Psorinum Therapy in Treating Stomach, Gall Bladder, Pancreatic, and Liver Cancers: A Prospective Clinical Study

We prospectively studied the clinical efficacy of an alternative cancer treatment “Psorinum Therapy” in treating stomach, gall bladder, pancreatic and liver cancers. Our study was observational, open level and single arm. The participants' eligibility criteria included histopathology/cytopathology confirmation of malignancy, inoperable tumor, and no prior chemotherapy or radiation therapy. The primary outcome measures of the study were (i) to assess the radiological tumor response (ii) to find out how many participants survived at least 1 year, 2 years, 3 years, 4 years and finally 5 years after the beginning of the study considering each type of cancer. Psorinum-6x was administered orally to all the participants up to 0.02 ml/Kg body weight as a single dose in empty stomach per day for 2 years along with allopathic and homeopathic supportive cares. 158 participants (42 of stomach, 40 of gall bladder, 44 of pancreatic, 32 of liver) were included in the final analysis of the study. Complete tumor response occurred in 28 (17.72%) cases and partial tumor response occurred in 56 (35.44%) cases. Double-blind randomized controlled clinical trial should be conducted for further scientific exploration of this alternative cancer treatment

Analysis of different deleted regions in chromosome 11 and their interrelations in early and late onset breast tumors: association with cyclin D1 amplification and survival

Previous studies have shown that younger women exhibit more aggressive pathologic features of breast cancer (BC) in comparison to older women; young age could be an independent predictor of adverse prognosis. In order to find any existing differences in the molecular progression of BC in both younger and older women, chromosome 11 (chr.11) was taken as a tool, due to its frequent deletion and amplification, particularly of CyclinD1 (CCND1) locus in BC. In the present work, the comparative analysis in the frequency of deletion in different regions in chr.11 and CCND1 amplification in BC in the two age groups was studied, as well as the interrelation and prognostic significance of these chromosomal alterations. The chr. 11 alterations were also studied in types of breast lesions other than carcinoma to see the prevalence of the alterations in these diseases. For this purpose, comparative deletion mapping of chr.11 using 17 microsatellite markers and CCND1 amplification was examined in 30 early-onset (≤40 years) and 33 late-onset (>40 years) breast carcinomas, as well as 11 other types of breast lesions. The frequency of deletion and CCND1 amplification was much higher in carcinomas than with other types of breast lesions. A total of six highly deleted regions, namely, 11p15.5, 11p11.2, 11q13.2, 11q22.3-23.1, 11q23.3-24.1, and 11q25, were identified in carcinomas of the two age groups. The 11q13.2 deletion and CCND1 amplification was comparatively higher in the carcinoma of younger women. The following significant associations were observed for (a) LOH at 11q25 with LOH at 11q13.2, 11q22.3-23.1, 11q23.3-24.1 and CCND1 amplification, respectively, and (b) LOH at 11p15.5 with LOH at 11q22.3-23.1 in carcinoma of younger women. On the other hand, the significant associations in older women were (a) LOH at 11q25 with LOH at 11q22.3-23.1, 11q23.3-24.1, respectively, and (b) LOH at 11q22.3-23.1 with LOH at 11q23.3-24.1. Deletion at 11q13.2 was also associated with reduced overall survival in the younger group, indicating its prognostic significance. It is evident from our data that the pattern of chromosomal alterations are not exactly same in the carcinomas in the two age groups. Differential interrelationship of the chromosomal alterations and prognosis in these two age groups indicate that the molecular pathogenesis of the carcinomas is not similar

Differential Association of BRCA1 and BRCA2 Genes with Some Breast Cancer–Associated Genes in Early and Late Onset Breast Tumors

Accumulating evidence indicating more aggressive features of breast carcinoma (BC) in young women than their older counterparts have raised the question of whether these differences are present at the genetic level. Methods: For this purpose, we performed a comparative analysis of the frequency of deletions of BRCA1, BRCA2, BRCAX, TP53, ATM, and RB1 and amplification of Cyclin D1 and also studied the interrelation and prognostic significance of these genetic alterations in 30 early onset (�40 years) and 33 late onset (�40 years) cases of BC. These gene alterations were also studied in 11 other types of breast lesions. Results: A differential pattern of alterations (deletion/amplification) was observed in the two age groups, with the sequence in younger women being BRCA1 (72%), TP53 (71%), ATM (64%), BRCA2 (62%), RB1 (60%), Cyclin D1 (43%), and BRCAX (24%) and that in the older group being TP53 (66%), RB1 (63%), BRCA1 (56%), ATM (53%), BRCA2 (45%), Cyclin D1 (24%), and BRCAX (23%). Similar, differential correlations were also seen with several clinicopathological parameters, prognosis, and combinations of alterations among these genes in the two age groups. Conclusions: Differential frequencies and interrelationships of genetic alterations and prognoses in these two age groups indicate that the molecular pathways for the development of tumors in both age groups may not be similar, though the ultimate effect is deregulation of cell cycle checkpoints and defects in the DNA repair pathway

Deletion mapping of chromosome 1 in early onset and late onset breast tumors - a comparative study in Eastern India

Younger women exhibit more aggressive pathologic features of breast cancer (BC) compared to their older counterparts. Young age has been shown to be an independent predictor of adverse prognosis. These findings have raised the question of whether these differences are also present at the genetic level. Twenty-five early onset (age ≤ 40 years) tumors including 4 bilateral tumors, and 26 late onset(> 40 years) breast tumors, including 2 bilateral tumors, were xamined for loss of heterozygosity (LOH) at chromosome 1 using 11 polymorphic microsatellite markers. A comparative study revealed high frequencies of LOH in chr.1p36 (61%), 1p31.3 (40%), 1p21.3 (50%) and 1q22–23.2 (56%) in a younger group, and chr. 1p36 (46%), 1p34.2 (48%), and 1q22–23.2 (52%) in an older group. These differences in LOH frequency in these two age groups were significant for chr. 1p21.3(p = 0.025) only. These data suggest that the deletion pattern in early onset breast tumors is not fully identical to late onsetbreast tumors. Similar differential deletion patterns of LOH in the 5 highly deleted regions were seen in premenopausal and postmenopausal groups. An association was seen between LOH at chr.1p34.2 and chr. 23.2 and higher grade of the tumors in older women. Among the highly deleted regions, the deletion at chr.1p36 was found to occur early in both groups because of common allelic loss in the bilateral tumors

Deletion in chromosome 11 and Bcl-1/Cyclin D1 alterations are independently associated with the development of uterine cervical carcinoma

The aim of this study was to understand whether there is any association between specific deleted regions in chromosome 11 (chr.11) and alteration (amplification/rearrangement) of Bcl-1/Cyclin D1 locus, located at 11q13, in uterine cervical carcinoma (CA-CX). Methods: The deletion mapping of chr.11 was studied using 17 highly polymorphic microsatellite markers in 65 primary uterine cervical lesions. The Bcl- 1/Cyclin D1 alterations were analyzed by Southern blot and/or polymerase chain reaction (PCR) method in respective cervical lesions. Results: Chr.11 deletion was found to be significantly associated with progression of CA-CX. High frequency (48–65%) of deletion was found in 11p15.5 (D1), 11q22.3–23.1(D2), and 11q23.3– 24.1(D3) regions and significant association was seen among deletions in D2 and D3 regions. Bcl-1/Cyclin D1 locus alteration was observed in overall 27% cervical lesions. Co-amplification of Bcl-1/Cyclin D1 locus was seen in 10% samples. However, no association was found between the deleted regions and Bcl-1/Cyclin D1 locus alterations. Conclusions: Our study suggests that there is no co-operativity between the deleted regions (D1- D3) in chr.11 and Bcl-1/Cyclin D1 alterations, but these alterations may provide cumulative effect in progression of the tumor. The D1–D3 regions may harbor candidate tumor suppressor gene(s) (TSGs) associated with the development of CA-CX