Options for Cholangiocarcinoma

More  “centisble” (safe, effective and cost-effective) ways to deal with Cholangiocarcinoma include Corrective  Cancer Care  and SOUL.  But these three articles below are astonishing both in their promise and, sadly, in their being ignored by conventional oncologists – hobbled as they are to yesterday’s medicine… the standard of care.

The first agent  “thymoquinone”  is in Black cumin seed – the primary ingredient in   (SOUL)

 The second is a safe blood sugar lowering drug which I had recommended to all my cancer patients  (see www.weeksmd.com and search “metformin  and cancer”)

 The third is from pepper – cayenne etc. who myriad benefits are well know to athletes, arthritics, folks suffering with headaches and other inflammatory processes… like cancer in general.




Oncol Rep. 2014 May;31(5):2063-70. doi: 10.3892/or.2014.3059. Epub 2014 Mar 5.

Thymoquinone induces G2/M arrest, inactivates PI3K/Akt and nuclear factor-κB pathways in human cholangiocarcinomas both in vitro and in vivo.

Xu D1, Ma Y1, Zhao B1, Li S1, Zhang Y2, Pan S1, Wu Y1, Wang J1, Wang D1, Pan H1, Liu L1, Jiang H1. 



Cholangiocarcinoma (CCA) is a notoriously lethal tumor mostly due to the de novo or acquired resistance to traditional chemotherapy besides gemcitabine and, therefore, an increasing need for effective strategies to prevent and treat the poor prognosis of this tumor is required. Thymoquinone (TQ), a hopeful natural product derived from black cumin (Nigella sativa) has shown considerable antineoplastic properties. Whether TQ exerts antitumor effects on CCA cells in vitro and in vivo remains unknown. Examinations of cell viability assay, detection of cell cycle and apoptosis, electrophoretic mobility shift assay (EMSA), western blotting and immunohistochemistry were used in the present study. We demonstrated that TQ inhibited the growth of human CCA cell lines (TFK-1 and HuCCT1) in a dose- and time-dependent manner. Firstly, our results provided evidence that TQ not only inhibits the proliferation of CCA cells, induces cell cycle arrest and prompts cell apoptotic effect in vitro, but it also exhibits inhibitory effects of tumor growth and angiogenesis in vivo. The responsible mechanism is at least partially due to TQ inhibiting the growth of CCA cell lines induced by downregulation of PI3K/Akt and NF-κB and regulated gene products, including p-AKT, p65, XIAP, Bcl-2, COX-2, VEGF. Taken together, these results provide strong evidence of our hypothesis that TQ alone presents a promising therapeutic regimen for the treatment of CCA cells with better efficiency.





Oncol Rep. 2014 Jun;31(6):2611-8. doi: 10.3892/or.2014.3151. Epub 2014 Apr 23.

Metformin inhibits proliferation and enhances chemosensitivity of intrahepatic cholangiocarcinoma cell lines.

Ling S1, Feng T2, Ke Q3, Fan N2, Li L2, Li Z1, Dong C1, Wang C2, Xu F4, Li Y2, Wang L1.




Metformin is an oral anti-hyperglycemic agent of the biguanide family, which is used first-line for type II diabetes with few side-effects. A recent epidemiological study that included 1,828 potential intrahepatic cholangiocarcinoma (ICC) patients showed that metformin use was significantly associated with a 60% reduction in ICC risk in diabetic patients, demonstrating the potential value of metformin in ICC management. In the present study, we firstly showed that metformin exhibited a dose- and time-dependent anti-proliferation effect on ICC cell lines, by mechanisms including apoptosis induction and cell cycle arrest. Metformin targeted the AMPK/mTORC1 pathway in ICC cells. Furthermore, metformin sensitized ICC cells to certain chemotherapeutic agents, such as sorafenib, 5-fluorouracil and As2O3 by targeting the AMPK/mTOR/HIF-1α/MRP1 pathway and ERK. As it is an inexpensive and widely used antidiabetic drug without severe adverse effects, metformin may be a prospective chemotherapeutic agent or a chemosensitizer in future ICC treatment.

PMID: 24788596 [PubMed – in process]

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PLoS One. 2014 Apr 18;9(4):e95605. doi: 10.1371/journal.pone.0095605. eCollection 2014.

Capsaicin treatment attenuates cholangiocarcinoma carcinogenesis.

Wutka A1, Palagani V1, Barat S1, Chen X1, El Khatib M1, Götze J1, Belahmer H1, Zender S2, Bozko P1, Malek NP1, Plentz RR1.

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Capsaicin, the most abundant pungent molecule produced by pepper plants, represents an important ingredient in spicy foods consumed throughout the world. Studies have shown that capsaicin can relieve inflammation and has anti-proliferative effects on various human malignancies. Cholangiocarcinoma (CC) is a cancer disease with rising incidence. The prognosis remains dismal with little advance in treatment. The aim of the present study is to explore the anti-tumor activity of capsaicin in cultured human CC cell lines. Capsaicin effectively impaired cell proliferation, migration, invasion, epithelial to mesenchymal transition and growth of softagar colonies. Further, we show that capsaicin treatment of CC cells regulates the Hedgehog signaling pathway. Conclusion: Our results provide a basis for capsaicin to improve the prognosis of CCs in vivo and present new insights into the effectiveness and mode of action of capsaicin.

PMID: 24748170 [PubMed – in process] PMCID: PMC3991659 Free PMC Article

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