Thread by @_HeartofGrace_

1/ 🧵💉BOOSTERS: There's much talk about BOOSTERS containing something different compared to the previous formulations--theories that they lead to cancer/disease because of a different ingredient.

Instead, perhaps, it is what is called the "multi-hit" cancer theory.

2/ The multi-hit theory states cancer is not caused by a single genetic mutation but a series of genetic "hits" which accumulate over time. These genetic changes occur in specific genes, leading to uncontrolled cell growth and the formation of a tumor, leading to cancer.

3/ The steps in the "multi hit" cancer theory are:
1. initiation of the cancer process is caused by a single point mutation of a gene. This mutation can be spontaneous or triggered by exposure to carcinogens such as tobacco smoke, radiation, or...(plasmid DNA?)

4/ 2. After initiation, the mutated cell needs more genetic changes to develop full-blown cancer. These additional mutations are acquired during the promotion stage. Promotion can involve various factors like inflammation, hormonal influences, and additional genetic mutations.

5/ 3. In the final stage, called "progression" the tumor continues to evolve and grow. More genetic mutations accumulate, leading to malignancy and invasiveness. This can result in tumor spreading to nearby tissues and eventually metastasizing to distant organs.

6/ The types of cancer depend on how many HITS occur. Some only take TWO hits.
The following are examples which can occur, and how many "hits" it takes to get there.
A. Mutations in BRCA1/BRCA2 genes are associated with an increased risk of breast, ovarian, and other cancers.

7/ B. Mutations in the TP53 gene, also known as "guardian of the genome," are found in many types of cancer, including breast, colorectal, and lung cancer.
C. KRAS mutations are commonly found in pancreatic, colorectal, and lung cancer.
D. Epidermal Growth Factor Receptor:

8/ (EGFR) mutations are seen in lung cancer.
E. Human Epidermal Growth Factor Receptor 2 (HER2) mutations are associated with breast and ovarian cancer.
F. BRAF mutations are found in melanoma, colorectal, and thyroid cancer.

Not all cancers will do this. Many mechanisms

9/ exist in the body to fight back against these things--some people are more genetically predispositioned to have a higher risk of cancer. Two people could have the same exposures--one might develop cancer, one might not. My friend's mom and her sister are in their 90s, and they

10/ are Irish Catholic, drink Mickey's, and smoke every day. They are both sharp as tacks, love debating politics, have fun, and are still physically active. No cancer there (I love them).

There have been reports that appendicitis is a safety signal of the current vaccines:

11/ Appendiceal cancer ( mucinous adenocarcinoma )of the appendix, is associated with mutations in KRAS gene. Reports are coming in from Pathologists seeing an increase in the tissues they are testing as having appendiceal cancer.

.pubmed.ncbi.nlm.nih.gov/34746743/#:~:t…

12/ Risk factors for cancer: Genetic predisposition, environmental, random mutations, infectious agents, and diversity in population.

It would be a terrible thing, if viruses were reactivated in people, that are linked to cancers.

The following are viruses linked to cancer:

13/ HPV, Hep B and C, Epstein-Barr, and Human T-cell Lymphotropic Virus-1.
HPV: cervical, anal, and oropharyngeal cancers.
Hep: liver cancer (hepatocellular carcinoma.
EBV: Burkitt's lymphoma, nasopharyngeal carcinoma, and certain types of lymphomas.
HTLV-1:leukemia/lymphoma

14/Back to hits and cancer: Somatic mutations are genetic alterations that occur in a person's cells during their lifetime and are not inherited. These mutations can accumulate over time due to various factors, including exposure to carcinogens, DNA replication errors, etc.

15/ In these cancers, we are looking at somatic mutations.
Somatic mutations are limited to the specific tissues or cells in which they occur. They do not affect the entire organism or get passed on to offspring.

16/ Regarding DNA plasmids landing in a transfection agent, containing a nuclear localization signal (to help it get into the nucleus of cells) at a rate of billion(s) per dose, they can enter during telophase. During telophase,

17/the nuclear envelope reforms around separated sets of chromosomes, enclosing the genetic material in the nucleus. For genetic material to enter the nucleus during this phase, it would need to pass through the reformed nuclear envelope, which is a highly regulated process.

18/ cell type most susceptible to genetic mutations vary, but rapidly dividing cells might be more susceptible. Cells actively undergoing mitosis or meiosis, such as certain stem cells or cells involved in tissue repair, have a higher propensity for DNA replication and division.

20/Cells that undergo frequent cell division in the human body: 1:Skin Epithelial Cells,2: Intestinal Epithelial Cells, 3: Blood Cells, 4:Bone Cells,5: Stem Cells, and 6: Liver Cells.
Respective cancers:
1: basal cell carcinoma, squamous cell carcinoma, and melanoma.

21/ 2: colorectal cancer and other gastrointestinal cancers
3:blood cancers, such as leukemia, lymphoma, and multiple myeloma.
6:liver cancer, including hepatocellular carcinoma.
5: breast cancer

22/ Not meant to treat or DX. This is the multi hit theory. These are not happening to everyone, but this theory might explain why the more exposure you have to a carcinogen or gene mutation event, the higher risk you are at.

ncbi.nlm.nih.gov/pmc/articles/P…

23/ Are either of you gentlemen seeing a higher number of specific cancers that are lower in hits on your data sets?

@EthicalSkeptic
@DowdEdward

@NestCommander
@Doctor_I_am_The
@53v3n0fn1n3
@SenatorRennick
@Johnincarlisle
@JohnBoweActor
@PierreKory

Type of cancer by estimated new cases by estimated deaths.
Anxious to see @EthicalSkeptic and @DowdEdward data confirmations.

cancer.gov/types/common-c…