Devastating aggressive (TURBO) cancer, B-cell lymphoblastic malignant lymphoma, after Pfizer mRNA technology based gene injection vaccine (Malone, Kariko, Weissman) in a mouse model, n=14 mice (note,

by Paul Alexander

only 8 mice were used for FDA to grant EUA approval for the fraud failed BIVALENT (Wuhan and BA4/BA5 sub-variants) booster where the mice even got sick; 8 mice, vs 14 here, so no smack talk on methods

‘case of B-cell lymphoblastic lymphoma following intravenous high-dose mRNA COVID-19 vaccination (Pfizer BNT162b2) in a BALB/c mouse. Two days following booster vaccination (i.e., 16 days after prime), at only 14 weeks of age, our animal suffered spontaneous death with marked organomegaly and diffuse malignant infiltration of multiple extranodal organs (heart, lung, liver, kidney, spleen) by lymphoid neoplasm.’

‘Immunohistochemical examination revealed organ sections positive for CD19, terminal deoxynucleotidyl transferase, and c-MYC, compatible with a B-cell lymphoblastic lymphoma immunophenotype. Our murine case adds to previous clinical reports on malignant lymphoma development following novel mRNA COVID-19 vaccination.’


‘(n=14) was immunized intravenously via the lateral tail vein with the BNT162b2 mRNA COVID-19 vaccine (Pfizer-BioNTech) following a two-dose regimen, while another group (n=14) received normal saline injections and served as control. The second dose of BNT162b2 was administered 14 days after the first priming dose, at 12 and 14 weeks of age, respectively. Each dose contained 6 µg of BNT162b2 diluted in a total volume of 60 µl of normal saline (± 0.25 µg BNT162b2 per gram of body weight). All animals were housed in standard type III plastic cages (with a maximum of seven mice per cage) and maintained at controlled room temperature (20-24°C) and relative humidity (45-65%) under a 12-h light/dark (L/D) cycle. Animals were fed standard pelleted rodent chow and had access to water ad libitum. All treatments and tests were carried out during the light phase of the L/D cycle.’

This is what we mean, Makis, me, McCullough, Hodkinson et al., by TURBO cancer. Aggressive cancer, from initial symtoms to death, often now in days and we have never seen this aggressiveness before, the metastasis is unbelievable, all over the body.

Figure 2

Necropsy examination of organs following spontaneous death. (A) A disproportional enlargement of several of the animal’s major organs was observed at necropsy, including the liver, kidneys, spleen, and intestines (black arrows). (B) Animal with normal phenotype for reference.

Figure 3

Histopathological and immunohistochemical analysis of organs following spontaneous death. (A) At necropsy two days following BNT162b2 booster, heart, liver, kidneys, spleen, lungs, and skeletal muscle were collected and processed for hematoxylin and eosin (HE) staining. Histopathological examination of the organ sections revealed a diffuse and extensive infiltration by medium-sized atypical cells, often completely obliterating the normal parenchyma. The skeletal muscle section showed evidence of systemic leukocytosis without parenchymal abnormalities. (B) Immunohistochemical findings showing staining of medium-sized atypical cells positive for B-cell marker CD19 (left panel), with further nuclear staining positive for terminal deoxynucleotidyl transferase (TdT) (middle panel) and the c-MYC oncoprotein (right panel). Stainings are compatible with a B-cell lymphoblastic lymphoma (B-LBL) immunophenotype.

‘The above histopathological observations suggested extensive, systemic infiltration of the organs by a malignant lymphoid neoplasm, morphologically most suggestive of a Burkitt lymphoma (BL) or B-cell lymphoblastic lymphoma (B-LBL). For confirmation and further differentiation of the lymphoma diagnosis, immunohistochemistry (IHC) was performed using commercially available antibodies against CD19, terminal deoxynucleotidyl transferase (TdT) and c-MYC (see Figure 3B). Anti-CD19 staining (diluted 1:100, catalog no. 90176, Cell Signaling, Danvers, US) confirmed the B-cell origin of the neoplastic cells. Moreover, staining with anti-TdT (diluted 1:200, catalog no. ab85148, Abcam, Cambridge, UK) showed nuclear expression of TdT in the neoplastic cells. TdT is a marker of immaturity expressed in nearly all (i.e., 90 - 95%) LBL cases but lacks in BL (10). Lastly, anti-c-MYC staining (diluted 1:200, catalog no. ab32072, Abcam, Cambridge, UK) demonstrated increased c-MYC expression in the neoplastic cell nuclei, potentially indicating a c-MYC rearrangement as one of the lymphoma driver mutations. Such rearrangement is associated with several hematologic malignancies, including both BL and B-LBL (11). However, in the present case, BL is unlikely due to the TdT expression of the neoplastic cells, strengthening the B-LBL diagnosis.’