Background: Pancreatic cancer is the fourth leading cause of cancer deaths worldwide, a particularly lethal cancer, with the majority of cases dead inside the first year. Mortality statistics have barely changed in over fifty years. Case history: This case history recounts the atypical presentation of a rare pancreatic adenocarcinoma as an aggressive pancreatic pseudocyst, that required multiple drainage/ablative surgeries, mostly in a short time span of 3 months, and recurring. Biopsy revealed its true nature as a rare mucinous adenocarcinoma, by then stage 4 with peritoneal metastases, therefore deemed inoperable, the worst prognosis. Palliative FOLFOX chemotherapy followed by SABR radiotherapy were proposed, with the PARP inhibitor, Olaparib planned as maintenance treatment. These therapies were not expected to radically change the prognostic outlook. However, on compassionate grounds, some experimental therapies, were combined, intended to synergise with the palliative protocols. These therapies included daily high dose methylcobalamin injections, twice weekly, intravenous high dose, vitamin C, liposomal alpha lipoic acid, a ketogenic diet, anti-cachectic medium chain triglyceride oil, high dose vitamin D and a functional food containing colostrum, naturally high in the activated vitamin D binding protein, as well as in lactoferrin, haptocorrin and other immune modulating components. In addition, a quartet of off label drugs, which early research shows have some anti-cancer actions, were prescribed: doxycycline, metformin, atorvastatin and the antiprotozoan drug, mebendazole. Outcome: The patient responded well to these protocols, and was on the road to recovery within 6 months, and in complete remission for almost two years now. The rationale for such therapies is reviewed and analysed, and weighting is assessed for the individual therapies. We propose that such an integrative combination of standard/non standard, research based therapies may provide a blueprint for survival in pancreatic cancer that deserves formal clinical trials. &&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&

Background: Supposed ‘spontaneous’ remissions in chronic lymphocytic leukemia/CLL are extremely rare. By the most stringent immunophenotypic criteria, there are only seven cases to date of unexplained, immune system effected cures. A historic review of this phenomenon is presented as context for this eighth case of CLL immunophenotypic reversal. Case history: A 59-year-old, molecular biologist, stage I CLL, whose diagnosis and recovery were both thoroughly documented, not content to watch and wait, chose to treat himself, after individual tumour susceptibility testing, with evidence based, biological response modifiers, which initially seemed to keep his CLL stable. This included 1mg of hydroxocobalamin injected i.m. daily. However, after some years his lymphocytosis began slowly to drift upwards. At that point, he was persuaded to change his injection protocol to methylcobalamin, at 50 mg i.m. a day, a dose whose clinical safety is sufficiently well established, and a form of cobalamin that the research literature shows has anticancer actions. Outcome: This change in cobalamin form and dose proved a critical turning point. Complete disappearance of the lymphocytosis also coincided with a severe infection and an even further temporary increase of the parenteral methylcobalamin dose, both catalytic factors. In the 4th & 5th years following this, the patient’s repeated immunophenotyping showed no clonal disease present. A brief review of the field of cobalamin in cancer research and treatment is given, with discussion of the various mechanisms by which cobalamins may impact on cancer/CLL. Historic analysis reveals that cyanocobalamin is generally cancer promotional, whereas hydroxocobalamin, methylcobalamin and adenosylcobalamin are cancer protective and cytotoxic. It is hypothesised that the actions of cobalamin in cancer aetiology and oncogenesis/progression are intertwined with those of nitric oxide, which tumours regulate to dupe the immune system to their presence, by causing a functional cobalamin deficiency in the host.