COFFEE: More than once daily...if you have the right genes, shows a "protective effect" for cutaneous melanoma. Not sure exactly what that means, and not really clear if these genes might be the protection in and of themselves, without the addition of coffee. Presumably they looked at that, but????
DOXYCYCLINE: An older antibiotic, causes some nausea, but pretty good in treating acne, but...apparently...it kills and inhibits growth of melanoma cells.
CURCUMIN: The yellow part of curry and mustard also stops melanoma in its tracks, at least in a petri dish.
CIMETADINE: aka: tagamet, taken for heart burn, ulcers, etc, as it decreases stomach acid, helped get rid of melanoma in at least three horses. There's a smattering of human "data" out there, too.
NSAID's: Non steroidal anti-iflammatory drugs like Advil seem to decrease the risk of melanoma and squamous cell skin cancers.
SHIITAKES: Good old Lentinula edodes mycelia! If you're a mouse with melanoma and you have access to mushroom juice...you are in luck, my friend.
THE DATA: Read at your own risk (the stuff on NAID's and Shiitakes I've posted before)!!
The protective effect of coffee consumption on
cutaneous melanoma risk and the role of GSTM1 and GSTT1 polymorphisms.
Source Clinical
Epidemiology Unit, Istituto Dermopatico dell'Immacolata, IDI-IRCSS, Via dei
Monti di Creta, 104, 00167, Rome, Italy, c.fortes@idi.it. 2013 Jul 17. [Epub ahead of print]
Abstract
PURPOSES:
The authors examined the association
between coffee consumption and cutaneous melanoma and the implication of GSTM1
and GSTT1 polymorphisms.
METHODS:
A hospital-based case-control study
was conducted in the inpatient wards of IDI-San Carlo Rome, Italy, including
304 incident cases of cutaneous melanoma and 305 controls. Information on
socio-demographic characteristics, medical history, smoking, sun exposure,
pigmentary characteristics and diet was collected for all subjects. Within the
study, individual patterns at two polymorphic genes (GSTM1 and GSTT1) belonging
to glutathione S-transferases family were investigated in 188 cases of
cutaneous melanoma and 152 controls. Logistic regression was the method used to
estimate odds ratio and 95 % confidence intervals.
RESULTS:
High frequency of coffee drinking
(>once daily), compared with low-frequency consumption of coffee (≤7 times
weekly) was associated with a protective effect for cutaneous melanoma (OR
0.46; 95 % CI 0.31-0.68) after adjusting for sex, age, education,
hair colour, common nevi, skin phototype, and sunburn episodes in childhood.
When stratified by GSTM1 and GSTT1 genotype, the protective effect of coffee
was extremely high for subjects with both GSTM1 and GSTT1 null polymorphisms
(OR 0.01; 95 % CI 0.0003-0.54).
CONCLUSIONS:
Our results show a protective effect
of coffee consumption for cutaneous melanoma, in particular for those with
homozygous deletion for GSTM1 and GSTT1.
Doxycycline inhibits the adhesion and migration of
melanoma cells by inhibiting the expression and phosphorylation of focal
adhesion kinase (FAK).
Sun T, Zhao N, Ni CS, Zhao XL, Zhang WZ, Su X, Zhang DF, Gu Q, Sun BC. Source: Department
of Pathology, Tianjin Medical University, Tianjin 300070, PR China.Cancer Lett.
2009 Nov. Epub 209 May 30.
Abstract: Doxycycline
has been found to induce apoptosis and to inhibit the growth of a variety of
tumor cells, in addition to its use as an antibiotic. However, the mechanism of
its actions, especially at the molecular level, remains unknown and needs to be
resolved. A crucial step possibly lies in the early period of doxycycline
administration, which leads to a series of cascading effects depicting the
consequential biological action of doxycycline on tumor cells. The present
study focuses on the early-stage effects of doxycycline administration,
specifically at the stages of treatment (before 16h). In this paper, we report
that doxycycline inhibits the adhesion and migration of melanoma cells.
Afterwards, the cells undergo apoptosis (aniokis). Remarkably, doxycycline also
inhibits the expression and phosphorylation of focal adhesion kinase (FAK), a
protein tyrosine kinase involved in the regulation of cell adhesion and
migration. We further demonstrate that doxycycline down-regulates the
activities of MMP-2 and MMP-9, and its effects are stronger than those of an
Integrin beta1 antibody. Finally, we suggest that doxycycline might exert its
anti-tumor effects by inhibiting FAK signaling pathway. These results provide
an insight into the possible mechanisms that underlie the multiple drug actions
of doxycycline. The potential use of doxycycline in anti-tumor treatment is
promising and warrants further studies.
Activation of c-Jun N-terminal kinase is essential for
mitochondrial membrane potential change and apoptosis induced by doxycycline in
melanoma cells.
Shieh JM, Huang TF, Hung CF, Chou KH, Tsai YJ, Wu WB. Source: Department of Internal Medicine, Chi-Mei Medical Center,
Tainan, Taiwan. Br J Pharmacol. 2010
Jul.
Abstract
BACKGROUND
AND PURPOSE: Tetracyclines were recently found to
induce tumour cell death, but the early processes involved in this cytotoxic
effect remain unclear.
EXPERIMENTAL
APPROACH: Viability of human and mouse
melanoma cells was determined by MTT assay and flow cytometry.
Kinase/protein/caspase activation was measured by Western blotting and
mitochondrial membrane potential (DeltaPsi(m)) was analyzed by fluorescence
microscopy and flow cytometry.
KEY
RESULTS: Human and mouse melanoma cells were
treated with doxycycline or minocycline but only doxycycline was cytotoxic.
This cell death (apoptosis) in A2058 cells involved activation of caspase-3, -7
and -9 and contributed to inhibition, by doxycycline, of matrix
metalloproteinase (MMP) activity and migration of these cells. Doxycycline
induced intra-cellular reactive oxygen species (ROS) production, apoptosis
signal-regulated kinase 1 (ASK1), c-Jun N-terminal kinase (JNK) and p38
mitogen-activated protein kinase (MAPK) activation at an early stage of
treatment and induced mitochondrial cytochrome c release into cytosol and
DeltaPsi(m) change during apoptosis. The JNK inhibitor/small interference RNA
inhibited doxycycline-induced JNK activation, DeltaPsi(m) change and apoptosis,
but did not affect ASK1 activation, suggesting a role of ASK1 for JNK
activation in melanoma cell apoptosis. Two ROS scavengers reduced
doxycycline-induced JNK and caspase activation, and apoptosis. Taken together,
the results suggest the involvement of a ROS-ASK1-JNK pathway in doxycycline-induced
melanoma cell apoptosis.
CONCLUSIONS
AND IMPLICATIONS: We have shown a promising cytotoxic
effect of doxycycline on melanoma cells, have identified ROS and ASK1 as the
possible initiators and have demonstrated that JNK activation is necessary for
doxycycline-induced melanoma cell apoptosis.
Curcumin-induced
antiproliferative and proapoptotic effects in melanoma cells are associated
with suppression of IκB kinase and nuclear factor κB activity and are
independent of the B-Raf/mitogen-activated/extracellular signal-regulated
protein kinase pathway and the Akt pathway
Doris R. Siwak M.S., Shishir Shishodia Ph.D., Bharat B.
Aggarwal Ph.D., Razelle Kurzrock M.D.†,*
Article first published online: 11 JUL 2005
Abstract
BACKGROUND Nuclear factor-κB (NF-κB) plays a central role in cell survival and proliferation in human melanoma; therefore, the authors explored the possibility of exploiting NF-κB for melanoma treatment by using curcumin, an agent with known, potent, NF-κB-inhibitory activity and little toxicity in humans.
METHODS Three melanoma cell lines (C32, G-361, and WM 266-4), all of which had B-raf mutations, were treated with curcumin, and the authors assessed its effects on viability ((3-[4,5-dimethylthiazol-2-yl]2,5-diphenyltetrazolium bromide assay) and apoptosis (flow-cytometric analysis of annexin V/propidium iodide-stained cells). Curcumin-treated cells also were examined for NF-κB binding activity (electrophoretic mobility shift assay) and for the activity of its upstream regulator, IκB kinase (IKK) (immune complex kinase assay). In addition, relevant signaling, as reflected by B-Raf kinase activity (kinase cascade assay), and steady-state levels of activated, downstream effectors, as reflected by mitogen-activated signal-regulated protein kinase (MEK), extracellular signal-regulated protein kinase (ERK), and Akt phosphorylation levels (immunoblots), were assessed.
RESULTS Curcumin treatment decreased cell viability of all 3 cell lines in a dose-dependent manner (50% inhibitory concentration = 6.1–7.7 μM) and induced apoptosis. However, curcumin did not inhibit the activities of B-Raf, MEK, or ERK, and Akt phosphorylation was enhanced. Furthermore, in the presence of curcumin, the Akt inhibitor 1L-6-hydroxymethyl-chiro-inositol 2-[(R)-2-O-methyl-3-O-octadecylcarbonate] no longer suppressed Akt phosphorylation.
CONCLUSIONS Curcumin has potent antiproliferative and proapoptotic effects in melanoma cells. These effects were associated with the suppression of NF-κB and IKK activities but were independent of the B-Raf/MEK/ERK and Akt pathways. Cancer 2005.
Cimetidine for treatment of melanomas in three horses.
Goetz
TE, Ogilvie
GK, Keegan
KG, Johnson
PJ. Source: Department of Veterinary Clinical Medicine,
College of Veterinary Medicine, University of Illinois, Urbana 61801. J AM Vet
Med Assoc. 1990
Talking about pain...=:o) I think Dr W's nurse Cabell must think I am one in her duff...I asked her in e-mail in the wee hours last night..what patient I was in our trial...I am patient number 4!! -Lynn
ReplyDeleteI have bookmarked your blog, the articles are way better than other similar blogs.. thanks for a great blog!
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