Does anyone know if there is a correlation between low thyroid activity (TSH levels) and multiple myeloma?
One of my neighbors who is in the health care field mentioned to me that, since my thyroid count was so low (0.197), I should check to see if that has thrown off some of my other blood counts. (I had thyroid cancer years ago & my specialist has always kept my thyroid count very low).
It seems weird but since I have had no symptoms since I was diagnosed with multiple myeloma seven months ago, I just wondered.
Forums
-
barbara1200 - Name: barb
- Who do you know with myeloma?: myself
- When were you/they diagnosed?: 2013
- Age at diagnosis: 75
Re: Low thyroid activity (TSH levels) & multiple myeloma
There are no known links between myeloma and low thyroid levels .
-
Dr. Jatin Shah - Name: Jatin Shah, M.D.
Beacon Medical Advisor
Re: Low thyroid activity (TSH levels) & multiple myeloma
Thanks so much for answering this question for me. Guess I have looked for a link for my M spike -- since it has been 7 months since diagnoses of multiple myeloma I have wondered why I have not had any symptoms. I will just quit wondering & enjoy it.
Thanks again.
Thanks again.
-
barbara1200 - Name: barb
- Who do you know with myeloma?: myself
- When were you/they diagnosed?: 2013
- Age at diagnosis: 75
Re: Low thyroid activity (TSH levels) & multiple myeloma
The study described in this article from Molecular Cancer Research,
http://mcr.aacrjournals.org/content/9/10/1385.full
concludes that "Thyroid hormones induce myeloma cell viability and proliferation". It also lists sources that have documented increased surviveability in individuals with hypothyroidism, such as that induced by your specialist.
Keren Cohen et al, "Thyroid Hormone Is a MAPK-Dependent Growth Factor for Human Myeloma Cells Acting via αvβ3 Integrin", Molecular Cancer Res October 2011 9; 1385
Abstract:
Experimental and clinical observations suggest that thyroid hormone [L-thyroxine (T4) and 3,5,3′-triiodo-L-thyronine (T3)] can support cancer cell proliferation. T3 and T4 promote both tumor cell division and angiogenesis by activating mitogen-activated protein kinase (MAPK) via binding to a hormone receptor on the αvβ3 integrin, overexpressed on many cancer cells. We have studied the responsiveness of several multiple myeloma cell lines to T3 and T4 and characterized hormonal effects on cell survival, proliferation, and MAPK activation. Overnight T3 (1–100 nmol/L) and T4 (100 nmol/L) incubation enhanced, up to 50% (P < 0.002), multiple myeloma cell viability (WST-1 assay) and increased cell proliferation by 30% to 60% (P < 0.01). Short exposure (10 minutes) to T3 and T4 increased MAPK activity by 2.5- to 3.5-fold (P < 0.03). Pharmacologic MAPK inhibition blocked the proliferative action of T3 and T4. Antibodies to the integrin αvβ3 dimer and αv and β3 monomers (but not β1) inhibited MAPK activation and subsequent cell proliferation in response to thyroid hormone, indicating dependence upon this integrin. Moreover, tetraiodothyroacetic acid (tetrac), a non-agonist T4 analogue previously shown to selectively block T3/T4 binding to αvβ3 receptor site, blocked induction of MAPK by the hormones in a dose-dependent manner. This demonstration of the role of thyroid hormones as growth factors for multiple myeloma cells may offer novel therapeutic approaches.
http://mcr.aacrjournals.org/content/9/10/1385.full
concludes that "Thyroid hormones induce myeloma cell viability and proliferation". It also lists sources that have documented increased surviveability in individuals with hypothyroidism, such as that induced by your specialist.
Keren Cohen et al, "Thyroid Hormone Is a MAPK-Dependent Growth Factor for Human Myeloma Cells Acting via αvβ3 Integrin", Molecular Cancer Res October 2011 9; 1385
Abstract:
Experimental and clinical observations suggest that thyroid hormone [L-thyroxine (T4) and 3,5,3′-triiodo-L-thyronine (T3)] can support cancer cell proliferation. T3 and T4 promote both tumor cell division and angiogenesis by activating mitogen-activated protein kinase (MAPK) via binding to a hormone receptor on the αvβ3 integrin, overexpressed on many cancer cells. We have studied the responsiveness of several multiple myeloma cell lines to T3 and T4 and characterized hormonal effects on cell survival, proliferation, and MAPK activation. Overnight T3 (1–100 nmol/L) and T4 (100 nmol/L) incubation enhanced, up to 50% (P < 0.002), multiple myeloma cell viability (WST-1 assay) and increased cell proliferation by 30% to 60% (P < 0.01). Short exposure (10 minutes) to T3 and T4 increased MAPK activity by 2.5- to 3.5-fold (P < 0.03). Pharmacologic MAPK inhibition blocked the proliferative action of T3 and T4. Antibodies to the integrin αvβ3 dimer and αv and β3 monomers (but not β1) inhibited MAPK activation and subsequent cell proliferation in response to thyroid hormone, indicating dependence upon this integrin. Moreover, tetraiodothyroacetic acid (tetrac), a non-agonist T4 analogue previously shown to selectively block T3/T4 binding to αvβ3 receptor site, blocked induction of MAPK by the hormones in a dose-dependent manner. This demonstration of the role of thyroid hormones as growth factors for multiple myeloma cells may offer novel therapeutic approaches.
-
Tim Diener
Re: Low thyroid activity (TSH levels) & multiple myeloma
Tim Thank you so much for this information. I will copy it & give it to my oncologist. I had been complaining about my endocrinologist keeping my thyroid so low, but I see that she was just doing this for my protection. I appreciate this info so much. Thanks again.
-
barbara1200 - Name: barb
- Who do you know with myeloma?: myself
- When were you/they diagnosed?: 2013
- Age at diagnosis: 75
Re: Low thyroid activity (TSH levels) & multiple myeloma
Thanks, this is very interesting.
It's important to distinguish between a thyroid hormone stimulating or supporting proliferation of an underlying, already present myeloma, and a thyroid hormone being a causative factor, or driving development, of myeloma.
It's important to distinguish between a thyroid hormone stimulating or supporting proliferation of an underlying, already present myeloma, and a thyroid hormone being a causative factor, or driving development, of myeloma.
-
Dr. Jatin Shah - Name: Jatin Shah, M.D.
Beacon Medical Advisor
Re: Low thyroid activity (TSH levels) & multiple myeloma
Dr. Shah Is it possible to tell the difference? Thank you.
-
barbara1200 - Name: barb
- Who do you know with myeloma?: myself
- When were you/they diagnosed?: 2013
- Age at diagnosis: 75
Re: Low thyroid activity (TSH levels) & multiple myeloma
As a myeloma sufferer with hypothyroidism, I am not comforted by suggestions that several lab studies showing T3 and T4 levels to increase proliferation of myeloma cell lines, may not apply.
It sure looks like T4 levels in synthetic hormones could be a growth factor for myeloma.
For myself, I'm looking to be on the low side of the dosing, just to play it safe.
K Cohen et al., "Thyroid Hormone Is a MAPK-Dependent Growth Factor for Human Myeloma Cells Acting via αvβ3 Integrin," Molecular Cancer Research, 2011 (updated 2014) (full text pdf).
Abstract: Experimental and clinical observations suggest that thyroid hormone [L-thyroxine (T4) and 3,5,3′-triiodo-L-thyronine (T3)] can support cancer cell proliferation. T3 and T4 promote both tumor cell division and angiogenesis by activating mitogen-activated protein kinase (MAPK) via binding to a hormone receptor on the αvβ3 integrin, overexpressed on many cancer cells. We have studied the responsiveness of several multiple myeloma cell lines to T3 and T4 and characterized hormonal effects on cell survival, proliferation, and MAPK activation. Overnight T3 (1–100 nmol/L) and T4 (100 nmol/L) incubation enhanced, up to 50% (P < 0.002), multiple myeloma cell viability (WST-1 assay) and increased cell proliferation by 30% to 60% (P < 0.01). Short exposure (10 minutes) to T3 and T4 increased MAPK activity by 2.5- to 3.5-fold (P < 0.03). Pharmacologic MAPK inhibition blocked the proliferative action of T3 and T4. Antibodies to the integrin αvβ3 dimer and αv and β3 monomers (but not β1) inhibited MAPK activation and subsequent cell proliferation in response to thyroid hormone, indicating dependence upon this integrin. Moreover, tetraiodothyroacetic acid (tetrac), a non-agonist T4 analogue previously shown to selectively block T3/T4 binding to αvβ3 receptor site, blocked induction of MAPK by the hormones in a dose-dependent manner. This demonstration of the role of thyroid hormones as growth factors for multiple myeloma cells may offer novel therapeutic approaches
K Cohen et al., "Relevance of the thyroid hormones–αvβ3 pathway in primary myeloma bone marrow cells and to bortezomib action," Leukemia & Lymphoma, 2014.
Abstract: Thyroid hormones (T3 and T4) induce proliferation in multiple myeloma (multiple myeloma) cell lines via the αvβ3 integrin–mitogen-activated protein kinase (MAPK) pathway. We further show in primary multiple myeloma bone marrow (BM) samples (n = 9) induction of cell viability by 1 nM T3 (13%, p < 0.002) and more potently by 100 nM T4 (21–45%, p < 0.0002) and a quick (1 h) and long-lasting (24 h) pERK activation, which was inhibited in the presence of β3 but not β1 blocking antibodies. Involvement of the integrin was further shown by two disintegrins, Arg-Gly-Asp (RGD) and echistatin peptides, which occluded the effects of T3/T4 on viability, proliferating cell nuclear antigen (PCNA) (proliferation marker) and apoptotic gene expression. Lastly, T3/T4 significantly opposed bortezomib (25 nM) cytotoxicy, as confirmed by several methods. In summary, our results imply that endogenous thyroid hormones in myeloma are factors that may support cell growth, with relevance to bortezomib action.
It sure looks like T4 levels in synthetic hormones could be a growth factor for myeloma.
For myself, I'm looking to be on the low side of the dosing, just to play it safe.
K Cohen et al., "Thyroid Hormone Is a MAPK-Dependent Growth Factor for Human Myeloma Cells Acting via αvβ3 Integrin," Molecular Cancer Research, 2011 (updated 2014) (full text pdf).
Abstract: Experimental and clinical observations suggest that thyroid hormone [L-thyroxine (T4) and 3,5,3′-triiodo-L-thyronine (T3)] can support cancer cell proliferation. T3 and T4 promote both tumor cell division and angiogenesis by activating mitogen-activated protein kinase (MAPK) via binding to a hormone receptor on the αvβ3 integrin, overexpressed on many cancer cells. We have studied the responsiveness of several multiple myeloma cell lines to T3 and T4 and characterized hormonal effects on cell survival, proliferation, and MAPK activation. Overnight T3 (1–100 nmol/L) and T4 (100 nmol/L) incubation enhanced, up to 50% (P < 0.002), multiple myeloma cell viability (WST-1 assay) and increased cell proliferation by 30% to 60% (P < 0.01). Short exposure (10 minutes) to T3 and T4 increased MAPK activity by 2.5- to 3.5-fold (P < 0.03). Pharmacologic MAPK inhibition blocked the proliferative action of T3 and T4. Antibodies to the integrin αvβ3 dimer and αv and β3 monomers (but not β1) inhibited MAPK activation and subsequent cell proliferation in response to thyroid hormone, indicating dependence upon this integrin. Moreover, tetraiodothyroacetic acid (tetrac), a non-agonist T4 analogue previously shown to selectively block T3/T4 binding to αvβ3 receptor site, blocked induction of MAPK by the hormones in a dose-dependent manner. This demonstration of the role of thyroid hormones as growth factors for multiple myeloma cells may offer novel therapeutic approaches
K Cohen et al., "Relevance of the thyroid hormones–αvβ3 pathway in primary myeloma bone marrow cells and to bortezomib action," Leukemia & Lymphoma, 2014.
Abstract: Thyroid hormones (T3 and T4) induce proliferation in multiple myeloma (multiple myeloma) cell lines via the αvβ3 integrin–mitogen-activated protein kinase (MAPK) pathway. We further show in primary multiple myeloma bone marrow (BM) samples (n = 9) induction of cell viability by 1 nM T3 (13%, p < 0.002) and more potently by 100 nM T4 (21–45%, p < 0.0002) and a quick (1 h) and long-lasting (24 h) pERK activation, which was inhibited in the presence of β3 but not β1 blocking antibodies. Involvement of the integrin was further shown by two disintegrins, Arg-Gly-Asp (RGD) and echistatin peptides, which occluded the effects of T3/T4 on viability, proliferating cell nuclear antigen (PCNA) (proliferation marker) and apoptotic gene expression. Lastly, T3/T4 significantly opposed bortezomib (25 nM) cytotoxicy, as confirmed by several methods. In summary, our results imply that endogenous thyroid hormones in myeloma are factors that may support cell growth, with relevance to bortezomib action.
-
Danny Parker
Re: Low thyroid activity (TSH levels) & multiple myeloma
This potential relationship is very interesting.
In 2009 I was diagnosed with hypothyroidism (and began taking Synthroid) just a couple months before being diagnosed with MGUS, which progressed to smoldering myeloma and then to symptomatic multiple myeloma.
I had never thought about the possibility of the synthetic hormone stimulating / encouraging the myeloma cell growth. Instead, I've wondered whether there was some third agent that might have contributed to both the hypothyroidism and the MGUS / myeloma. Now this makes me think about that connection differently.
In 2009 I was diagnosed with hypothyroidism (and began taking Synthroid) just a couple months before being diagnosed with MGUS, which progressed to smoldering myeloma and then to symptomatic multiple myeloma.
I had never thought about the possibility of the synthetic hormone stimulating / encouraging the myeloma cell growth. Instead, I've wondered whether there was some third agent that might have contributed to both the hypothyroidism and the MGUS / myeloma. Now this makes me think about that connection differently.
-
mikeb - Name: mikeb
- Who do you know with myeloma?: self
- When were you/they diagnosed?: 2009 (MGUS at that time)
- Age at diagnosis: 55
Re: Low thyroid activity (TSH levels) & multiple myeloma
Hi Danny - thanks for the article about thyroid hormones.
In my late 30's I was diagnosed with low thyroid and my Synthyroid dose was eventually increased to 112 mcgs. Almost 3 years ago (age 56), I was diagnosed with MGUS. About a year+ ago, I read an article discussing T4 and possible relationship with multiple myeloma. I mentioned the article to my doctor and asked if my dose could be lowered. She was hesitant, but lowered the dose and now I am taking 88 mcgs with very little change in T3, T4, and TSH.
My first M spike was 1 (October 2011) a repeat test 2 months later (December 2011) showed a spike of 1.5. Now (August 2014), my spike is 0.8 - the lowest spike.
Have no idea if lowering Synthryoid is associated with the lower spike. Plus, I have not noticed any difference since lowering Synthyroid - same energy levels.
At my next appointment, I'm assuming my doctor will lower the dose to 75 mcgs. I agree with you, lowering may be better.
Diane
In my late 30's I was diagnosed with low thyroid and my Synthyroid dose was eventually increased to 112 mcgs. Almost 3 years ago (age 56), I was diagnosed with MGUS. About a year+ ago, I read an article discussing T4 and possible relationship with multiple myeloma. I mentioned the article to my doctor and asked if my dose could be lowered. She was hesitant, but lowered the dose and now I am taking 88 mcgs with very little change in T3, T4, and TSH.
My first M spike was 1 (October 2011) a repeat test 2 months later (December 2011) showed a spike of 1.5. Now (August 2014), my spike is 0.8 - the lowest spike.
Have no idea if lowering Synthryoid is associated with the lower spike. Plus, I have not noticed any difference since lowering Synthyroid - same energy levels.
At my next appointment, I'm assuming my doctor will lower the dose to 75 mcgs. I agree with you, lowering may be better.
Diane
-
Dianem
14 posts
• Page 1 of 2 • 1, 2