Traditional systems of medicine all over the world even traditional medicine and cancer have been using plants and plants products for therapeutic purposes. In this study, 34 patients with hematologic malignancy and other available cancers were entered in the study during 1993-2014.The complete remission (CR) was obtained in 24 of 34 (70.6%) hematology malignancy and other advanced cancers. During follow up, the survival time in three lung cancer was 10, 10 and 17 years, 1 jaundice cholangiocarcinoma was 2 years, 1 gallbladder cancer 15 years, 1 gastric cancer 7 years, 9 lymphoma over 10-20 years, 1 refractory anemia over 11 years, and 2 chronic granulocytic leukemia (CGL) 5 years and 8 years respectively. CR was once obtained after all-trans retinoic acid(RA) and low dose (1 mg) plant medicine homoharringtonine intravenously in one case of acute promyelocytic leukemia(APL). A CR was achieved by use of chlorambucil and traditional medicine in 1 chronic lymphocytic leukemia with his peripheral leukocytes 123.88 × 109/ L, with a leukocyte differential count of 85% small lymphocytes. A 62-year-old female multiple myeloma was in CR after low-dose thalidomide and plant medicine Vinca rosea (Catharanthus roseus). Traditional medicine consisted of Vinca rosea, astragalus membanaceus Bunge, ophiopogon japonicas, asparagus cochinchinensis, angelica sinensis, poria cocos, coix lacryma jobi L. var mayuen, solanum nigrum L, houttuynia cordata, scutellaria barbata d.don and oldenlandia diffusa roxb. During the follow up of three years, she remained CR. In this study, I experienced that a CR was a pivotal influencing factor in those longest survival patients, and traditional medicine was also recommended. As the mechanism of RA to APL treatment, RA (ATRA or cis RA) induce the APL CR and relieve the blockage of promyelocyte differentiation via binding to oncogenic pml/RARa whereas oncogenic pml/ RARa fusion act as a constitutive repressor of RAR and retinoic acid signaling, inducing a differentiation block at promyelocytic stage. This is first described in eukaryotes.

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EpCAM is a cell adhesion molecule. Its structure, its expression and the oncogenic potential, and its signaling network and target therapy were in concise reviewed. EpCAM is expressed in a broad variety of human carcinomas to varying degrees. The identification of EpCAM describing both a protective and a promoting role in carcinogenesis appears to be dependent on the cancer type. In recent advances, in addition to PI3K/akt and Raf/MAPK pathway involving in cell survival, antiapoptosis and proliferation, and malignant initiation and progression three distinct pathway are illustrated: EpCAM/E-cadherin-catenin-actin cytoskeleton,EpCAM/ wint-catenin signaling,and its major EpCAM/nuclear signaling presented by Munz M in 2004. Moreover, more accumulated data are needed in detail mechanism.The data may provide its cancer biology and clinical targeting therapy benefits. Indeed, the use of the EpCAM-specific monoclonal antibody has been successful in increasing disease-free survival in colon and breast cancer patients with minimal residual disease.