Doing some field work in Houston for 3 weeks.
We will be tracking new CPRIT Requests for Application
Have submitted preliminary summary of our newest submission to Dr. Jeffrey Larson for review and help. Hopefully we will meet the requirements.
This work in Houston is a continuation and preparedness for work to do under the CPRIT funded project if it comes to be.
DR K.
Tuesday, October 30, 2012
Survey Data Extraction
We are working hard to rapidly bring out the results of the surveys on breast cancer risk factors, smoking cessation, physical activity and nutrition collected during the PINK Event at Cielo Vista Mall in El Paso. Stay tuned!
Monday, October 29, 2012
Saturday, October 27, 2012
Building an Electronic Cancer Cell is a necessity
Natural death of cancer cells is the path to cure.
Experience of chemotherapy has shown that a blind and random attack of cancer cells is ineffective at assuring the death of cancer at a 100% curative rate. We believe that this is mostly due to the fact that chemotherapy most of the time does not inflict enough damage to the cell to lead to self destruction or Apoptosis. We believe that certain changes to the cell caused by chemotherapy could work counter the intended effect. This the basis of the trust in target therapy.
Now let us not approach Target therapy the same way we did for chemotherapy. Target therapy has proven to work, no doubt about it. We need now to organize coordinated attacks on the cancer cells. We know that Cancer cells' life processes seem to be organized in cascade, redundancy and escape mechanisms, but in a logical way. With one event following another. This is why Target therapy works by cutting off or promoting upstream events in the cascade.The thing is that cells have downstream escape mechanisms, therefore that mechanism needs also to be struck down in a staged or coordinated attack.
We believe that the construction of an electronic model of a cell will help us identify gaps in the cascade of molecular events, and help identify critical new targets to go after, once these gaps are filled.
Some of the current targets
1. Adhesion Molecules
2. Cell membrane receptors
3. Signal transduction pathways
4. Transcription genes
5. Histones and promoter genes
6. Mitochondrial/ribosomes Metabolism disruption
7. Nuclear genetic material
8. Gene repair and mismatch repair mechanism
This list is not exhaustive, therefore the potential for investigation appears endless.
Experience of chemotherapy has shown that a blind and random attack of cancer cells is ineffective at assuring the death of cancer at a 100% curative rate. We believe that this is mostly due to the fact that chemotherapy most of the time does not inflict enough damage to the cell to lead to self destruction or Apoptosis. We believe that certain changes to the cell caused by chemotherapy could work counter the intended effect. This the basis of the trust in target therapy.
Now let us not approach Target therapy the same way we did for chemotherapy. Target therapy has proven to work, no doubt about it. We need now to organize coordinated attacks on the cancer cells. We know that Cancer cells' life processes seem to be organized in cascade, redundancy and escape mechanisms, but in a logical way. With one event following another. This is why Target therapy works by cutting off or promoting upstream events in the cascade.The thing is that cells have downstream escape mechanisms, therefore that mechanism needs also to be struck down in a staged or coordinated attack.
We believe that the construction of an electronic model of a cell will help us identify gaps in the cascade of molecular events, and help identify critical new targets to go after, once these gaps are filled.
Some of the current targets
1. Adhesion Molecules
2. Cell membrane receptors
3. Signal transduction pathways
4. Transcription genes
5. Histones and promoter genes
6. Mitochondrial/ribosomes Metabolism disruption
7. Nuclear genetic material
8. Gene repair and mismatch repair mechanism
This list is not exhaustive, therefore the potential for investigation appears endless.
Friday, October 26, 2012
Ltd Governor David Dewhurst to Visit CPRIT
A surprise visit this morning at the closing of the 3rd CIPRIT Conference in Austin, Texas.
He reiterated his unwavering support for cancer research, prevention and commercialization in favor of reducing the burden of cancer on the Texas population with the hope that the findings and new developments will help save lives nationwide and worldwide. The sooner the better, we all agree!
He reiterated his unwavering support for cancer research, prevention and commercialization in favor of reducing the burden of cancer on the Texas population with the hope that the findings and new developments will help save lives nationwide and worldwide. The sooner the better, we all agree!
Thursday, October 25, 2012
Free LUNG CANCER Seminar TONIGHT!
You are welcome to our FREE LUNG CANCER Seminar at the Greater East Cancer Center & CRBCM located 2400 Trawood Dr, Suite 303 in the Sierra Providence Eastside Medical Center in El Paso, Texas.
Time: 6pm - 7pm
Your QUESTIONS are welcomed, take this opportunity to find out what you always wanted to know for sure!
We are looking forward to welcoming and meeting you tonight!
For info and directions call: 915-730-4535 or 765-969-2188
Time: 6pm - 7pm
Your QUESTIONS are welcomed, take this opportunity to find out what you always wanted to know for sure!
We are looking forward to welcoming and meeting you tonight!
For info and directions call: 915-730-4535 or 765-969-2188
Wednesday, October 24, 2012
Networking at the CPRIT Annual Conference Austin
It is greatly inspiring and encouraging to meet and speak with current grant recipients, whether in the field of pure research, prevention or intervention. Our various hypothesis seem well aligned with findings in other cities in Texas. I have the impression that thanks to CPRIT, never before was a 'minority' population so well and intensely studied and paid attention to through outreach programs: a totally new health care model may be derived from these experiences! As a consequence of the extremely positive reaction of the target population and their adherence to interventions such as screenings, exercise programs and classes in nutrition and diet, some research programs had to refuse access, being overwhelmed by the number of people wanting to participate in their healthy lifestyle program - isn't that living proof, once again, that education and customized health care will make an individual want to live more healthy and take better care of him or herself!
After our conference on Breast Cancer and discussion on the CRBCM objective
tomorrow in our monthly conference, we will discuss Lung Cancer
we will focus on risk factors, some of the attempts for primary prevention interventions and their results, and discuss some of the new target therapies already in place, and of course future therapeutic strategies/targets.
Come participate by calling 915-307-3354.
DR K.
tomorrow in our monthly conference, we will discuss Lung Cancer
we will focus on risk factors, some of the attempts for primary prevention interventions and their results, and discuss some of the new target therapies already in place, and of course future therapeutic strategies/targets.
Come participate by calling 915-307-3354.
DR K.
Tuesday, October 23, 2012
We believe in the cure for Cancer:
People talk about a cure and skeptics balk!
But the cure is possible and actually exists already in every survivor who had a remote history of cancer.
Remember this, a cancer cell is full of messages encrypted in chemical messages when to grow, when to start aging and when to die. Yes cancer cells have an internal message when to start apoptosis (self destruction).
It means you could tell it to start apoptosis and kill itself. Our challenge is to know how to speak to a cell.
Research are starting to learn that language in what is now known as Target Therapy. Cancer treatment is now becoming a Piano tune. if you hit the right keys in a song and the cancer cell get it, it will find its way to self destruction. We are at the early stage of this music, still learning it. Hitting this key here and seeing what happens. We are finding out that even tough cancers such as Melanoma, if you hit the BRAF key, things start happening. In some lung cancers, if you hit the EGFR key, you start getting somewhere. It is just a matter of time before we start asking to a cell, now time for an increase in BAX or Caspases, and self destruct. The cell has some redundancy and networking to complicate the road to self destruction, but we still believe that with the right tune, cancer cells will dance to self destruction, and yes cure is within our reach!
But the cure is possible and actually exists already in every survivor who had a remote history of cancer.
Remember this, a cancer cell is full of messages encrypted in chemical messages when to grow, when to start aging and when to die. Yes cancer cells have an internal message when to start apoptosis (self destruction).
It means you could tell it to start apoptosis and kill itself. Our challenge is to know how to speak to a cell.
Research are starting to learn that language in what is now known as Target Therapy. Cancer treatment is now becoming a Piano tune. if you hit the right keys in a song and the cancer cell get it, it will find its way to self destruction. We are at the early stage of this music, still learning it. Hitting this key here and seeing what happens. We are finding out that even tough cancers such as Melanoma, if you hit the BRAF key, things start happening. In some lung cancers, if you hit the EGFR key, you start getting somewhere. It is just a matter of time before we start asking to a cell, now time for an increase in BAX or Caspases, and self destruct. The cell has some redundancy and networking to complicate the road to self destruction, but we still believe that with the right tune, cancer cells will dance to self destruction, and yes cure is within our reach!
Monday, October 22, 2012
 |
| The CRBCM Team in Action |
 | |
| Questionnaires handed out |
 | |
| Interested visitors eager to fill out the survey |
 | |
| Concentrated on the surveys |
 | |
| Health is a Family Affair |
The first feed-back from the surveys shows that :
13 visitors need and want more information in general
3 Visitors want to volunteer with the CRBCM
1 Visitor wants to be trained to teach activities at the CRBCM
1 Visitor wants to become a Navigator for patients
1 Visitor and Survivor wants to teach Lymphedema classes
Participants with a special interest in several health topics signed up for follow-up contact regarding:
5 x Diet
4 x Physical Exercise
7 x Nutrition
4 x Weight Control
4 x Stress Management
5 x Breast Cancer
1 x Uterine Cancer
1 x Cervical Cancer
1 x Prostate Cancer
1 x Lung Cancer
1 x Anemia
2 x Smoking Cessation
Now we know what we need to do!
Sunday, October 21, 2012
Clinical Hypothesis in research, prevention and Commercialization Hypothesis in cancer therapeutics
Following our first article of October 14th, we believe it is time to suggest a second hypothesis
in therapeutic research in Cancer. The early years of cancer treatment, the objective was to blast the cancer cells with chemotherapy that was in our arsenal. Most of the time this approach was able to kill the cells partially. The cancer cells quickly however learned to escape the blast, creating wonderful resistance mechanisms. As we progress in molecular biology, we are increasingly shying away from these blast approaches, leaning more and more in identifying metabolic pathways, and identifying targets in that pathway and aiming our gun and shoot it, and see what happens. This is called Target Therapy.
One pathway that we have learned a bit about is the P53 ( and down the line the pathway the Rb which lead to cell stopping in the cell cycle to allow genetic repair). This pathway is mostly triggered by an abnormality in the gene.
Today, we go back to the blast approach when we have no good Target therapy option. In fact we always try to add the target therapy to the blast chemotherapy to see if we could have the most from our money.
combination of Avastin (a target therapy) to chemotherapy is standard therapy in the United states for stage IV Colon cancer. We know that chemotherapy mostly affect our gene. This change in gene should trigger the activation of our P53 system to stop the cancer cell in its track for growth. The question now is should we give chemotherapy in patient who has an altered P53 system. What is the benefit the gene with chemotherapy, if the system that should be triggered to clean up is out.
Hypothesis:
Altered P53 pathway predict a failure of chemotherapy which has gene disturbance as main effect.
second hypothesis: preservation of status of the wild type P53 during chemotherapy may predict for a successful chemotherapy treatment (Cisplatin).
if it is true, commercialization is possible...
Don't be shy, give me your opinion!
in therapeutic research in Cancer. The early years of cancer treatment, the objective was to blast the cancer cells with chemotherapy that was in our arsenal. Most of the time this approach was able to kill the cells partially. The cancer cells quickly however learned to escape the blast, creating wonderful resistance mechanisms. As we progress in molecular biology, we are increasingly shying away from these blast approaches, leaning more and more in identifying metabolic pathways, and identifying targets in that pathway and aiming our gun and shoot it, and see what happens. This is called Target Therapy.
One pathway that we have learned a bit about is the P53 ( and down the line the pathway the Rb which lead to cell stopping in the cell cycle to allow genetic repair). This pathway is mostly triggered by an abnormality in the gene.
Today, we go back to the blast approach when we have no good Target therapy option. In fact we always try to add the target therapy to the blast chemotherapy to see if we could have the most from our money.
combination of Avastin (a target therapy) to chemotherapy is standard therapy in the United states for stage IV Colon cancer. We know that chemotherapy mostly affect our gene. This change in gene should trigger the activation of our P53 system to stop the cancer cell in its track for growth. The question now is should we give chemotherapy in patient who has an altered P53 system. What is the benefit the gene with chemotherapy, if the system that should be triggered to clean up is out.
Hypothesis:
Altered P53 pathway predict a failure of chemotherapy which has gene disturbance as main effect.
second hypothesis: preservation of status of the wild type P53 during chemotherapy may predict for a successful chemotherapy treatment (Cisplatin).
if it is true, commercialization is possible...
Don't be shy, give me your opinion!
Saturday, October 20, 2012
The CRBCM is conducting 4 research survey this morning at Cielo Vista Mall
all related to life style modification to reverse mortality of breast cancer, I am glad to report a huge participation, already, a call for reprint of survey material has been placed, we can already predict
good data mining! The CRBCM is proud of the Cielo Vista Mall and its help for our cause! Other participating with us include The Susan G Komen, the National Cancer Society, the Rio Grande, UTEP, and another organization...CRBCM is standing its own! We are proud of being the CRBCM!
The Fight for the reversal of Breast Cancer mortality is on, we will not back down!
Dr Kankonde
all related to life style modification to reverse mortality of breast cancer, I am glad to report a huge participation, already, a call for reprint of survey material has been placed, we can already predict
good data mining! The CRBCM is proud of the Cielo Vista Mall and its help for our cause! Other participating with us include The Susan G Komen, the National Cancer Society, the Rio Grande, UTEP, and another organization...CRBCM is standing its own! We are proud of being the CRBCM!
The Fight for the reversal of Breast Cancer mortality is on, we will not back down!
Dr Kankonde
Friday, October 19, 2012
At Cielo mall, we will be conducting a survey
4 questionaires
1. Risk factor assessment for Breast Cancer
2. Nutrition Pattern
3. Physical Activity evaluation
4. smoking cessation
there will be a 5 dollars incentive/reward for the first 40 survey takers (who will take all the 4 surveys).
We have 8 Volunteers, we need more,
please call 915-307-3354 to volunteer or take a survey
4 questionaires
1. Risk factor assessment for Breast Cancer
2. Nutrition Pattern
3. Physical Activity evaluation
4. smoking cessation
there will be a 5 dollars incentive/reward for the first 40 survey takers (who will take all the 4 surveys).
We have 8 Volunteers, we need more,
please call 915-307-3354 to volunteer or take a survey
Wednesday, October 17, 2012
Rating of Breast Cancer Risk Factors by Cancer Survivors in El Paso
Rating of Breast Cancer Risk Factors from 1 to 10 among a list of 28 risk factors by Cancer Survivors from the Dialogue Group in El Paso, Texas, on October 9th, 2012:
The following Risk Factors were given a "Nr.1" importance each by one to four participants out of 18 participants in this small pilot survey that will now be conducted on a larger scale with the El Paso population
Were rated as Nr.1 Risk factor for Breast Cancer:
4x Personal History
3x Family History
3x Being a Woman
2x Smoking
2x Being Overweight
1x Age
1x Drinking Alcohol
1x Genetic
1x Race and Ethnicity
The full list of Risk Factors for Breast Cancer can be found on: breastcancer.org.
The following description of Risk Factors for Breast Cancer can be found on cancer.org:
Besides being female, age is the most important risk factor for breast cancer. A woman’s breast cancer risk may be higher or lower depending on her personal risk factors and other factors not yet fully understood.
Currently, a woman living in the US has a 12.15%, or a 1 in 8, lifetime risk of being diagnosed with breast cancer. In the 1970s, the lifetime risk of being diagnosed with breast cancer was 1 in 11. This increase in the likelihood of being diagnosed with breast cancer is due to longer life expectancy, as well as increases in breast cancer incidence due in part to changes in reproductive patterns, menopausal hormone use, the rising prevalence of obesity, and increased detection through screening. Lifetime risk reflects an average woman’s risk over an entire lifetime, including the possibility that she may die from another cause before she would have developed breast cancer, and should not be confused with risk over a shorter time period.
Relative Risk Factors (cancer.org)
Relative Risk Factor >4.0 •
Age (65+ vs. <65 years, although risk increases across all ages until age 80)
• Biopsy-confirmed atypical hyperplasia
• Certain inherited genetic mutations for breast cancer (BRCA1 and/or BRCA2)
• Mammographically dense breasts
• Personal history of breast cancer
Relative Risk Factor 2.1-4.0
• High endogenous estrogen or testosterone levels
• High bone density (postmenopausal)
• High-dose radiation to chest
• Two first-degree relatives with breast cancer
Relative Risk Factor 1.1-2.0
• Alcohol consumption
• Ashkenazi Jewish heritage
• Early menarche (<12 years)
• Height (tall)
• High socioeconomic status
• Late age at first full-term pregnancy (>30 years)
• Late menopause (>55 years)
• Never breastfed a child
• No full-term pregnancies
• Obesity (postmenopausal)/adult weight gain
• One first-degree relative with breast cancer
• Personal history of endometrium, ovary, or colon cancer
• Recent and long-term use of menopausal hormone therapy containing estrogen and progestin
• Recent oral contraceptive use
The following Risk Factors were given a "Nr.1" importance each by one to four participants out of 18 participants in this small pilot survey that will now be conducted on a larger scale with the El Paso population
Were rated as Nr.1 Risk factor for Breast Cancer:
4x Personal History
3x Family History
3x Being a Woman
2x Smoking
2x Being Overweight
1x Age
1x Drinking Alcohol
1x Genetic
1x Race and Ethnicity
The full list of Risk Factors for Breast Cancer can be found on: breastcancer.org.
The following description of Risk Factors for Breast Cancer can be found on cancer.org:
Besides being female, age is the most important risk factor for breast cancer. A woman’s breast cancer risk may be higher or lower depending on her personal risk factors and other factors not yet fully understood.
Currently, a woman living in the US has a 12.15%, or a 1 in 8, lifetime risk of being diagnosed with breast cancer. In the 1970s, the lifetime risk of being diagnosed with breast cancer was 1 in 11. This increase in the likelihood of being diagnosed with breast cancer is due to longer life expectancy, as well as increases in breast cancer incidence due in part to changes in reproductive patterns, menopausal hormone use, the rising prevalence of obesity, and increased detection through screening. Lifetime risk reflects an average woman’s risk over an entire lifetime, including the possibility that she may die from another cause before she would have developed breast cancer, and should not be confused with risk over a shorter time period.
Relative Risk Factors (cancer.org)
Relative Risk Factor >4.0 •
Age (65+ vs. <65 years, although risk increases across all ages until age 80)
• Biopsy-confirmed atypical hyperplasia
• Certain inherited genetic mutations for breast cancer (BRCA1 and/or BRCA2)
• Mammographically dense breasts
• Personal history of breast cancer
Relative Risk Factor 2.1-4.0
• High endogenous estrogen or testosterone levels
• High bone density (postmenopausal)
• High-dose radiation to chest
• Two first-degree relatives with breast cancer
Relative Risk Factor 1.1-2.0
• Alcohol consumption
• Ashkenazi Jewish heritage
• Early menarche (<12 years)
• Height (tall)
• High socioeconomic status
• Late age at first full-term pregnancy (>30 years)
• Late menopause (>55 years)
• Never breastfed a child
• No full-term pregnancies
• Obesity (postmenopausal)/adult weight gain
• One first-degree relative with breast cancer
• Personal history of endometrium, ovary, or colon cancer
• Recent and long-term use of menopausal hormone therapy containing estrogen and progestin
• Recent oral contraceptive use
Monday, October 15, 2012
Affordable Mammograms NOW AVAILABLE!
If you have not yet had your yearly mammogram, now is the right time!
Many imaging services offer a special promotional rates for self-paying patients, and not only in October.
Call us for details on where and how much the mammograms are right now in El Paso:
Call us on 915-730-4535
Many imaging services offer a special promotional rates for self-paying patients, and not only in October.
Call us for details on where and how much the mammograms are right now in El Paso:
Call us on 915-730-4535
Sunday, October 14, 2012
CLINICAL HYPOTHESIS IN CANCER RESEARCH AND COMMERCIALIZATION:
CLINICAL HYPOTHESIS IN CANCER RESEARCH AND COMMERCIALIZATION:
Of 186,000 Prostate cancers diagnosed each year, only 29,000 patients will die of this disease. In fact 70% of men over 80 years of age may be found with Prostate Cancer. Most will not die of this cancer. This fact has made almost futile the testing for prostate cancer in elderly patients. How does one chose who should be followed closely or treated? In other words how do you know what prostate cancer to observe versus which one to actually treat? In more scientific terms, which are the predictive factors that would prompt us to act versus observe the cancer? To make the matter more confusing, the success of PSA (prostate Specific Antigen) testing has complicated the issue. It has led to over-diagnosis, and experts are now recommending to use PSA findings with caution.
One thing is for sure: the difference between a benign and malignant tumor is that the malignant ones spread and invade our body. This is called "ability to metastasize". It is by invading other organs that cancer causes these organs to fail and finally causing death of the patient. Researchers have now started to look at cancer cells to try to predict which ones will spread and therefore kill the individual.
The Hypothesis:
For a cancer to spread, it has to detach itself from its surroundings and create a way to where it wants to go. Scientists have suggested that wherever a cell is located, it is maintained in place by ADHESION MOLECULES which tie them to the location. To make its move, the cancer cell has to lose these molecules.
This is why E-Cadherin has to be reduced by the cell, so that it can free itself from this environment. The question now is: Is a REDUCTION OF E-CADHERIN A PREDICTOR OF BAD CANCER? IN OTHER WORDS, SHOULD WE BE TESTING FOR THE REDUCTION OF E-CADHERIN IN PROSTATE CANCER TO PREDICT WHICH ONES NEEDS INTERVENTION? This is thought provoking.
P120 and beta- catenins are 2 molecules which could potentially be surrogates of cancer metastasis...who knows for sure!
After it has freed itself, the cancer cell has to move through tissues, it uses enzymes to break through the fibers. Some of these enzymes are called METALLOPROTEINASE. The current question is: SHOULD WE BE MEASURING LEVELS OF METALLOPROTEINASES TO DETECT CANCER CELLS ON THE MOVE?
These questions have been raised, it is time to work.
We could actually improve current means of screening for cancer by checking for reduction of E-Cadherin and increase of metalloproteinase in the tumor or blood if this is possible. Potential for commercialization is high if we can conquer this detection technology. "lets go to work!
12/3/2012
METASTATASIS AND SEEDING INTO NEW OR INVADED TISSUE
When the cancer cell reaches the new location, it uses the TGF beta to help its growth and to create exceptional advantage for its growth versus surrounding tissue. This Lead scientists to conclude that TGF beta presence is a sign of resistant disease. When in facts, it is first a late sign of metastasis already COMPLETED, TGF beta seems to be a sign of SEEDING INTO A NEW LOCATION. TGF BETA NOT ONLY STIMULATE GROWTH BUT COULD BE AN INHIBITORY PROTEIN FOR THE HOST DEFENSE AND REJECTION.
QUESTION:
SHOULD TGF BETA INCREASE BE THE THE SIGN OF SEEDING VS LATE STEP OF METASTASIS. WE BELIEVE THAT BY THE TIME TGF BETA IS BEING ELEVATED, SEEDING HAS ALREADY OCCURRED.
Of 186,000 Prostate cancers diagnosed each year, only 29,000 patients will die of this disease. In fact 70% of men over 80 years of age may be found with Prostate Cancer. Most will not die of this cancer. This fact has made almost futile the testing for prostate cancer in elderly patients. How does one chose who should be followed closely or treated? In other words how do you know what prostate cancer to observe versus which one to actually treat? In more scientific terms, which are the predictive factors that would prompt us to act versus observe the cancer? To make the matter more confusing, the success of PSA (prostate Specific Antigen) testing has complicated the issue. It has led to over-diagnosis, and experts are now recommending to use PSA findings with caution.
One thing is for sure: the difference between a benign and malignant tumor is that the malignant ones spread and invade our body. This is called "ability to metastasize". It is by invading other organs that cancer causes these organs to fail and finally causing death of the patient. Researchers have now started to look at cancer cells to try to predict which ones will spread and therefore kill the individual.
The Hypothesis:
For a cancer to spread, it has to detach itself from its surroundings and create a way to where it wants to go. Scientists have suggested that wherever a cell is located, it is maintained in place by ADHESION MOLECULES which tie them to the location. To make its move, the cancer cell has to lose these molecules.
This is why E-Cadherin has to be reduced by the cell, so that it can free itself from this environment. The question now is: Is a REDUCTION OF E-CADHERIN A PREDICTOR OF BAD CANCER? IN OTHER WORDS, SHOULD WE BE TESTING FOR THE REDUCTION OF E-CADHERIN IN PROSTATE CANCER TO PREDICT WHICH ONES NEEDS INTERVENTION? This is thought provoking.
P120 and beta- catenins are 2 molecules which could potentially be surrogates of cancer metastasis...who knows for sure!
After it has freed itself, the cancer cell has to move through tissues, it uses enzymes to break through the fibers. Some of these enzymes are called METALLOPROTEINASE. The current question is: SHOULD WE BE MEASURING LEVELS OF METALLOPROTEINASES TO DETECT CANCER CELLS ON THE MOVE?
Matrix metalloproteinases 2 and 9 increase permeability of sheep pleura in vitro
Eleni Apostolidou1*)These questions have been raised, it is time to work.
We could actually improve current means of screening for cancer by checking for reduction of E-Cadherin and increase of metalloproteinase in the tumor or blood if this is possible. Potential for commercialization is high if we can conquer this detection technology. "lets go to work!
12/3/2012
METASTATASIS AND SEEDING INTO NEW OR INVADED TISSUE
When the cancer cell reaches the new location, it uses the TGF beta to help its growth and to create exceptional advantage for its growth versus surrounding tissue. This Lead scientists to conclude that TGF beta presence is a sign of resistant disease. When in facts, it is first a late sign of metastasis already COMPLETED, TGF beta seems to be a sign of SEEDING INTO A NEW LOCATION. TGF BETA NOT ONLY STIMULATE GROWTH BUT COULD BE AN INHIBITORY PROTEIN FOR THE HOST DEFENSE AND REJECTION.
QUESTION:
SHOULD TGF BETA INCREASE BE THE THE SIGN OF SEEDING VS LATE STEP OF METASTASIS. WE BELIEVE THAT BY THE TIME TGF BETA IS BEING ELEVATED, SEEDING HAS ALREADY OCCURRED.
Conference with the Cancer Survivor Dialogue Group
On October 9, 2012, the CRBCM had a chance to submit a comprehensive mission and plan of activities intended for implementation annually. The plan was presented before the Dialogue Cancer Group, the largest Breast cancer survivors group in El Paso. Some members including a local physician were current patients undergoing chemotherapy. We took that opportunity to conduct a small survey to detect perception by El Pasoans as to what would be the most frequent or predominant risk factors for Breast cancer. Certainly, this was to tailor our education program for a potential primary prevention intervention. We asked the participants to rank the first 10 risk factors by importance out of 28 risk factors documented by BreastCancer.org on their web page. The list was randomly proposed for this small study. We have not concluded our analysis yet, but one can already suggest that 85% of survivors and current patients in El Paso feel that the 2 predominant Risk factors at equal rates were FAMILY HISTORY and GENETIC PREDISPOSITION.
This finding is striking because of the following reasons:
1. The group under observation is made of people who discuss monthly about Breast Cancer. Current patients speak with their Doctors almost everyday. This is a group of people that is clearly very well informed about this topic. But they still believe that the disease is either hereditary or follows a Mendelian inheritance pattern. That somehow the family history determines who will get Breast Cancer. Te truth is that 85 percent of newly diagnosed Breast cancers happen in women who are the first in their family to have the disease. In other words, just because there is no family history of breast cancer, women should not feel protected against the disease.
Take your mammogram if you are over 40 years of age: Please!
2. The consequence of the belief that "nobody in my family has it, so I am not at risk and so why would I want to go for a mammogram?" clearly is one of the barriers to taking a screening mammogram. Our Health Education material will feature it as a major objective to discuss in order to increase local rates of screening mammograms here in El Paso.
3. The Other truth is that most research literature suggests that only 5 to 10% of breast cancers (including BRCA 1 and BRCA 2) have a true genetic or familial hereditary or Mendelian inheritance pattern. The rest is random!
TO BE CONTINUED
This finding is striking because of the following reasons:
1. The group under observation is made of people who discuss monthly about Breast Cancer. Current patients speak with their Doctors almost everyday. This is a group of people that is clearly very well informed about this topic. But they still believe that the disease is either hereditary or follows a Mendelian inheritance pattern. That somehow the family history determines who will get Breast Cancer. Te truth is that 85 percent of newly diagnosed Breast cancers happen in women who are the first in their family to have the disease. In other words, just because there is no family history of breast cancer, women should not feel protected against the disease.
Take your mammogram if you are over 40 years of age: Please!
2. The consequence of the belief that "nobody in my family has it, so I am not at risk and so why would I want to go for a mammogram?" clearly is one of the barriers to taking a screening mammogram. Our Health Education material will feature it as a major objective to discuss in order to increase local rates of screening mammograms here in El Paso.
3. The Other truth is that most research literature suggests that only 5 to 10% of breast cancers (including BRCA 1 and BRCA 2) have a true genetic or familial hereditary or Mendelian inheritance pattern. The rest is random!
TO BE CONTINUED
Saturday, October 13, 2012
Our button for the STRIDES and EVERY DAY that we are KNOCKING CANCER OUT!
Our button for the STRIDES and EVERY DAY that we are KNOCKING CANCER OUT!
Own Your Power! Si Quieres, Puedes!
Wednesday, October 10, 2012
Dialogue Group of Cancer Survivors, Oct.9th,2012
 |
| Ready for the Presentation of the CRBCM |
 | ||
| Welcome to a large classroom |
 | |
| Lively discussions follow the presentation |
 | |
| A captive audience with many questions |
Monday, October 8, 2012
We have been invited to discuss the CRBCM mission and objectives before
the DIALOGUE CANCER GROUP, the largest Cancer support group in El Paso.
This will be up to an hour presentation. Join us on October 9th, 2012
at Sierra Medical Center located 1625 Medical Center Drive, El Paso TX
79902.
Lower level LL. at 6:00 PM
for more Information call Peggy at 915-307-3354
or Lupe Sanchez 915-592-7526
or Elaine Prensky at 915-584-3724
JOIN US PLEASE! on
This breast cancer month, the CRBCM has planned 3 events,
Presenting CRBCM plan before the cancer support group in EL PASO
participate to MAKE STRIDES against Breast Cancer 5k walk fundraising by the American cancer Society,
conducting a Pilot program about detecting Breast cancer risk factors in the people of El Paso
To join these activities, call 915-307-3354. on NEWS
Thursday, October 4, 2012
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