It was okay though triple A came out and changed the tire. I was going to it, but mom didn't want me to. Besides the triple A guy came very quickly after about 15 minutes. So, after that mom went home and I came over a little later and stayed the night. Thursday (today), mom rested this morning and then made her way to the courthouse. Her case was reset and she stayed for a little while downtown, but came home after. It was a little rough with some people there, but we forgive those who trespass against us. Anyway, I picked up some dinner which was good, but I think I'm going to buy a juicer and try to get more fresh vegetables in our diet. I've read so much about juicing and its just really good for you all around. Perhaps we can find some concoction that we will enjoy. Anyway, I am here with mom tonight and she is feeling better. We are enjoying each others company and having a nice night.
Thank you all for your prayers and compassion.
-Vanessa
Thank you all for your prayers and compassion.
-Vanessa
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