None of these practices are common among the peoples of Zimbabwe or South Africa. The Lemba are also divided into 12 tribes, and among the Buba, the priestly class, was found the exact same DNA element as among those Jews of the priestly class elsewhere around the world.

A number of genetic studies have confirmed the findings. Initial research in 1996 indicated that more than half of the Lemba Y chromosomes (the male chromosome) are Semitic in origin. That study was followed by another in 2000, that reported more specifically that a significant group of Lemba males carry the “Cohen [Kohen] modal haplotype” (CHM) on the Y chromosome, which indicates the Y-DNA Haplogroup J found among Jews and some other populations across the Middle East.

The Buba clan carried most of the CMH markers among the Lemba, similar to other Jewish groups around the world where the males of the priestly class, the Kohenim, carry the CHM marker. Lemba tradition states that it was the Buba clan that had a “leadership role in bringing the Lemba out of Israel” and into southern Africa.

The oral tradition handed down among the Yemenite Jews is similar, stating that after the expulsion following the destruction of the First Temple, the Levi’im (assistant priests) and Kohenim fled towards Yemen; the group then split, with some continuing on towards the south, in the direction of Africa.

The University of London’s Professor Tudor Parfitt , who spent six months living with the tribe, and 20 years researching their people, expressed his amazement in an interview this week with the British Broadcasting Corporation (BBC). Parfitt stated that it appears that the Jewish priesthood continued in the West by people called Cohen, and in the same way it was continued by the priestly clan of the Lemba. They have a common ancestor who geneticists state lived about 3,000 years ago somewhere in north Arabia, which is the time of Moses and Aaron, when the Jewish priesthood started.

The Lemba tradition states that their ancestors fled the Holy Land some 2,500 years ago, traveling first to “Sen’a” and then south to Africa. Their sacred prayer language is comprised of a mixture of Hebrew and Arabic. The tribe, approximately 80,000 strong, lives in central Zimbabwe and the northern part of South Africa, and prizes above all its holiest object: the ngoma lungundu, “the drum that thunders.” According to tribal leaders, it is this, a wooden replica of the Biblical Ark of the Covenant, that connects the Lemba to their Jewish ancestry.

The oral traditions regarding the ngoma lungundu said it had been used in battles, and thus was rebuilt several times, possibly from original remnants, Parfitt explained. He added that the replica that recently went on display at the Harare museum, about 700 years old, is “the closest descendant of the Ark that we know of.”

The Lemba people of today, however, are Christians and Muslims, although many define their ties to Judaism as their “culture.”

When leadership roles were being clarified, the staff of Aaron sprouted almond buds to show that he was chosen by G-d in Numbers 17.  Jeremiah also was shown an almond branch by G-d in his first prophetic vision (Jeremiah 1). The beautifully-blossomed almond tree featured prominently in Israeli celebrations of Tu b’Shevat has a dark side.

Nectar of almond flowers contains 4-10 milligrams per litre of amygdalin, which yields the potent poison cyanide. While sweet almonds are safe for eating (though causing an allergic reaction in some people), wild bitter almonds also contain amounts of amygdalin and could be toxic, especially for young children.

A group of researchers at the Department of Environmental and Evolutionary Biology and the Department of Science Education at the University of Haifa-Oranim investigated why the almond tree produces poison, especially when the purpose of flower nectar is to attract bees, which will pollinate them. They discovered that the lethal substance is actually there to give the lushly-flowered tree an advantage over nearby competitors.

The research team exposed honey bees to plates of nectar that had varying concentrations of the toxin and a plate of nectar without the toxin. The team first monitored four different amygdalin concentrations in the range of the natural levels of toxin typically found in almond tree nectar. A second experiment monitored levels much higher than those found in the natural form. In all cases, the bees preferred nectar containing amygdalin over the amygdalin-free variety. While amygdalin is poisonous for mammals, it is not poisonous for insects, such as the honey bee. In fact, it may act as a stimulant which attracts them.

Another theory is that “expert” bees”, the ones who have been pollinating for some time – will have built up a tolerance to amygdalin, resulting in the arrival of only the most seasoned pollinators at the almond tree. There is a posibility that the nectar toxin prevents bacteria from harming the nectar and threatening the pollination of the tree. Honey made from these almond trees is known to have medicinal properties, such as natural anti-biotics

Two genetic factors were identified. The study, funded by the British Heart Foundation, used gene-chip technology to scan DNA that had previously been identified to contain potential risk areas for heart disease. Farrall emphasized that “the increase in risk to people from high Lp(a) levels is significantly less severe that the risk from high LDL cholesterol levels. Lp(a) doesn’t trump LDL, which has a larger impact and which we can already control pretty effectively.” The aim, he added, is to find a medication that will simultaneously control both.

Another new form of “bad” cholesterol was identified earlier this year by a researcher at the Chinese University of Hong Kong. Khen-Yu Chen, Ph.D. presented his findings at the 238th National Meeting of the American Chemical Society earlier in the year. In an interview published by Science Daily this past August, Chen stated oxycholesterol which at present cannot be controlled by diet or current medications on the market might turn out to be the most serious threat of all to gene-chip technology health.

Oxycholesterol was proved to reduce the elasticity of arteries and impaired their ability to expand and carry more blood throughout the body. It also produced more deposits of cholesterol in the lining of arteries and a tendency to develop larger fatty deposits or atherosclerotic plaques which increase the risk for heart attack and stroke. The work demonstrated that oxycholesterol boosts total cholesterol levels and promotes atherosclerosis (hardening of the arteries) more than non-oxidized cholesterol.

Oxidation occurs when fatty foods are heated. Foods containing high amounts of oxycholesterol include anything fried or highly processed, including the average “fast food.” The good news is that a diet rich in antioxidants can counter these effects and might block the process that forms oxycholesterol. Such a diet includes fresh fruit and vegetables, whole grains, nuts and seeds, and certain herbs and spices.

Under the agreement, OncoGenex retains the right to co-promote the new medication in the United States and Canada. Teva will add the new treatment to its family of branded oncology products elsewhere in the world, including Israel. OGX-011 is a second-generation antisense drug that was co-discovered by OncoGenex and Isis Pharmaceuticals, Inc., which will receive a $10 million payment from OncoGenex as a result of the deal with Teva.

OGX-011 is designed to block production of clusterin, a cell survival protein. Increased clusterin production is observed in many human cancers and in response to many cancer treatments as well. It is linked to faster rates of cancer progression, treatment resistance and shorter survival. OncoGenex conducted five Phase II trials studies in which OGX-011 demonstrated effectiveness in fighting prostate and advanced non-small cell lung cancers. It also appeared to show potential benefit when added to therapy for breast cancer.

They currently have five product candidates in development: OGX-011, OGX-427, OGX-225, SN2310 and CSP-9222.

OGX-011, also known as custirsen sodium, inhibits the production of clusterin, a protein that is associated with treatment resistance in a number of solid tumors, including prostate, breast, non-small cell lung, ovarian, and bladder cancers. It has potential applicability as a therapeutic in a broad number of cancers at different stages and can potentially be used in combination with a variety of commonly used cancer treatments, including chemotherapy, radiation therapy, and hormone ablation therapy. Preliminary data in a Phase 2 clinical trial evaluating OGX-011 in combination with second-line chemotherapy in patients with hormone refractory prostate cancer has shown that retreatment with docetaxel in combination with OGX-011 may reverse docetaxel resistance and improve patient survival. In July 2008, OncoGenex reached an agreement with the U.S. Food and Drug Administration (FDA) on the design of a Phase 3 registration trial of OGX-011 via the Special Protocol Assessment (SPA) process;

OGX-427 is designed to reduce production of Hsp27, a protein that is over-produced in response to many cancer treatments including hormone ablation therapy, chemotherapy and radiation therapy. Hsp27 production has been shown to inhibit cell death in tumor cells through a variety of mechanisms. OGX-427 is in a Phase 1 clinical trial for the treatment of solid tumors including prostate, non-small cell lung, breast, ovarian, and bladder cancers. The company anticipates that the safety profile for OGX-427 as a single agent will be completed in the second half of 2008, and for OGX-427 in combination with chemotherapy in the first half of 2009. Like OGX-011, this product candidate has potential as a treatment in a broad number of cancers;

SN2310 is a novel prodrug of SN-38, which is a potent anti-cancer drug belonging to the class of topoisomerase I inhibitors. SN2310 is designed to enhance the delivery and exposure of SN-38 to the tumor by providing greater prodrug conversion and a longer half-life than achieved with irinotecan. It is currently in a Phase 1 trial and progress is being made to determine its safety and pharmacokinetic profile, in addition to the maximum tolerated dose;

CSP-9222 is a caspase activator presently in pre-clinical development. Caspase activators consist of small molecules that have been identified in preclinical research as activators of programmed cell death. Unlike normal cells, many tumor cell types have lost the ability to undergo the normal process of programmed cell death, known as apoptosis. CSP-9222 has demonstrated anti-tumor activity in a range of pre-clinical animal tumor models, including taxane-resistant tumors, following both intravenous and oral administration. The company expects to move this compound into Phase 1 clinical development within 12-18 months. The caspase program was in-licensed in August 2008 through an exclusive agreement with Bayer HealthCare LLC; and

OGX-225 aims to reduce the production of both Insulin-Like Growth Factor Binding Protein -2 and Insulin-Like Growth Factor Binding Protein -5 with a single product to enhance treatment sensitivity and delay tumor progression. IGFBP-2 and IGFBP-5 are both hormones that make an alternate hormone, IGF-1, available to the tumor that facilitates continued tumor growth. Employing OGX-225 as a single product to simultaneously inhibit the production of both IGFBP-2 and IGFBP-5 has the potential to delay disease progression in a number of cancers that are dependent upon IGF-1 for tumor growth. OGX-225 is in pre-clinical development and has completed pre-clinical pharmacology.

OGX-427 is a second generation antisense drug which in preclinical experiments, inhibits production of Heat Shock Protein 27 (Hsp27) a cell survival protein found at elevated levels in many human cancers including prostate, lung, breast, ovarian, bladder, renal, pancreatic, multiple myeloma and liver cancer. Many anti-cancer therapies are known to further elevate Hsp27 levels. For example, Hsp27 levels increased four-fold in prostate cancer patients after treatment with chemo- or hormone therapy. Increased levels of Hsp27 in some human cancers are associated with metastases, poor prognosis and resistance to radiation or chemotherapy.

Preclinical studies show that OGX-427 significantly decreases levels of Hsp27, induces apoptosis in several human cancer cell lines, has single agent anti-tumor activity, and acts as a chemosensitizer in combination with several cytotoxic drugs including docetaxel.

OGX-427 is being evaluated in a Phase 1 study in patients with breast, prostate, ovarian, non-small cell lung, or bladder cancer who have failed potentially curative treatments or for which a curative treatment does not exist. Patients are being enrolled at clinical sites in Canada and the United States.

Preliminary results of this phase 1 trial were presented during an oral presentation at the ASCO 2009 Annual Meeting. OGX-427 treatment was well tolerated as a monotherapy. No evidence of altered cardiac activity was observed. A majority of adverse events were mild and mainly occurred during the loading doses. The combination of OGX-427 with docetaxel at both dose levels was also well tolerated. This data is subject to further analysis.

Circulating tumor cells (“CTCs”), an emerging metric to assess treatment effect, were evaluated at baseline before treatment and during OGX-427 treatment as a monotherapy. Both total and Hsp27-positive CTCs were evaluated. Declines of 50% or greater in both total and Hsp27-positive CTCs were observed in over one-half of the patients in each cohort and in each type of cancer. Declines in Hsp27 CTCs to 5 or less cells occurred in 27% of patients who had greater than 5 CTCs at baseline. Reduction in tumor markers defined as declines of prostate specific antigen, or PSA, levels in prostate cancer or CA-125 levels in ovarian cancer were also observed. A reduction in PSA level was observed in 7 of 20 patients (35%) with prostate cancer and a reduction in CA-125 levels was observed in 3 of 5 patients (60%) with ovarian cancer.

A second investigator-sponsored phase 1 clinical trial evaluating OGX-427 when administered directly into the bladder in patients with bladder cancer was initiated in August 2009. The study, which will enroll up to 30 patients with bladder cancer, is designed to determine the safety and potential benefit of OGX-427 administered directly into the bladder using a catheter, which is known as intravesical instillation. In addition, the study will measure the direct effect of OGX-427 on expression of Hsp27 in bladder tumor cells as well as determine the pharmacokinetics and pharmacodynamics of OGX-427 when delivered by intravesical instillation. This investigator-sponsored study is funded by the National Cancer Institute of Canada (“NCIC”).

SN2310 is a novel camptothecin for the treatment of cancer. Camptothecins are potent anticancer agents that belong to the family of drugs called topoisomerase I inhibitors that bind reversibly to the TOPO-I-DNA complex causing breaks in the DNA strands during replication resulting in cell death.

There are two camptothecins approved by the FDA: irinotecan (Camptosar) and topotecan (Hycamtin). Irinotecan is approved for the treatment of metastatic colorectal cancer when used as a component of first-line therapy with 5-FU and leucovorin or when disease has recurred or progressed following initial 5-FU- based therapy. Topotecan is approved for second-line treatment of ovarian cancer and small-cell lung cancer. The combined sales of the two drugs were over $1 billion in 2006, with irinotecan sales of over $900 million.

SN-38 is the active metabolite of irinotecan. A major limitation of irinotecan is that the pro-drug requires enzymatic hydrolysis to the active drug, SN-38, and only approximately 3% is hydrolyzed. Based on literature reports, SN-38 is 200 to 2000 times more cytotoxic than irinotecan. SN-38 has not been successfully developed, at least in part due to its poor solubility.

SN2310 Injectable Emulsion is an oil-and-water emulsion that incorporates a new derivative of SN-38, SN2310. The conjugation of SN-38 to Vitamin E succinate enables increased solubility in a vitamin E-based, oil-in-water emulsion that can be administered without dilution. The difference in the structure is shown in the right sidebar.

SN2310 Injectable Emulsion is being developed with the objective of demonstrating improved anti-tumor activity as a result of increased exposure to SN-38 based on a longer half-life. In addition, the product is more convenient, with a shorter duration of administration and no requirement for reconstitution.

In preclinical studies, comparable or better cytotoxic activity in vitro was observed when results after administration of SN2310 were compared to results after administration of irinotecan or topotecan. Similarly, the anti-tumor activity of SN2310 was comparable or better than activity of irinotecan when compared in human tumor xenograft studies. To-date, we have demonstrated that SN2310 provides similar exposure of SN38 as irinotecan at approximately a 15-fold lower dose, with a half-life that is approximately seven-fold higher. Additionally, the Vitamin E chain is separated from SN38 via both enzymatic and hydrolytic cleavage, and in vitro studies suggest that this results in conversion of about 10 times more prodrug to active drug than irinotecan.

In September 2006, Sonus initiated a Phase 1 study of SN2310 which is presently ongoing.

CSP-9222 is the lead compound from a family of caspase activators that have been in-licensed from Bayer Healthcare LLC. These novel, small molecules have been identified as activators of programmed cell death.

Unlike normal cells, many tumor cell types have lost the ability to undergo the normal process of programmed cell death, known as apoptosis. By activating the caspase pathway, tumor cells can be triggered to undergo apoptosis resulting in cell death.

Preclinical data with CSP-9222 in numerous preclinical animal models, including taxane-resistant tumor cells, indicate anti-tumor activity across a broad spectrum of tumor cell types. Both intravenous and oral administration of CSP-9222 has resulted in anti-tumor activity in various animal models. Thus, CSP-9222 offers the potential for a novel therapy in the treatment of a variety of cancers.

They have conducted five Phase 2 clinical trials to evaluate the ability of custirsen sodium (OGX-011), our lead product candidate, to enhance the effects of therapy in prostate, non-small cell lung and breast cancers. Data from these Phase 2 studies demonstrates the potential benefit of adding OGX-011, a second generation antisense molecule, to existing cancer therapies. Based on our Phase 2 results in 294 patients, we believe that registration trials for market approval of OGX-011 are warranted in Castrate Resistant Prostate Cancer (CRPC) and Nonsmall Cell Lung Cancer (NSCLC). Our initial registration trials will focus on the CRPC indication.

OGX-011 is designed to block production of clusterin, a cell survival protein that is over-produced in several cancer indications and in response to many cancer treatments, including hormone ablation therapy, chemotherapy and radiation therapy. Increased clusterin production is observed in many human cancers, including prostate, non-small cell lung, breast, ovarian, bladder, renal, pancreatic, anaplastic large cell lymphoma and colon cancers and melanoma. Increased clusterin production is linked to faster rates of cancer progression, treatment resistance and shorter survival duration. Clusterin levels may be further increased in response to standard cancer therapies, including hormone ablation therapy, chemotherapy and radiation therapy. Clusterin expression is linked to disease progression, treatment resistance, poor prognosis and survival in scientific publications. For example, increased expression of clusterin in prostate cancer is closely correlated with increasing Gleason score, which is a strong prognostic factor for poor survival of patients with prostate cancer.

A broad range of preclinical studies show that OGX-011 decreases clusterin levels and sensitizes tumor cells to standard chemotherapeutic drugs, resulting in increased rates of tumor cell death. Preclinical results also show that reducing clusterin production sensitizes prostate tumor cells to hormone ablation therapy and sensitizes prostate and non-small cell tumor cells to radiation therapy. The Clinical program for OGX-011 is summarized below.

Three Phase 1 clinical trials, involving a total of 75 patients, have been completed with OGX-011. In all of these clinical trials, OGX-011 was well tolerated by the patients.

In the first Phase 1 clinical trial, OGX-011 was intravenously administered once per week in combination with hormone ablation therapy to patients with localized prostate cancer in advance of surgery to remove the prostate gland. This clinical trial showed that once weekly administration of OGX-011 reduced clusterin mRNA levels by approximately 92 percent in prostate cancer tissue and approximately 98 percent in lymph node tissue, and more than doubled the rate of prostate tumor cell death compared to hormone ablation therapy alone.

In the second Phase 1 clinical trial, OGX-011 was intravenously administered once per week in combination with docetaxel chemotherapy to patients with solid tumors known to express clusterin. This clinical trial showed that serum clusterin levels dropped in patients while on treatment with 640 mg OGX-011 in combination with docetaxel.

In the third Phase 1 clinical trial, OGX-011 was intravenously administered once per week in combination with two commonly used chemotherapeutic agents to patients with advanced non-small cell lung cancer. The one-year survival rate for patients that received at least one dose of OGX-011 in combination with these chemotherapies was approximately 60 percent. This compares with results from prior published Phase 3 clinical trials which reported one-year survival rates of 33 to 43 percent for patients that received chemotherapy treatment alone.

They have conducted five phase 2 clinical trials to evaluate the ability of OGX-011 to enhance the effects of therapy in prostate, non-small cell lung and breast cancer. Data is available from each of the five phase 2 studies which demonstrate that adding OGX-011 to therapy shows potential benefit of OGX 011:

• longer survival duration when adding OGX-011 to first-line docetaxel compared to first-line docetaxel alone in patients with CRPC within a randomized phase 2 trial;
• longer survival duration when adding OGX-011 to either mitoxantrone or docetaxel as second-line chemotherapy compared to survival duration observed in two published studies of CRPC patients receiving second-line chemotherapy;
  increased frequency and duration of pain palliation when adding OGX-011 to either mitoxantrone or docetaxel as second-line chemotherapy compared to the frequency and duration of pain palliation observed in the TAX 327 Study for first-line chemotherapy alone in patients with CRPC;
• and longer survival duration when adding OGX-011 to gemcitabine and a platinum-containing chemotherapy compared to the survival duration reported in prior published results from randomized clinical trials in NSCLC patients receiving gemcitabine and a platinum-containing chemotherapy.

Final results of a randomized phase 2 trial evaluating the benefit of combining OGX-011 with first-line docetaxel chemotherapy were presented during an oral presentation at the American Society of Clinical Oncology (“ASCO”) 2009 Annual Meeting. Analyses indicating a survival benefit in patients treated with OGX-011 in combination with first-line docetaxel compared to docetaxel alone, the latter of which being the current standard care for patients with advanced, progressive metastatic prostate cancer, are described below:

• The median overall survival in patients with advanced metastatic prostate cancer who were treated with OGX-011 plus docetaxel in a randomized phase 2 trial was 23.8 months compared to 16.9 months for patients treated with docetaxel alone, indicating a 6.9 month survival advantage in the OGX-011 arm;
• The unadjusted hazard ratio (“HR”), a measure used to compare the death rates between treatment groups, was 0.61, representing a 39% lower rate of death for patients treated with OGX-011;and
• A prospectively defined multivariate analysis indicated that the significant predictors of overall survival were treatment arm, performance status and presence of metastases other than in bone or lymph nodes. In the multivariate analysis, patients treated with OGX-011 had a rate of death of 51% lower than patients treated with docetaxel alone (HR=0.49; p=0.012).
• Additional exploratory analyses found that the lower rate of death was associated with the effect of OGX-011 treatment even when varying amounts of chemotherapy were administered (i.e. OGX-011 treatment resulted in a lower rate of death when compared to the control arm for patients receiving 6 or less cycles of chemotherapy as well as for patients receiving 10 cycles of chemotherapy).
  OGX-011 is being developed to work in combination with therapies that are broadly used by clinicians and considered highly effective in the treatment of each cancer indication that we are targeting with the intent of delaying treatment resistance to those therapies. Since production of clusterin and the resulting treatment resistance occurs in an array of cancer indications and in response to a variety of cancer treatments, we believe that our development options for OGX-011 are numerous.

Phase 1 Clinical Results

• OGX-011 in Combination with Hormone Ablation Therapy in Patients with Localized Prostate Cancer (Clinical Trial OGX-011-01)

For men with localized prostate cancer, hormone ablation therapy with surgery remains the initial standard of care. Hormone ablation causes death of prostate tumor cells.

The purpose of this clinical trial was to:

• determine safety and tolerability and define the recommended Phase 2 dose of OGX-011 when given in combination with hormone ablation therapy;
• determine the concentration and elimination profile of OGX-011 in serum and in the prostate when administered in combination with hormone ablation therapy;
  measure clusterin mRNA and protein levels in the prostate and other tissues and correlate with dose of OGX-011;
  measure serum clusterin levels and correlate with dose of OGX-011; and
• attempt to establish possible correlations between plasma and/or prostate concentrations of OGX-011 with patient response or toxicity measures.
  In order to determine these objectives, OGX-011 was administered in combination with hormone ablation therapy to patients with localized prostate cancer in advance of a surgical procedure to remove the prostate gland.

There were a total of 25 patients enrolled into treatment groups who received increasing doses of OGX-011 from 40 milligrams (mg) up to 640 mg. There was no dose limiting toxicity observed during OGX-011 dose escalation and adverse events were mild to moderate (grade 1 or 2). In summary, the results of the Phase 1 clinical trial of OGX-011 in combination with hormone ablation therapy were that:

• OGX-011 achieved high drug concentrations in the prostate and lymph nodes through once weekly intravenous administration;
• clusterin mRNA was inhibited in prostate tumor cells by more than 92 percent in patients receiving the highest dose of OGX-011 (640 mg);
• approximately double the amount of tumor cell death occurred in the prostate of patients receiving the highest dose of OGX-011 (640 mg) compared to hormone ablation therapy alone;
• OGX-011 was well-tolerated, with no dose limiting toxicity observed; and
• the recommended Phase 2 dose of OGX-011 was established at 640 mg.
• OGX-011 concentration in prostate tissue increased with higher doses, as shown in Figure 1 above. Dose-dependent decreases in clusterin mRNA in prostate tissue were also observed. At the highest dose (640 mg) of OGX-011, clusterin mRNA was decreased by more than 92 percent in prostate tissue when compared to the lowest dose level and other historical controls (patients with no prior hormone ablation therapy and patients with less than two months of hormone ablation therapy).
• Similarly, clusterin mRNA was decreased by approximately 98 percent in lymph node tissue when compared to the lowest dose level (data not shown).

To determine whether suppression of clusterin levels by OGX-011 treatment could increase tumor cell death in prostate cancer tissue, the percentage of dying tumor cells per high powered field of the microscope were counted as shown in Figure 3 below. At the Phase 2 dose (640 mg) the addition of OGX-011 more than doubled the percentage of dying tumor cells compared to hormone ablation therapy alone.

These data demonstrate that OGX-011 was able to:

• be delivered to prostate tumors and lymph nodes;
  get inside tumor cells where it is required in order to potentially have a therapeutic effect;
• significantly decrease clusterin production; and
  increase tumor cell death when combined with hormone ablation therapy.
• Based on achieving high drug concentration in prostate tissue and over 92 percent inhibition of clusterin mRNA in prostate tumor cells and lymph nodes, and a favorable safety profile, 640 mg was selected as the optimal dose for Phase 2 clinical trials of OGX-011.

Patients in this clinical trial experienced various “adverse events”, the majority of which are known to be associated with the other treatments in the protocol (hormone ablation therapy or prostate surgery). An adverse event is any unfavorable and unintended clinical laboratory value or symptom which is encountered during or after the use of an investigational product (i.e. OGX-011). These events may or may not be related to the patient’s disease, other therapies administered to the patient or the investigational product.

None of the events that occurred resulted in patients discontinuing OGX-011 and the majority of the adverse events were considered mild. The adverse events thought to be possibly related to OGX-011 occurred mainly within the first week and decreased with continued dosing. These events included mild suppression of white blood cell counts; flu-like symptoms that included fever, fatigue, and rigors; and mild elevations in liver enzyme levels. Most symptoms went away after one to three weeks despite continued administration of OGX-011.

There were no “serious adverse events” reported during this clinical trial. Serious adverse event means any adverse experience that results in any of the following outcomes: death, a life-threatening experience, inpatient hospitalization or prolongation of existing hospitalization, a persistent or significant disability/incapacity, or a congenital anomaly/birth defect.

OGX-011 in Combination with Docetaxel Chemotherapy in the Treatment of Solid Tumors (Clinical Trial OGX-011-02)

OGX-011 treatment in animal models has been shown to enhance chemosensitivity and to reverse chemotherapy resistance to docetaxel, a chemotherapeutic agent used in a number of cancers including lung, breast, ovarian, bladder, renal cell and hormone refractory prostate cancer. This clinical trial was undertaken to evaluate the safety profile of OGX-011 in combination with docetaxel chemotherapy.

The purpose of this clinical trial was to:

• determine safety and tolerability and define the recommended Phase 2 dose of OGX-011 when given in combination with docetaxel chemotherapy given either weekly or every three weeks;
• determine the concentration of OGX-011 and docetaxel in serum when administered in combination;
  measure evidence of the effect of OGX-011 on serum clusterin levels; and
• document any objective tumor responses.

In order to determine these objectives, OGX-011 was administered in combination with docetaxel chemotherapy to patients with cancers known to over-produce clusterin (prostate, non-small cell lung, breast, ovary, bladder and renal cell).

There were a total of 40 patients enrolled into treatment groups who received increasing doses of OGX-011 from 40 mg up to 640 mg. In addition to OGX-011 treatment, patients also received docetaxel chemotherapy given either as a weekly or every three week schedule as one cycle. The clinical trial was conducted at multiple clinical sites.

Although this was a group of patients with various cancer types, responses and stable disease were documented. OGX-011 treatment resulted in a trend towards dose dependent decreases in serum clusterin levels with the 640 mg dose level having the greatest change from baseline. There was no evidence that administration of OGX-011 affected the metabolism of docetaxel chemotherapy or that docetaxel chemotherapy affected the metabolism of OGX-011.

The recommended OGX-011 dose for treatment in combination with docetaxel chemotherapy was determined as 640 mg, based on acceptable safety results, documented responses/stable disease, and lowering of serum clusterin levels observed from this Phase 1 clinical trial.

Patients in this clinical trial experienced various adverse events, the majority of which are known to be associated with the other treatment in the protocol (docetaxel chemotherapy). Adverse events associated with docetaxel chemotherapy include reduced appetite, nausea, hair loss and decrease in blood counts.

Adverse events were primarily mild to moderate. The incidence of reduced appetite, nausea and hair loss increased as the OGX-011 dose levels increased. The decrease in white blood cell counts was consistent with other trials using docetaxel and did not decrease further with increased doses of OGX-011. Five of the 40 patients experienced dose-limiting toxicity. Four of these events were attributed to the docetaxel chemotherapy and one, fatigue, was attributed to the combination of OGX-011, docetaxel and the disease. Six of the 40 patients experienced a serious adverse event. All of these events were attributed to the docetaxel chemotherapy, except a case of upper gastrointestinal bleeding which was attributed to the combination of OGX-011 and docetaxel chemotherapy.

Phase 2 Clinical Trial Results

The Phase 1 clinical trials evaluated the safety and established the recommended Phase 2 dose of OGX-011 in combination with either docetaxel chemotherapy (two different schedules), gemcitabine/cisplatin chemotherapy or hormone ablation therapy. In all clinical trials, 640 mg was established as the Phase 2 dose.

They have conducted five Phase 2 clinical trials of OGX-011 to further evaluate the safety and efficacy of OGX-011 in combination with various cancer therapies for prostate, non-small cell lung and breast cancer, as further described below on the OncoGenex web site.

Prostate Cancer
Final Results of Phase 2 Clinical Trial in Patients Receiving
First-Line Chemotherapy Treatment for Castrate Resistant Prostate Cancer (Study OGX-011-03)
Phase 2 Clinical Trial - Hormone Ablation Therapy in Patients with Localized Prostate Cancer (Study OGX-011-04)
Preliminary Results of a Phase 2 Clinical Trial in Patients Receiving Second-Line Chemotherapy for Treatment of Hormone Refractory Prostate Cancer (Study OGX-011-07)

Lung Cancer
Preliminary Results of Phase 2 Clinical Trial in Patients Treated with First-Line Chemotherapy for Non-Small Cell Lung Cancer (Study OGX-011-05)

Breast Cancer
Preliminary Results of Phase 2 Clinical Trial in Patients with Advanced Breast Cancer (OGX-011-06)

G-d Bless Israel: Teva shares trading on the Tel Aviv Stock Exchange on December 22, 2009, rose 2.42% from their previous day’s level, and continued to rise in after hours trading. The stock reached its all time high on the TASE Tuesday, closing at 206.5 shekels a share. The rise was partially due to Teva’s announcement of its purchase on Monday of OncoGenex.

The dwelling and older discoveries of nearby tombs in burial caves suggest that Nazareth was an out-of-the-way hamlet of around 50 houses on a patch of about 1.6 hectares. Archaeologist Yardena Alexandre, stated it was evidently populated by Jews of modest means who kept camouflaged grottos to hide from Roman invaders.
Alexandre’s team found a camouflaged entry way into a grotto, which was used by Jews at the time to hide from Roman soldiers who were battling Jewish rebels at the time for control of the area. The grotto would have hid around six people for a few hours. Similar camouflaged grottos were found in other ancient Jewish communities of the lower Galilee such as the nearby biblical village of Cana, which did witness battle between Jews and Romans. However, Roman soldiers did not end up battling Nazareth’s Jews because the hamlet had little strategic value at the time. The Roman army was more interested in larger towns and strategic hilltop communities.

Alexandre’s team found remains of a wall, a hideout, a courtyard and a water system that appeared to collect water from the roof and supply it to the home. The discovery was made when builders dug up the courtyard of a former convent to make room for a new Christian centre, just meters away from a Basilica. It was not clear how big the dwelling is, however Alexandre’s team have uncovered about 85 square metres of the house, which may have been for an extended family and could be much larger.

As workers at the site carefully chipped away at mud with small pickaxes to reveal stone walls, archaeologists found clay and chalk vessels which were likely used by Galilean Jews of the time. Based on clay and chalk shards found at the site, the dwelling appeared to house a “simple Jewish family.” The scientists concluded a Jewish family lived there because of the chalk, which was used by Jews at the time to ensure the purity of the food and water kept inside the vessels. The shards date back to the time of Jesus, which includes the late Hellenic, early Roman period that ranges from around 100 B.C. to 100 A.D.. The determination was made by comparing the findings to shards and remains found in other parts of the Galilee typical of that period.

The absence of any remains of glass vessels or imported products suggested the family who lived in the dwelling were “simple,” since the remains did not indicate whether they were traders or farmers. The only other artifacts that archeologists have found in the Nazareth area from the time of Jesus are ancient burial caves outside the hamlet, providing a rough idea of the village’s population at the time.

Work is now taking place to clear newer ruins built above the dwelling, which will be preserved. The dwelling will become a part of a new international Christian centre being constructed close to the site and funded by a French Roman Catholic group. Alexandre stated limited space and population density in Nazareth means it is unlikely that archeologists can carry out any further excavations in the area, leaving this dwelling to tell the story of what Jesus’ boyhood home may have looked like.

The shroud was found in this 1 CE cemetery (Israel Antiquities Authority)

The Hebrew University’s Prof. Mark Spigelman, one of the leading researchers who studied the molecular evidence from the tomb, believes the isolation was due to the fact that the shrouded man suffered from leprosy and died of tuberculosis. The DNA of both diseases was found in his bones. The excavation also found a clump of the shrouded man’s hair, which had been ritually cut prior to his burial. These are both unique discoveries, as explained by Hebrew University spokespeople, because organic remains are hardly ever preserved in the Jerusalem area owing to high humidity levels in the ground.

The evidence revealed by the remains indicate that tuberculosis and leprosy may have crossed social boundaries in the first-century C.E. Jerusalem. A number of clues included the size of the tomb, its location alongside a High Priest, the type of textiles used as shroud wrappings and the clean state of the man’s hair; suggest that the shrouded individual was a fairly affluent member of society in Jerusalem or a priest himself. According to Prof. Shimon Gibson of Hebrew University, the tomb would have faced directly toward the Jewish Temple of the time.

This is the first time fragments of a burial shroud have been found from the time Jesus was alleged to have been active in Jerusalem. The shroud found in the cave known as the Tomb of the Shroud, is very different from that of the Shroud of Turin, which was claimed to be the one used to wrap the body of Jesus. Unlike the complex weave of the Turin Shroud, the recently discovered shroud is made up of a simple two-way weave, as the textiles historian Dr. Orit Shamir was able to show.

The burial shroud may disprove the claim that the Shroud of Turin is from first-century Jerusalem. Based on the assumption that this is representative of a typical burial shroud widely used at the time of Jesus, researchers concluded that the Turin Shroud did not originate from Second Temple-era Jerusalem. Further details of the discovery are published in the December 16, 2009, issue of PloS ONE Journal for peer-reviewed scientific and medical research.

There are two entrances to the ruins

The ruins were first discovered in 1934. The synagogue dates back to the fourth century, and Jews apparently abandoned it in the eighth century, during the beginning of Muslim rule. Dr. Doron Sar-Avi, explained that most ruins, such as those from the same period of time near Susiya (a Jewish town in the southern Hevron hills), happen to be in Jewish communities. Several Arab homes in Samoa include doorposts that stood in the ruins, including a depiction of menorahs.

Former place of altar and Holy Ark

Shavei Israel works in nine countries to bring back to Judaism “hidden Jews,” who themselves or their parents or ancestors were forced to practice the religion secretly. Its founder Michael Freund stated that iIn recent years, an increasing number of Poles have rediscovered their Jewish ancestry, seeking to reclaim the precious heritage that was so brutally taken from them and their forebears. It is our hope that this book will…enable a new generation of Polish Jews to celebrate Chanukah with joy, as well as gain a better understanding of our eternal faith, its principles and beliefs.

Approximately 4,000 Jews are officially registered as living in Poland, but according to various estimates, there are tens of thousands of others who have concealed their true identity, or are simply unaware of it.

Many of the “hidden Jews” in Poland lost all contact with Judaism due to extreme anti-Semitism after the Holocaust, and some of them even converted. Others concealed their Jewishness from the Communist authorities and now feel free to resume their true identity.

Another phenomenon pertains to Jewish young people who were adopted by Catholic families and institutions during the Holocaust. They were told nothing of their Jewish identity, and only in recent years have they or their descendants gradually begun to rediscover it.

Shavei Israel also provides assistance to different communities, such as the Bnei Menashe of India, the Bnei Anousim in Spain, Portugal and South America, the Subbotnik Jews of Russia, the Jewish community of Kaifeng in China as well as the “hidden Jews” of Poland.

Its emissaries in Poland conduct seminars in Poland and provide assistance for the process of conversion to those who choose to immigrate to Israel.

Through the years, the British military’s investigations generated thousands of pages of secret documents, many of which have been released by the National Archives after they were declassified. The UFO document release made clear that the British military had devoted considerable resources to the question of extraterrestrial life. Some UFO sightings seemed credible, such as a 1984 report by a number of air traffic controllers who stated they saw an unidentified aircraft land at a small airport, then take off at tremendous speed.

The U.S. Air Force says it has not investigated UFO sightings since 1969, when it ended Project Blue Book, which examined more than 12,600 reported UFO sightings; including 700 that were never explained. The federal funding for the U.S. SETI project listened for any signals from alien civilizations. Canada still investigates UFO reports or any other “threat to the Canadian sovereignty.

Such investigations of “The EX-Files, Extraterrestrial life and UFO’s” has been one of the biggest mysteries of all time. Is it possible that Biblical scholars have the answer?

The treatment is non-invasive, has no side effects and damages only the cancerous cell, without damaging the healthy cells that surround it.

The laboratory is located at the Laurie I. Lokey Interdisciplinary Center for Life Sciences and Engineering, which was built in 2006 with major support of $30 million from philanthropist Lauri Lokey.

The cutting-edge research has stimulated interest both locally and on the international front, winning additional grants of two million euros from the European Union and more than $1 million from the Israel Science Foundation. Millions of dollars were invested to equip the new laboratory, headed by Nobel Laureate, Professor Aaron Ciechanover.

The multidisciplinary laboratory includes researchers from the fields of physics, optics, biology, engineering and biomedical nanotechnology and is currently engaged in a number of innovative projects, all of which are linked to advanced diagnostics and medical treatment.

Dr. Dvir Yelin, a researcher at the center explained the tumor is illuminated via an endoscopic laser-based miniature optical fiber. The laser has two parameters: one, it consists of very short pulses, at millions of billionths of a second that can break down the cell without heat; and two, the laser has a wavelength that precisely fits the resonant frequency of nano-particles, which makes it possible to highly increase the efficiency of the laser.

Under these conditions, the laser operates at a distance of nanometers (a millionth of a millimeter) from a nanoparticle, and creates sufficiently intense laser illumination to dismantle, through ionization, the material within the cancer cell, which then dies without damage to the surrounding healthy cells, he explained.

The treatment is relative to an equally cutting-edge diagnostic test recently developed by a research group headed by Hossam Haick, also at the Technion, in which a breath test using an array of sensors based on gold nanoparticles is used to distinguish the breath of lung cancer patients from that of healthy individuals in an atmosphere of high humidity.

The team is working to develop an inexpensive and non-invasive diagnostic test for lung cancer based on the study, which was published in the journal Nature Nanotechnology.